Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
Immunoglobulins produced in response to VIRAL ANTIGENS.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
Antibodies produced by a single clone of cells.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
Antibodies that reduce or abolish some biological activity of a soluble antigen or infectious agent, usually a virus.
A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
A form of fluorescent antibody technique commonly used to detect serum antibodies and immune complexes in tissues and microorganisms in specimens from patients with infectious diseases. The technique involves formation of an antigen-antibody complex which is labeled with fluorescein-conjugated anti-immunoglobulin antibody. (From Bennington, Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
A measure of the binding strength between antibody and a simple hapten or antigen determinant. It depends on the closeness of stereochemical fit between antibody combining sites and antigen determinants, on the size of the area of contact between them, and on the distribution of charged and hydrophobic groups. It includes the concept of "avidity," which refers to the strength of the antigen-antibody bond after formation of reversible complexes.
A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Local surface sites on antibodies which react with antigen determinant sites on antigens (EPITOPES.) They are formed from parts of the variable regions of FAB FRAGMENTS.
A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.
Antibodies reactive with HIV ANTIGENS.
Serological reactions in which an antiserum against one antigen reacts with a non-identical but closely related antigen.
Sites on an antigen that interact with specific antibodies.
Immunoglobulins induced by antigens specific for tumors other than the normally occurring HISTOCOMPATIBILITY ANTIGENS.
Immunoglobulins produced in a response to PROTOZOAN ANTIGENS.
Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement.
Chronic inflammatory and autoimmune disease in which the salivary and lacrimal glands undergo progressive destruction by lymphocytes and plasma cells resulting in decreased production of saliva and tears. The primary form, often called sicca syndrome, involves both KERATOCONJUNCTIVITIS SICCA and XEROSTOMIA. The secondary form includes, in addition, the presence of a connective tissue disease, usually rheumatoid arthritis.
A chronic self-perpetuating hepatocellular INFLAMMATION of unknown cause, usually with HYPERGAMMAGLOBULINEMIA and serum AUTOANTIBODIES.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
An idiopathic vascular disorder characterized by bilateral Raynaud phenomenon, the abrupt onset of digital paleness or CYANOSIS in response to cold exposure or stress.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
Arthritis of children, with onset before 16 years of age. The terms juvenile rheumatoid arthritis (JRA) and juvenile idiopathic arthritis (JIA) refer to classification systems for chronic arthritis in children. Only one subtype of juvenile arthritis (polyarticular-onset, rheumatoid factor-positive) clinically resembles adult rheumatoid arthritis and is considered its childhood equivalent.
Inflammation of the iris characterized by circumcorneal injection, aqueous flare, keratotic precipitates, and constricted and sluggish pupil along with discoloration of the iris.
Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals.
A syndrome with overlapping clinical features of systemic lupus erythematosus, scleroderma, polymyositis, and Raynaud's phenomenon. The disease is differentially characterized by high serum titers of antibodies to ribonuclease-sensitive extractable (saline soluble) nuclear antigen and a "speckled" epidermal nuclear staining pattern on direct immunofluorescence.
Autoantibodies directed against cytoplasmic constituents of POLYMORPHONUCLEAR LEUKOCYTES and/or MONOCYTES. They are used as specific markers for GRANULOMATOSIS WITH POLYANGIITIS and other diseases, though their pathophysiological role is not clear. ANCA are routinely detected by indirect immunofluorescence with three different patterns: c-ANCA (cytoplasmic), p-ANCA (perinuclear), and atypical ANCA.
Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory IgA (IMMUNOGLOBULIN A, SECRETORY) is the main immunoglobulin in secretions.
Immunoglobulins produced in a response to FUNGAL ANTIGENS.
A term used to describe a variety of localized asymmetrical SKIN thickening that is similar to those of SYSTEMIC SCLERODERMA but without the disease features in the multiple internal organs and BLOOD VESSELS. Lesions may be characterized as patches or plaques (morphea), bands (linear), or nodules.
FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cirrhosis involves the destruction of small intra-hepatic bile ducts and bile secretion. Secondary biliary cirrhosis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).
The measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).
The processes triggered by interactions of ANTIBODIES with their ANTIGENS.
Antibodies, often monoclonal, in which the two antigen-binding sites are specific for separate ANTIGENIC DETERMINANTS. They are artificial antibodies produced by chemical crosslinking, fusion of HYBRIDOMA cells, or by molecular genetic techniques. They function as the main mediators of targeted cellular cytotoxicity and have been shown to be efficient in the targeting of drugs, toxins, radiolabeled haptens, and effector cells to diseased tissue, primarily tumors.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Antibodies which elicit IMMUNOPRECIPITATION when combined with antigen.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Inflammation of any part of the KIDNEY.
A form of antibodies consisting only of the variable regions of the heavy and light chains (FV FRAGMENTS), connected by a small linker peptide. They are less immunogenic than complete immunoglobulin and thus have potential therapeutic use.
The protein components that constitute the common core of small nuclear ribonucleoprotein particles. These proteins are commonly referred as Sm nuclear antigens due to their antigenic nature.
Immunologic techniques based on the use of: (1) enzyme-antibody conjugates; (2) enzyme-antigen conjugates; (3) antienzyme antibody followed by its homologous enzyme; or (4) enzyme-antienzyme complexes. These are used histologically for visualizing or labeling tissue specimens.
Antibodies that inhibit the reaction between ANTIGEN and other antibodies or sensitized T-LYMPHOCYTES (e.g., antibodies of the IMMUNOGLOBULIN G class that compete with IGE antibodies for antigen, thereby blocking an allergic response). Blocking antibodies that bind tumors and prevent destruction of tumor cells by CYTOTOXIC T-LYMPHOCYTES have also been called enhancing antibodies. (Rosen et al., Dictionary of Immunology, 1989)
Inflammation of a serous membrane.
A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.
Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Substances that are recognized by the immune system and induce an immune reaction.
Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
Inflammation of a muscle or muscle tissue.
Immunologically detectable substances found in the CELL NUCLEUS.
Antiphospholipid antibodies found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase IMMUNOASSAY employing the purified phospholipid antigen CARDIOLIPIN.
Antibodies elicited in a different species from which the antigen originated. These antibodies are directed against a wide variety of interspecies-specific antigens, the best known of which are Forssman, Hanganutziu-Deicher (H-D), and Paul-Bunnell (P-B). Incidence of antibodies to these antigens--i.e., the phenomenon of heterophile antibody response--is useful in the serodiagnosis, pathogenesis, and prognosis of infection and latent infectious states as well as in cancer classification.
Diagnostic procedures involving immunoglobulin reactions.
Antibodies that can catalyze a wide variety of chemical reactions. They are characterized by high substrate specificity and share many mechanistic features with enzymes.
Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.
Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)
A form of lupus erythematosus in which the skin may be the only organ involved or in which skin involvement precedes the spread into other body systems. It has been classified into three forms - acute (= LUPUS ERYTHEMATOSUS, SYSTEMIC with skin lesions), subacute, and chronic (= LUPUS ERYTHEMATOSUS, DISCOID).
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.
A genus of parasitic protozoans found in the digestive tract of invertebrates, especially insects. Organisms of this genus have an amastigote and choanomastigote stage in their life cycle.
Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure MONOCLONAL ANTIBODIES or T-cell products, identical to those produced by the immunologically competent parent cell.
Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.
A chronic form of cutaneous lupus erythematosus (LUPUS ERYTHEMATOSUS, CUTANEOUS) in which the skin lesions mimic those of the systemic form but in which systemic signs are rare. It is characterized by the presence of discoid skin plaques showing varying degrees of edema, erythema, scaliness, follicular plugging, and skin atrophy. Lesions are surrounded by an elevated erythematous border. The condition typically involves the face and scalp, but widespread dissemination may occur.
A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.
Methods used for studying the interactions of antibodies with specific regions of protein antigens. Important applications of epitope mapping are found within the area of immunochemistry.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).
Small RNAs found in the cytoplasm usually complexed with proteins in scRNPs (RIBONUCLEOPROTEINS, SMALL CYTOPLASMIC).
Established cell cultures that have the potential to propagate indefinitely.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
Positive test results in subjects who do not possess the attribute for which the test is conducted. The labeling of healthy persons as diseased when screening in the detection of disease. (Last, A Dictionary of Epidemiology, 2d ed)
Elements of limited time intervals, contributing to particular results or situations.
Complexes of RNA-binding proteins with ribonucleic acids (RNA).
Substances elaborated by bacteria that have antigenic activity.
An encapsulated lymphatic organ through which venous blood filters.
A subacute or chronic inflammatory disease of muscle and skin, marked by proximal muscle weakness and a characteristic skin rash. The illness occurs with approximately equal frequency in children and adults. The skin lesions usually take the form of a purplish rash (or less often an exfoliative dermatitis) involving the nose, cheeks, forehead, upper trunk, and arms. The disease is associated with a complement mediated intramuscular microangiopathy, leading to loss of capillaries, muscle ischemia, muscle-fiber necrosis, and perifascicular atrophy. The childhood form of this disease tends to evolve into a systemic vasculitis. Dermatomyositis may occur in association with malignant neoplasms. (From Adams et al., Principles of Neurology, 6th ed, pp1405-6)
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.
Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of the Wassermann-type antigen that is used in nontreponemal SYPHILIS SERODIAGNOSIS.
Transfer of immunity from immunized to non-immune host by administration of serum antibodies, or transplantation of lymphocytes (ADOPTIVE TRANSFER).
The presence of antibodies directed against phospholipids (ANTIBODIES, ANTIPHOSPHOLIPID). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (ANTIBODIES, ANTICARDIOLIPIN). Present also are high levels of lupus anticoagulant (LUPUS COAGULATION INHIBITOR).
Proteins prepared by recombinant DNA technology.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
Serum globulins that migrate to the gamma region (most positively charged) upon ELECTROPHORESIS. At one time, gamma-globulins came to be used as a synonym for immunoglobulins since most immunoglobulins are gamma globulins and conversely most gamma globulins are immunoglobulins. But since some immunoglobulins exhibit an alpha or beta electrophoretic mobility, that usage is in decline.
A broad-specificity HLA-DR antigen that is associated with HLA-DRB1 CHAINS encoded by DRB1*11 and DRB1*12 alleles.
Partial immunoglobulin molecules resulting from selective cleavage by proteolytic enzymes or generated through PROTEIN ENGINEERING techniques.
The sum of the weight of all the atoms in a molecule.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
Substances elaborated by viruses that have antigenic activity.
Highly conserved nuclear RNA-protein complexes that function in RNA processing in the nucleus, including pre-mRNA splicing and pre-mRNA 3'-end processing in the nucleoplasm, and pre-rRNA processing in the nucleolus (see RIBONUCLEOPROTEINS, SMALL NUCLEOLAR).
Glands that secrete SALIVA in the MOUTH. There are three pairs of salivary glands (PAROTID GLAND; SUBLINGUAL GLAND; SUBMANDIBULAR GLAND).
Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.
Antigens determined by leukocyte loci found on chromosome 6, the major histocompatibility loci in humans. They are polypeptides or glycoproteins found on most nucleated cells and platelets, determine tissue types for transplantation, and are associated with certain diseases.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
Within most types of eukaryotic CELL NUCLEUS, a distinct region, not delimited by a membrane, in which some species of rRNA (RNA, RIBOSOMAL) are synthesized and assembled into ribonucleoprotein subunits of ribosomes. In the nucleolus rRNA is transcribed from a nucleolar organizer, i.e., a group of tandemly repeated chromosomal genes which encode rRNA and which are transcribed by RNA polymerase I. (Singleton & Sainsbury, Dictionary of Microbiology & Molecular Biology, 2d ed)
Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.
A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Sensitive tests to measure certain antigens, antibodies, or viruses, using their ability to agglutinate certain erythrocytes. (From Stedman, 26th ed)
Measurement of rate of settling of erythrocytes in anticoagulated blood.
Serologic tests in which a known quantity of antigen is added to the serum prior to the addition of a red cell suspension. Reaction result is expressed as the smallest amount of antigen which causes complete inhibition of hemagglutination.
That region of the immunoglobulin molecule that varies in its amino acid sequence and composition, and comprises the binding site for a specific antigen. It is located at the N-terminus of the Fab fragment of the immunoglobulin. It includes hypervariable regions (COMPLEMENTARITY DETERMINING REGIONS) and framework regions.
EPIDEMIOLOGIC STUDIES based on the detection through serological testing of characteristic change in the serum level of specific ANTIBODIES. Latent subclinical infections and carrier states can thus be detected in addition to clinically overt cases.
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
Commercially prepared reagent sets, with accessory devices, containing all of the major components and literature necessary to perform one or more designated diagnostic tests or procedures. They may be for laboratory or personal use.
INFLAMMATION of salivary tissue (SALIVARY GLANDS), usually due to INFECTION or injuries.
An excess of GAMMA-GLOBULINS in the serum due to chronic infections or PARAPROTEINEMIAS.
Unique genetically-controlled determinants present on ANTIBODIES whose specificity is limited to a single group of proteins (e.g., another antibody molecule or an individual myeloma protein). The idiotype appears to represent the antigenicity of the antigen-binding site of the antibody and to be genetically codetermined with it. The idiotypic determinants have been precisely located to the IMMUNOGLOBULIN VARIABLE REGION of both immunoglobin polypeptide chains.
Techniques used to demonstrate or measure an immune response, and to identify or measure antigens using antibodies.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
The acquired form of infection by Toxoplasma gondii in animals and man.
Mouse strains constructed to possess identical genotypes except for a difference at a single gene locus.
Proteins, glycoprotein, or lipoprotein moieties on surfaces of tumor cells that are usually identified by monoclonal antibodies. Many of these are of either embryonic or viral origin.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Techniques for removal by adsorption and subsequent elution of a specific antibody or antigen using an immunosorbent containing the homologous antigen or antibody.
Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
A mouse substrain that is genetically predisposed to the development of systemic lupus erythematosus-like syndrome, which has been found to be clinically similar to the human disease. It has been determined that this mouse strain carries a mutation in the fas gene. Also, the MRL/lpr is a useful model to study behavioral and cognitive deficits found in autoimmune diseases and the efficacy of immunosuppressive agents.
Enlargement of the spleen.
The phenomenon of immense variability characteristic of ANTIBODIES. It enables the IMMUNE SYSTEM to react specifically against the essentially unlimited kinds of ANTIGENS it encounters. Antibody diversity is accounted for by three main theories: (1) the Germ Line Theory, which holds that each antibody-producing cell has genes coding for all possible antibody specificities, but expresses only the one stimulated by antigen; (2) the Somatic Mutation Theory, which holds that antibody-producing cells contain only a few genes, which produce antibody diversity by mutation; and (3) the Gene Rearrangement Theory, which holds that antibody diversity is generated by the rearrangement of IMMUNOGLOBULIN VARIABLE REGION gene segments during the differentiation of the ANTIBODY-PRODUCING CELLS.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
A collection of cloned peptides, or chemically synthesized peptides, frequently consisting of all possible combinations of amino acids making up an n-amino acid peptide.
Enzymes which catalyze the hydrolases of ester bonds within DNA. EC 3.1.-.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
Antibodies to the HEPATITIS C ANTIGENS including antibodies to envelope, core, and non-structural proteins.
Proteins conjugated with nucleic acids.
Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.
The classes of immunoglobulins found in any species of animal. In man there are nine classes that migrate in five different groups in electrophoresis; they each consist of two light and two heavy protein chains, and each group has distinguishing structural and functional properties.
A chronic inflammatory condition affecting the axial joints, such as the SACROILIAC JOINT and other intervertebral or costovertebral joints. It occurs predominantly in young males and is characterized by pain and stiffness of joints (ANKYLOSIS) with inflammation at tendon insertions.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.
Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each.
Antibodies obtained from a single clone of cells grown in mice or rats.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
Antibodies to the HEPATITIS B ANTIGENS, including antibodies to the surface (Australia) and core of the Dane particle and those to the "e" antigens.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Study of intracellular distribution of chemicals, reaction sites, enzymes, etc., by means of staining reactions, radioactive isotope uptake, selective metal distribution in electron microscopy, or other methods.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
Resistance to a disease-causing agent induced by the introduction of maternal immunity into the fetus by transplacental transfer or into the neonate through colostrum and milk.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
Antibodies specific to INSULIN.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
Drugs that are used to treat RHEUMATOID ARTHRITIS.
The statistical reproducibility of measurements (often in a clinical context), including the testing of instrumentation or techniques to obtain reproducible results. The concept includes reproducibility of physiological measurements, which may be used to develop rules to assess probability or prognosis, or response to a stimulus; reproducibility of occurrence of a condition; and reproducibility of experimental results.
The clear constricted portion of the chromosome at which the chromatids are joined and by which the chromosome is attached to the spindle during cell division.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Serologic tests in which a positive reaction manifested by visible CHEMICAL PRECIPITATION occurs when a soluble ANTIGEN reacts with its precipitins, i.e., ANTIBODIES that can form a precipitate.
A single chain of deoxyribonucleotides that occurs in some bacteria and viruses. It usually exists as a covalently closed circle.
The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.
Any part or derivative of any protozoan that elicits immunity; malaria (Plasmodium) and trypanosome antigens are presently the most frequently encountered.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease.
The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IMMUNOGLOBULIN G whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent.
A characteristic symptom complex.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
An immunoglobulin fragment composed of one variable domain from an IMMUNOGLOBULIN HEAVY CHAIN or IMMUNOGLOBULIN LIGHT CHAIN.
Polysaccharides found in bacteria and in capsules thereof.
The rate dynamics in chemical or physical systems.
A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Unstable isotopes of iodine that decay or disintegrate emitting radiation. I atoms with atomic weights 117-139, except I 127, are radioactive iodine isotopes.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
The total number of cases of a given disease in a specified population at a designated time. It is differentiated from INCIDENCE, which refers to the number of new cases in the population at a given time.
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Suspensions of attenuated or killed bacteria administered for the prevention or treatment of infectious bacterial disease.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Field of chemistry that pertains to immunological phenomena and the study of chemical reactions related to antigen stimulation of tissues. It includes physicochemical interactions between antigens and antibodies.
Layers of protein which surround the capsid in animal viruses with tubular nucleocapsids. The envelope consists of an inner layer of lipids and virus specified proteins also called membrane or matrix proteins. The outer layer consists of one or more types of morphological subunits called peplomers which project from the viral envelope; this layer always consists of glycoproteins.

Autoantibodies to RNA polymerases recognize multiple subunits and demonstrate cross-reactivity with RNA polymerase complexes. (1/2145)

OBJECTIVE: To determine the subunit specificity of autoantibody directed to RNA polymerases (RNAP) I, II, and III, which is one of the major autoantibody responses in patients with systemic sclerosis (SSc). METHODS: Thirty-two SSc sera with anti-RNAP antibodies (23 with anti-RNAP I/III, 5 with anti-RNAP I/III and II, and 4 with anti-RNAP II alone) were analyzed by immunoblotting using affinity-purified RNAP and by immunoprecipitation using 35S-labeled cell extracts in which RNAP complexes were dissociated. Antibodies bound to individual RNAP subunits were eluted from preparative immunoblots and were further analyzed by immunoblotting and immunoprecipitation. RESULTS: At least 15 different proteins were bound by antibodies in anti-RNAP-positive SSc sera in various combinations. All 9 sera immunoprecipitating RNAP II and all 28 sera immunoprecipitating RNAP I/III recognized the large subunit proteins of RNAP II and III, respectively. Reactivity to RNAP I large subunits was strongly associated with bright nucleolar staining by indirect immunofluorescence. Affinity-purified antibodies that recognized a 62-kd subunit protein cross-reacted with a 43-kd subunit protein and immunoprecipitated both RNAP I and RNAP III. Antibodies that recognized a 21-kd subunit protein obtained from sera that were positive for anti-RNAP I/III and II antibodies immunoprecipitated both RNAP II and RNAP III. CONCLUSION: Anti-RNAP antibodies recognize multiple subunits of RNAP I, II, and III. Moreover, the results of this study provide the first direct evidence that antibodies that recognize shared subunits of human RNAPs or epitopes present on different human RNAP subunits are responsible for the recognition of multiple RNAPs by SSc sera.  (+info)

Estrogen enhancement of anti-double-stranded DNA antibody and immunoglobulin G production in peripheral blood mononuclear cells from patients with systemic lupus erythematosus. (2/2145)

OBJECTIVE: To study the in vitro effect of estrogen on IgG anti-double-stranded DNA (anti-dsDNA) antibody and total IgG production in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE), in order to elucidate its regulatory role in SLE. METHODS: PBMC from SLE patients and normal donors were cultured with 17beta-estradiol (E2). IgG anti-dsDNA antibodies, total IgG, and cytokine activity in the culture supernatants were measured by enzyme-linked immunosorbent assay. RESULTS: E2 enhanced production of IgG anti-dsDNA antibodies as well as total IgG in PBMC from SLE patients. Anti-dsDNA production in patients with inactive disease was less responsive to E2 than that in patients with active disease. E2 also enhanced total IgG, but not anti-dsDNA, production in the PBMC of normal donors. Antibody production was increased by E2 to a lesser extent in patients' B cells than in their PBMC. Anti-interleukin-10 (anti-IL-10) antibodies partially blocked the E2-induced increase in antibody production in patients' PBMC, but anti-IL-10 had no effect on B cells. E2 increased IL-10 production by patients' monocytes. Exogenous IL-10 acted additively with E2 in increasing antibody production in patients' B cells. CONCLUSION: These results suggest that E2 may polyclonally increase the production of IgG, including IgG anti-dsDNA, in SLE patients' PBMC by enhancing B cell activity and by promoting IL-10 production in monocytes. These findings support the involvement of E2 in the pathogenesis of SLE.  (+info)

Up-regulation of glomerular extracellular matrix and transforming growth factor-beta expression in RF/J mice. (3/2145)

BACKGROUND: RF/J mice were first reported as a murine model of spontaneous glomerulosclerosis by Gude and Lupton in 1960, but the precise histologic characteristics and immunopathological background of this mouse have not been investigated further. METHODS: Measurements of serum levels of immunoglobulins, anti-single strand DNA (anti-ss-DNA) antibody, complement (C3), and circulating immune complex (IC) were performed. Analyses of glomerular histological and immunopathological lesions in association with the detection of mRNA expression of collagen IV, TGF-beta, matrix protein turnover related enzymes, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2) and platelet-derived growth factor (PDGF) were also performed in young (10-week-old) and elderly (60-week-old) RF/J mice with age-matched BALB/C mice as the controls. RESULTS: High levels of serum IgA and IgG from as early as 20 weeks of age were noted in the RF/J mice. Serum anti-ss-DNA antibody of aged RF/J mice increased up to 23% of that of aged MRL-lpr/lpr mice, and serum C3 concentration significantly decreased with age, reaching lower levels than that of BALB/c mice. IgA-IC levels were significantly high compared to BALB/C mice both in the early and late stages of life, whereas IgG-IC levels were high only in mice younger than 20 weeks. Semiquantitative and quantitative analyzes of renal histopathological findings revealed significantly marked and age-related mesangial matrix expansion in RF/J mice, with increasing frequency of global glomerular sclerosis and tubulointerstitial damage. On the other hand, although precise measurements of glomerular cell numbers also showed an apparent augmentation in both young and old RF/J mice compared to BALB/C mice, glomerular cellularity decreased with age in RF/J mice. Immunohistochemical study revealed massive immunoglobulin deposition from a young age in association with significantly higher accumulation of matrix proteins, such as types I and IV collagen and laminin from the early stage of life. In addition, in these glomeruli, transforming growth factor-beta1 (TGF-beta1) was highly expressed both in young and old mice. The mRNA expression of MMP-2 was up-regulated only in the early stage of life. Although PDGF mRNA of RF/J mice was significantly up-regulated in the early stage of life, the differences between the mice disappeared in the late stage of life. CONCLUSIONS: These findings suggest that in RF/J mice, an immunopathological background inducing high serum immunoglobulin and IC levels from the early stage of life is closely related to mesangioproliferative glomerular lesions mediated by PDGF, and that development of massive extracellular matrix accumulation in glomeruli was induced by up-regulated expression of TGF-beta with inappropriate regulation of protein turnover-related enzyme production.  (+info)

Cryoglobulinaemia and rheumatic manifestations in patients with hepatitis C virus infection. (4/2145)

OBJECTIVES: To investigate the association of cryoglobulinaemia and rheumatic manifestations in Korean patients with hepatitis C virus (HCV) infection. METHODS: Forty nine Korean patients with HCV infection were recruited. The prevalence, concentration, and type of cryoglobulin (by immunofixation), rheumatoid factor (RF), antinuclear antibody (ANA), and various rheumatological symptoms were investigated and HCV genotype was determined by polymerase chain reaction with genotype specific primer. RESULTS: The prevalence of cryoglobulin was 59% in Korean HCV patients and the concentration of cryoglobulin was 9.8 (7.9) g/l (mean (SD)). The type of cryoglobulinaemia was identified in 23 (80%) of 29 HCV patients with cryoglobulinaemia and they were all type III. There were no differences in age, sex, history of operation and transfusion, proportion of liver cirrhosis between the patients with cryoglobulinaemia and those without cryoglobulinaemia. The frequencies of RF and ANA were 14% and 3.4% respectively in HCV patients with cryoglobulinaemia. There was no difference in HCV genotype between the patients with cryoglobulinaemia and those without cryoglobulinaemia. Clinical features of HCV patients were as follows: arthralgia/arthritis (35%), cutaneous manifestation (37%), Raynaud's phenomenon (8%), paresthesia (44%), dry eyes (22%), dry mouth (10%), oral ulcer (33%), and abdominal pain (14%). However, these rheumatological symptoms did not differ between the two groups. CONCLUSION: Although the rheumatological symptoms were not different between HCV patients with and without cryoglobulinaemia, HCV patients showed various rheumatological manifestations. These result suggests that HCV infection could be included as one of the causes in patients with unexplained rheumatological symptoms.  (+info)

A critical evaluation of enzyme immunoassays for detection of antinuclear autoantibodies of defined specificities. I. Precision, sensitivity, and specificity. (5/2145)

OBJECTIVE: To determine the performance characteristics of enzyme-based immunoassay (EIA) kits for the detection of antinuclear and other autoantibodies of defined specificities. METHODS: Nine manufacturers of EIA kits to detect antibodies of defined specificities participated in a study in which they received coded sera from the Centers for Disease Control and Prevention. These coded sera contained different dilutions of antibody of one specificity mixed with sera containing antibodies of other specificities. The manufacturers were asked to use their standard technology to determine antibody content and send the data to a committee of the International Union of Immunological Societies for analysis. The data were analyzed for sensitivity and specificity in the detection of anti-double-stranded DNA (anti-dsDNA), anti-single-stranded DNA, antihistone, anti-Sm, anti-U1 RNP, anti-SSA/Ro, anti-SSB/La, anti-Scl-70 (DNA topoisomerase I), anticentromere, and anti-Jo-1 antibodies. In addition, replicate samples were included in the coded sera to evaluate the precision of each EIA method. RESULTS: Lack of sensitivity and specificity was most evident in the anti-dsDNA and anti-Sm kits, although 2 kits for anti-dsDNA achieved acceptable sensitivity and specificity. Generally, anti-SSA/Ro, anti-SSB/La, anti-Scl-70, anticentromere, and anti-Jo-1 kits performed well. Many false-positive results were obtained with a multiple myeloma serum containing cryoprecipitates, but multiple myeloma sera without cryoprecipitates presented no problem in the EIA system. Precision, based on evaluation of replicate samples, varied from very good to poor. CONCLUSION: No single manufacturer was clearly superior to others in terms of their products' overall sensitivity, specificity, and precision. Areas that needed improvement were in kits for the detection of antibodies to dsDNA and to Sm antigen. Some EIA kits achieved good sensitivity and specificity. Individual manufacturers were informed of the performance of their respective kits so they could take measures to correct perceived deficiencies and thus improve the reliability of a group of important diagnostic assays used in the evaluation of systemic rheumatic diseases.  (+info)

Influence of ethnic background on clinical and serologic features in patients with systemic sclerosis and anti-DNA topoisomerase I antibody. (6/2145)

OBJECTIVE: To investigate the effect of ethnicity on clinical and serologic expression in patients with systemic sclerosis (SSc) and anti-DNA topoisomerase I (anti-topo I) antibody. METHODS: Clinical and serologic features, as well as HLA class II allele frequencies, were compared among 47 North American white, 15 North American black, 43 Japanese, and 12 Choctaw Native American SSc patients with anti-topo I antibody. RESULTS: The frequency of progressive pulmonary interstitial fibrosis was lower, and cumulative survival rates were better in white compared with black and Japanese patients. Sera of white and black patients frequently recognized the portion adjacent to the carboxyl terminus of topo I, sera of Japanese patients preferentially recognized the portion adjacent to the amino terminus of topo I, and sera of Choctaw patients recognized both portions of topo I. Anti-RNA polymerase II and anti-SSA/Ro antibodies were present together with anti-topo I antibody more frequently in sera of Japanese patients than in sera of white patients. The HLA-DRB1 alleles associated with anti-topo I antibody differed; i.e., DRB1*1101-*1104 in whites and blacks, DRB1*1502 in Japanese, and DRB1*1602 in Choctaws. Multivariate analysis showed that ethnic background was an independent determinant affecting development of severe lung disease as well as survival. CONCLUSION: Clinical and serologic features in SSc patients were strongly influenced by ethnic background. The variability of disease expression in the 4 ethnic groups suggests that multiple factors linked to ethnicity, including genetic and environmental factors, modulate clinical manifestations, disease course, and autoantibody status in SSc.  (+info)

Disparate T cell requirements of two subsets of lupus-specific autoantibodies in pristane-treated mice. (7/2145)

Intraperitoneal injection of pristane induces a lupus-like disease in BALB/c and other non-autoimmune mice characterized by autoantibody production and the development of immune complex disease closely resembling lupus nephritis. Two subsets of autoantibodies are induced by pristane: IgG anti-DNA DNA and -chromatin autoantibodies are strongly IL-6-dependent, whereas IgG anti-nRNP/Sm and -Su antibodies are not. The present studies were carried out to examine the role of T cells in establishing this dichotomy between the production of anti-nRNP/Sm/Su versus anti-DNA/chromatin autoantibodies. Autoantibody production and renal disease were evaluated in athymic (nude) mice treated with pristane. BALB/c nu/nu mice spontaneously developed IgM and IgG anti-single-stranded (ss)DNA and -chromatin, but not anti-nRNP/Sm or -Su, autoantibodies. Pristane treatment increased the levels of IgG anti-chromatin antibodies in nu/nu mice, but did not induce production of anti-nRNP/Sm or -Su antibodies. In contrast, BALB/c nu/+ and +/+ control mice did not spontaneously produce autoantibodies, whereas anti-nRNP/Sm and -Su autoantibodies were induced by pristane in approx. 50% of nu/+ and +/+ mice and anti-DNA/chromatin antibodies at lower frequencies. Nude mice spontaneously developed mild renal lesions that were marginally affected by pristane, but were generally milder than the lesions developing in pristane-treated nu/+ and +/+ mice. The data provide further evidence that two distinct pathways with different cytokine and T cell requirements are involved in autoantibody formation in pristane-induced lupus. This dichotomy may be relevant to understanding differences in the regulation of anti-DNA versus anti-nRNP/Sm autoantibodies in systemic lupus erythematosus, as well as the association of anti-DNA, but not anti-nRNP/Sm, with lupus nephritis.  (+info)

Electrocardiographic abnormalities in a murine model injected with IgG from mothers of children with congenital heart block. (8/2145)

BACKGROUND: It is a widely held view that congenital heart block (CHB) is caused by the transplacental transfer of maternal autoantibodies (anti-SSA/Ro and/or anti-SSB/La) into the fetal circulation. To test this hypothesis and to reproduce human CHB, an experimental mouse model (BALB/c) was developed by passive transfer of human autoantibodies into pregnant mice. METHODS AND RESULTS: Timed pregnant mice (n=54) were injected with a single intravenous bolus of purified IgG containing human anti-SSA/Ro and anti-SSB/La antibodies from mothers of children with CHB. To parallel the "window period" of susceptibility to CHB in humans, 3 groups of mice were used: 8, 11, and 16 days of gestation. Within each group, we tested 10, 25, 50, and 100 microg of IgG. At delivery, ECGs were recorded and analyzed for conduction abnormalities. Bradycardia and PR interval were significantly increased in 8-, 11-, and 16-day gestational groups when compared with controls (P<0.05). QRS duration was not significantly different between all groups. Antibody levels measured by ELISA in both mothers and their offspring confirmed the transplacental transfer of the human antibodies to the pups. CONCLUSIONS: The passive transfer model demonstrated bradycardia, first-degree but not complete atrioventricular block in pups. The greater percentage and degree of bradycardia and PR prolongation in the 11-day mouse group correlates with the "window period" of susceptibility observed in humans. The high incidence of bradycardia suggests possible sinoatrial node involvement. All together, these data provide relevant insights into the pathogenesis of CHB.  (+info)

The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.

There are several subtypes of LES, including:

1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.

There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.

It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.

Some common types of connective tissue diseases include:

1. Rheumatoid arthritis (RA): A chronic autoimmune disorder that causes inflammation and joint damage.
2. Systemic lupus erythematosus (SLE): An autoimmune disorder that can affect multiple systems in the body, including the skin, joints, and kidneys.
3. Sjogren's syndrome: An autoimmune disorder that causes dry eyes and mouth, as well as joint pain and swelling.
4. Fibromyalgia: A chronic condition characterized by widespread muscle pain and fatigue.
5. Myositis: Inflammatory diseases that affect the muscles, such as dermatomyositis and polymyositis.
6. Giant cell arteritis: A condition that causes inflammation of the blood vessels, particularly in the head and neck.
7. Takayasu arteritis: A condition that causes inflammation of the blood vessels in the aorta and its branches.
8. Polyarteritis nodosa: A condition that causes inflammation of the blood vessels, particularly in the hands and feet.
9. IgG4-related disease: A condition characterized by inflammation and damage to various organs, including the pancreas, salivary glands, and liver.

Connective tissue diseases can cause a wide range of symptoms, including joint pain and stiffness, fatigue, skin rashes, fever, and weight loss. Treatment options vary depending on the specific disease and its severity, but may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). In some cases, surgery or physical therapy may also be necessary.

Examples of autoimmune diseases include:

1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.

The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.

There are two main types of systemic scleroderma: diffuse cutaneous systemic sclerosis (DCSS) and limited cutaneous systemic sclerosis (LCSS). DCSS is characterized by skin thickening and scar formation over the trunk, arms, and legs, while LCSS is characterized by skin tightening and patches of scaly skin on the hands and face.

The symptoms of systemic scleroderma can include:

* Skin hardening and tightening
* Fatigue
* Joint pain and stiffness
* Muscle weakness
* Swallowing difficulties
* Heartburn and acid reflux
* Shortness of breath
* Raynaud's phenomenon (pale or blue-colored fingers and toes in response to cold temperatures or stress)

The exact cause of systemic scleroderma is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment options for systemic scleroderma include medications to manage symptoms such as pain, stiffness, and swallowing difficulties, as well as physical therapy and lifestyle modifications to improve quality of life.

In summary, systemic scleroderma is a chronic autoimmune disease that affects multiple systems in the body, causing skin hardening and thickening, fatigue, joint pain, and other symptoms. While there is no cure for systemic scleroderma, treatment options are available to manage symptoms and improve quality of life.

1. Rheumatoid arthritis (RA): An autoimmune disease that causes inflammation in the joints, leading to pain, stiffness, and swelling.
2. Osteoarthritis (OA): A degenerative condition that occurs when the cartilage in the joints wears down over time, causing pain and stiffness.
3. Psoriatic arthritis (PsA): An inflammatory disease that affects both the skin and joints, often occurring in people with psoriasis.
4. Ankylosing spondylitis (AS): A condition that causes inflammation in the spine and peripheral joints, leading to stiffness and pain.
5. Lupus: An autoimmune disease that can affect multiple systems in the body, including the joints, skin, and kidneys.
6. Juvenile idiopathic arthritis (JIA): A condition that affects children under the age of 16, causing inflammation in the joints and potentially leading to long-term complications.
7. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dryness in the eyes and mouth.
8. Fibromyalgia: A condition characterized by widespread pain, fatigue, and sleep disturbances.
9. Gout: A type of inflammatory arthritis caused by excessive levels of uric acid in the blood, leading to sudden and severe attacks of joint pain.
10. Osteoporosis: A condition characterized by brittle bones and an increased risk of fractures, often occurring in older adults.

Rheumatic diseases can be challenging to diagnose and treat, as they often involve complex symptoms and a range of possible causes. However, with the help of rheumatology specialists and advanced diagnostic tools, it is possible to manage these conditions effectively and improve quality of life for patients.

Sjögren's syndrome can affect people of all ages, but it most commonly occurs in women between the ages of 40 and 60. The exact cause of the disorder is not known, but it is believed to be an autoimmune response, meaning that the immune system mistakenly attacks the glands as if they were foreign substances.

Symptoms of Sjögren's syndrome can vary in severity and may include:

* Dry mouth (xerostomia)
* Dry eyes (dry eye syndrome)
* Fatigue
* Joint pain
* Swollen lymph nodes
* Rash
* Sores on the skin
* Numbness or tingling in the hands and feet
* Sexual dysfunction

There is no cure for Sjögren's syndrome, but various treatments can help manage the symptoms. These may include:

* Medications to stimulate saliva production
* Eye drops to moisturize the eyes
* Mouthwashes to stimulate saliva production
* Pain relief medication for joint pain
* Anti-inflammatory medication to reduce swelling
* Immunosuppressive medication to suppress the immune system
* Hormone replacement therapy (HRT) to treat hormonal imbalances.

Sjögren's syndrome can also increase the risk of developing other autoimmune disorders, such as rheumatoid arthritis or lupus. It is important for people with Sjögren's syndrome to work closely with their healthcare provider to manage their symptoms and monitor their condition over time.

The exact cause of autoimmune hepatitis is not fully understood, but it is believed to involve a combination of genetic and environmental factors. The condition can occur in people of all ages, although it is most common in women between the ages of 20 and 40.

Symptoms of autoimmune hepatitis may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, and yellowing of the skin and eyes (jaundice). If left untreated, the condition can lead to liver failure and even death.

Treatment for autoimmune hepatitis typically involves medications to suppress the immune system and reduce inflammation in the liver. In severe cases, a liver transplant may be necessary. Early diagnosis and treatment can improve the chances of a successful outcome.

The exact cause of Raynaud disease is not fully understood, but it is believed to be related to an autoimmune disorder, in which the body's immune system mistakenly attacks healthy tissue. The condition can occur on its own or as a secondary symptom of another underlying medical condition such as scleroderma or rheumatoid arthritis.

Symptoms of Raynaud Disease:

1) Discoloration: Raynaud disease causes the affected areas to turn white or blue in response to cold temperatures or stress.

2) Pain: The constriction of blood vessels can cause pain in the affected areas.

3) Numbness or tingling: The lack of blood flow can cause numbness or tingling sensations in the fingers and toes.

4) Swelling: In severe cases, swelling may occur in the affected areas.

5) Burning sensation: Some people with Raynaud disease may experience a burning sensation in their hands and feet.

Diagnosis of Raynaud Disease:

1) Medical history: A doctor will ask about symptoms, medical history, and any triggers that may cause the condition.

2) Physical examination: The doctor will perform a physical examination to look for signs of discoloration or swelling in the affected areas.

3) Tests: Additional tests such as nailfold capillary microscopy, pulse volume recording and thermography may be ordered to confirm the diagnosis.

Treatment options for Raynaud Disease:

1) Medications: Drugs such as calcium channel blockers, alpha-blockers, and anticoagulants can help to relax blood vessels and improve blood flow.

2) Lifestyle changes: Avoiding triggers such as cold temperatures and taking steps to keep hands and feet warm can help manage the condition.

3) Alternative therapies: Some people with Raynaud disease may find relief with alternative therapies such as acupuncture or biofeedback.

It is important to note that in some cases, Raynaud disease can be a symptom of an underlying autoimmune disorder, such as lupus or scleroderma. If you suspect you have Raynaud disease, it is essential to seek medical attention to rule out any other conditions.

There are several types of JA, including:

1. Systemic juvenile idiopathic arthritis (SJIA): A severe form of JA that affects the entire body, causing fever, rash, and swollen lymph nodes in addition to joint inflammation.
2. Polyarticular juvenile idiopathic arthritis (PJIA): A common form of JA that affects multiple joints, especially in the hands and feet.
3. Oligoarticular juvenile idiopathic arthritis (OJIA): A mild form of JA that affects only a few joints.
4. Juvenile psoriatic arthritis (JPsA): A type of JA that is associated with psoriasis, a skin condition characterized by red, scaly patches.
5. Enthesitis-related juvenile idiopathic arthritis (ER-JIA): A rare form of JA that affects the areas where tendons and ligaments attach to bones.
6. Undifferentiated arthritis: A type of JA that does not fit into any of the other categories.

The symptoms of JA can vary depending on the specific type and severity of the condition, but may include:

* Joint pain and stiffness
* Swelling and redness in the affected joints
* Fatigue and fever
* Loss of mobility and range of motion
* Difficulty walking or standing

The exact cause of JA is not known, but it is believed to involve a combination of genetic and environmental factors. There is no cure for JA, but treatment options are available to help manage symptoms and prevent long-term joint damage. These may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying anti-rheumatic drugs (DMARDs), as well as physical therapy and lifestyle modifications.

Iritis, also known as anterior uveitis, is a type of inflammatory eye disease that affects the iris, which is the coloured part of the eye. It is a condition where the iris becomes inflamed, leading to pain, redness, and blurred vision.

Causes:

The exact cause of iritis is not known, but it is believed to be an autoimmune response, where the body's immune system mistakenly attacks healthy tissue in the eye. It can also be triggered by an infection or injury.

Symptoms:

The symptoms of iritis can vary depending on the severity of the condition, but common signs include:

* Eye pain, which can be severe
* Redness and inflammation of the eye
* Blurred vision or sensitivity to light
* Seeing floaters or flashes of light
* Sensitivity to touch or pressure on the eye

Diagnosis:

Iritis is diagnosed based on a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and tonometry. The doctor may also perform additional tests such as a fluorescein dye test or imaging studies to rule out other conditions.

Treatment:

The treatment of iritis typically involves a combination of medications and therapies, including:

* Corticosteroids to reduce inflammation
* Anti-inflammatory eye drops or ointments
* Pain relief medication
* Warm compresses to the affected eye
* Eye exercises to improve vision
* In severe cases, surgery may be necessary to remove the inflamed tissue

Prognosis:

The prognosis for iritis is generally good if treated promptly and effectively. However, if left untreated, it can lead to complications such as cataracts, glaucoma, or permanent vision loss. It is important to seek medical attention immediately if symptoms persist or worsen over time.

Prevention:

There is no known prevention for iritis, but early detection and treatment can help reduce the risk of complications. Regular eye exams and awareness of the signs and symptoms can help identify the condition in its early stages.

Complications:

Iritis can lead to several complications if left untreated or if the inflammation is not properly managed. These may include:

* Cataracts: The inflammation can cause clouding of the lens, leading to vision loss.
* Glaucoma: The increased pressure in the eye can lead to damage to the optic nerve and vision loss.
* Permanent vision loss: If the inflammation is not properly managed, it can lead to permanent vision loss.
* Increased risk of infection: Iritis can increase the risk of infection, particularly if the eye is not properly cleaned and cared for.

Conclusion:

Iritis is a painful and potentially sight-threatening condition that can cause inflammation in the iris of the eye. Early detection and prompt treatment are crucial to prevent complications and preserve vision. A comprehensive understanding of the signs, symptoms, diagnosis, treatment, prognosis, prevention, and complications of iritis is essential for effective management of this condition. If you suspect you or someone you know may have iritis, it is important to seek medical attention promptly to ensure proper diagnosis and treatment.

The exact cause of MCTD is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissues in the body. The disease is more common in women than men and typically affects people between the ages of 20 and 50.

Symptoms of MCTD can vary widely and may include:

* Skin rashes or lesions
* Joint pain and stiffness
* Fatigue
* Fever
* Raynaud's phenomenon (digits turn white or blue in response to cold or stress)
* Swollen lymph nodes
* Shortness of breath
* Chest pain
* Abdominal pain
* Weakness and wasting of muscles

There is no cure for MCTD, but treatment focuses on managing symptoms and preventing complications. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive drugs may be used to reduce inflammation and suppress the immune system. Physical therapy and exercise may also be helpful in maintaining joint mobility and strength.

The prognosis for MCTD varies depending on the severity of the disease and the presence of certain complications, such as lung or heart involvement. Some people with MCTD may experience a gradual worsening of symptoms over time, while others may experience periods of remission. With appropriate treatment, many people with MCTD are able to manage their symptoms and lead active lives.

There are several subtypes of localized scleroderma, including:

* Linear morphea: This is the most common form of localized scleroderma and appears as a linear or polylinear band of hardened skin on the arms, legs, or torso.
* Plaque morphea: This type of scleroderma causes flat, disk-shaped patches of thickened skin that can be red, purple, or brown.
* Guttate morphea: This form of localized scleroderma is characterized by numerous small, drop-like lesions on the arms, legs, or torso.

The exact cause of localized scleroderma is not known, but it is believed to be an autoimmune disorder that triggers the immune system to attack healthy tissue in the skin. The condition can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or imaging studies.

Treatment for localized scleroderma typically involves topical medications, such as corticosteroids or immunosuppressants, to reduce inflammation and slow the progression of the disease. In some cases, phototherapy or physical therapy may also be recommended to improve symptoms and prevent complications.

While there is no cure for localized scleroderma, early diagnosis and appropriate treatment can help manage the condition and improve quality of life for those affected.

The condition is often caused by gallstones or other blockages that prevent the normal flow of bile from the liver to the small intestine. Over time, the scarring can lead to the formation of cirrhosis, which is characterized by the replacement of healthy liver tissue with scar tissue.

Symptoms of liver cirrhosis, biliary may include:

* Jaundice (yellowing of the skin and eyes)
* Itching
* Fatigue
* Abdominal pain
* Dark urine
* Pale stools

The diagnosis of liver cirrhosis, biliary is typically made through a combination of physical examination, medical history, and diagnostic tests such as ultrasound, CT scans, and blood tests.

Treatment for liver cirrhosis, biliary depends on the underlying cause of the condition. In some cases, surgery may be necessary to remove gallstones or repair damaged bile ducts. Medications such as antioxidants and anti-inflammatory drugs may also be prescribed to help manage symptoms and slow the progression of the disease. In severe cases, a liver transplant may be necessary.

Prognosis for liver cirrhosis, biliary is generally poor, as the condition can lead to complications such as liver failure, infection, and cancer. However, with early diagnosis and appropriate treatment, it is possible to manage the symptoms and slow the progression of the disease.

There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:

* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.

Lupus Nephritis can cause a range of symptoms, including:

* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Fatigue
* Fever
* Joint pain

Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.

Nephritis is often diagnosed through a combination of physical examination, medical history, and laboratory tests such as urinalysis and blood tests. Treatment for nephritis depends on the underlying cause, but may include antibiotics, corticosteroids, and immunosuppressive medications. In severe cases, dialysis may be necessary to remove waste products from the blood.

Some common types of nephritis include:

1. Acute pyelonephritis: This is a type of bacterial infection that affects the kidneys and can cause sudden and severe symptoms.
2. Chronic pyelonephritis: This is a type of inflammation that occurs over a longer period of time, often as a result of recurrent infections or other underlying conditions.
3. Lupus nephritis: This is a type of inflammation that occurs in people with systemic lupus erythematosus (SLE), an autoimmune disorder that can affect multiple organs.
4. IgA nephropathy: This is a type of inflammation that occurs when an antibody called immunoglobulin A (IgA) deposits in the kidneys and causes damage.
5. Mesangial proliferative glomerulonephritis: This is a type of inflammation that affects the mesangium, a layer of tissue in the kidney that helps to filter waste products from the blood.
6. Minimal change disease: This is a type of nephrotic syndrome (a group of symptoms that include proteinuria, or excess protein in the urine) that is caused by inflammation and changes in the glomeruli, the tiny blood vessels in the kidneys that filter waste products from the blood.
7. Membranous nephropathy: This is a type of inflammation that occurs when there is an abnormal buildup of antibodies called immunoglobulin G (IgG) in the glomeruli, leading to damage to the kidneys.
8. Focal segmental glomerulosclerosis: This is a type of inflammation that affects one or more segments of the glomeruli, leading to scarring and loss of function.
9. Post-infectious glomerulonephritis: This is a type of inflammation that occurs after an infection, such as streptococcal infections, and can cause damage to the kidneys.
10. Acute tubular necrosis (ATN): This is a type of inflammation that occurs when there is a sudden loss of blood flow to the kidneys, causing damage to the tubules, which are tiny tubes in the kidneys that help to filter waste products from the blood.

The most common types of serositis include:

1. Pleurisy: Inflammation of the pleura, the membrane that surrounds the lungs.
2. Pericarditis: Inflammation of the pericardium, the membrane that surrounds the heart.
3. Peritonitis: Inflammation of the peritoneum, the membrane that lines the abdominal cavity.
4. Pneumoperitoneum: Accumulation of air in the peritoneal cavity.
5. Pyopericardium: Fluid accumulation within the pericardial sac.

Causes of serositis can include bacterial or viral infections, autoimmune disorders, injury, or cancer. Symptoms may include chest pain, fever, cough, shortness of breath, and abdominal pain.

Diagnosis is typically made through physical examination, medical imaging, and laboratory tests such as blood cultures, electrolyte panels, and inflammatory markers. Treatment depends on the underlying cause and may involve antibiotics, anti-inflammatory medications, or surgical intervention.

1. Polymyositis: This is an inflammatory disease that affects the muscles and can cause muscle weakness, pain, and stiffness.
2. Dercum's disease: This is a rare condition that causes fatty degeneration of the muscles, leading to muscle pain, weakness, and wasting.
3. Inflammatory myopathy: This is a group of conditions that cause inflammation in the muscles, leading to muscle weakness and pain.
4. Dermatomyositis: This is an inflammatory condition that affects both the skin and the muscles, causing skin rashes and muscle weakness.
5. Juvenile myositis: This is a rare condition that affects children and can cause muscle weakness, pain, and stiffness.

The symptoms of myositis can vary depending on the type of condition and its severity. Common symptoms include muscle weakness, muscle pain, stiffness, and fatigue. Other symptoms may include skin rashes, fever, and joint pain.

The diagnosis of myositis typically involves a combination of physical examination, medical history, and laboratory tests such as blood tests and muscle biopsies. Treatment for myositis depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy. In some cases, surgery may be necessary to remove affected muscle tissue.

There are three main types of CLE:

1. Discoid lupus erythematosus (DLE): Characterized by the presence of discrete, flat, round lesions with a scaly border. These lesions can scar and leave behind pale or dark patches on the skin.
2. Subacute cutaneous lupus erythematosus (SCLE): Characterized by the sudden appearance of red, painful, tender lesions that may resemble hives or folliculitis. These lesions can resolve on their own within weeks to months but can leave behind scarring.
3. Chronic cutaneous lupus erythematosus (CCLE): Characterized by the presence of widespread, thickened, darkened skin that can resemble leather or violet-colored plaques. This type is less common than DLE and SCLE.

CLE can be caused by a combination of genetic and environmental factors, including exposure to sunlight, hormonal changes, and certain medications. The disease is more common in women, especially those of childbearing age, and in people with a family history of autoimmune disorders.

The diagnosis of CLE is based on the presence of characteristic skin lesions and can be confirmed by a skin biopsy. Treatment options for CLE include topical corticosteroids, antimalarials, and immunosuppressive medications. In severe cases, phototherapy or systemic corticosteroids may be necessary. Prognosis is generally good, but the disease can be challenging to treat and recurrences are common.

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

The symptoms of lupus vulgaris typically include:

* Rough, scaly patches on the skin that may be dark red or purple in color
* Itching or burning sensation on the skin
* Skin thickening or hardening
* Painless ulcers or sores on the skin
* Swollen lymph nodes
* Fever
* Headache
* Joint pain or swelling

The diagnosis of lupus vulgaris is based on a combination of clinical findings and laboratory tests. A physical examination of the skin and mucous membranes can reveal characteristic signs of the condition, such as scaly patches or ulcers. Laboratory tests, such as blood tests or biopsies, may be performed to confirm the diagnosis and rule out other conditions.

Treatment of lupus vulgaris typically involves antibiotics, which can help to clear the infection and reduce symptoms. In severe cases, surgical debridement or laser therapy may be necessary to remove damaged tissue and promote healing. In addition, patients with lupus vulgaris may require supportive care to manage symptoms such as pain, itching, and swelling.

Overall, lupus vulgaris is a chronic skin condition that can cause significant discomfort and disfigurement if left untreated. It is important for individuals in regions where the condition is common to be aware of the signs and symptoms and seek medical attention if they suspect they may have the condition. With proper diagnosis and treatment, however, most patients with lupus vulgaris can experience significant improvement in their symptoms and quality of life.

It is important for individuals with discoid lupus erythematosus to be aware of their condition and seek medical attention if they experience any changes in their symptoms or if new lesions develop, as the disease can lead to complications such as skin cancer, scarring, and joint pain if left untreated. Early diagnosis and treatment can help prevent these complications and improve quality of life for those affected by the condition.

The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:

* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure

Glomerulonephritis can be caused by a variety of factors, including:

* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia

The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.

Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:

* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases

The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.

The symptoms of dermatomyositis can vary in severity and may include:

* Rashes and lesions on the skin, particularly on the face, neck, and hands
* Muscle weakness and fatigue
* Joint pain and stiffness
* Swelling and redness in the affected areas
* Fever
* Headaches
* Fatigue

Dermatomyositis is often associated with other autoimmune disorders, such as polymyositis, and can be triggered by certain medications or infections. There is no cure for dermatomyositis, but treatment options are available to manage the symptoms and prevent complications. Treatment may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy to maintain muscle strength and flexibility.

The term "dermatomyositis" is derived from the Greek words "derma," meaning skin, "myo," meaning muscle, and "-itis," indicating inflammation. The condition was first described in the medical literature in the early 20th century, and since then has been studied extensively to better understand its causes and develop effective treatments.

In summary, dermatomyositis is a rare autoimmune disease that affects both the skin and muscles, causing inflammation and various symptoms such as rashes, weakness, and joint pain. While there is no cure for the condition, treatment options are available to manage the symptoms and prevent complications.

The syndrome is typically diagnosed based on the presence of anticardiolipin antibodies (aCL) or lupus anticoagulant in the blood. Treatment for antiphospholipid syndrome may involve medications to prevent blood clots, such as heparin or warfarin, and aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce pain and inflammation. In some cases, intravenous immunoglobulin (IVIG) may be given to reduce the levels of antibodies in the blood. Plasmapheresis, a process that removes antibodies from the blood, may also be used in some cases.

Antiphospholipid syndrome is associated with other autoimmune disorders, such as systemic lupus erythematosus (SLE), and may be triggered by certain medications or infections. It is important for individuals with antiphospholipid syndrome to work closely with their healthcare provider to manage their condition and reduce the risk of complications.

There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:

1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.

The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.

Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.

In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:

1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.

It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.

Osteoarthritis (OA) is a degenerative condition that occurs when the cartilage that cushions the joints breaks down over time, causing the bones to rub together. It is the most common form of arthritis and typically affects older adults.

Rheumatoid arthritis (RA) is an autoimmune condition that occurs when the body's immune system attacks the lining of the joints, leading to inflammation and pain. It can affect anyone, regardless of age, and is typically seen in women.

Other types of arthritis include psoriatic arthritis, gouty arthritis, and lupus-related arthritis. Treatment for arthritis depends on the type and severity of the condition, but can include medications such as pain relievers, anti-inflammatory drugs, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy and lifestyle changes, such as exercise and weight loss, can also be helpful. In severe cases, surgery may be necessary to repair or replace damaged joints.

Arthritis is a leading cause of disability worldwide, affecting over 50 million adults in the United States alone. It can have a significant impact on a person's quality of life, making everyday activities such as walking, dressing, and grooming difficult and painful. Early diagnosis and treatment are important to help manage symptoms and slow the progression of the disease.

The term "immune complex disease" was first used in the 1960s to describe a group of conditions that were thought to be caused by the formation of immune complexes. These diseases include:

1. Systemic lupus erythematosus (SLE): an autoimmune disorder that can affect multiple organ systems and is characterized by the presence of anti-nuclear antibodies.
2. Rheumatoid arthritis (RA): an autoimmune disease that causes inflammation in the joints and can lead to joint damage.
3. Type III hypersensitivity reaction: a condition in which immune complexes are deposited in tissues, leading to inflammation and tissue damage.
4. Pemphigus: a group of autoimmune diseases that affect the skin and mucous membranes, characterized by the presence of autoantibodies against desmosomal antigens.
5. Bullous pemphigoid: an autoimmune disease that affects the skin and is characterized by the formation of large blisters.
6. Myasthenia gravis: an autoimmune disorder that affects the nervous system, causing muscle weakness and fatigue.
7. Goodpasture's syndrome: a rare autoimmune disease that affects the kidneys and lungs, characterized by the presence of immune complexes in the glomeruli of the kidneys.
8. Hemolytic uremic syndrome (HUS): a condition in which red blood cells are destroyed and waste products accumulate in the kidneys, leading to kidney failure.

Immune complex diseases can be caused by various factors, including genetic predisposition, environmental triggers, and exposure to certain drugs or toxins. Treatment options for these diseases include medications that suppress the immune system, such as corticosteroids and immunosuppressive drugs, and plasmapheresis, which is a process that removes harmful antibodies from the blood. In some cases, organ transplantation may be necessary.

In conclusion, immune complex diseases are a group of disorders that occur when the body's immune system mistakenly attacks its own tissues and organs, leading to inflammation and damage. These diseases can affect various parts of the body, including the skin, kidneys, lungs, and nervous system. Treatment options vary depending on the specific disease and its severity, but may include medications that suppress the immune system and plasmapheresis.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Symptoms of sialadenitis may include:

* Swelling and tenderness of the salivary gland
* Pain in the jaw, cheek, or neck
* Difficulty swallowing
* Fever
* Redness and warmth of the affected area

The diagnosis of sialadenitis is based on a combination of physical examination, medical history, and imaging studies such as ultrasound or CT scan. Treatment depends on the underlying cause, but may include antibiotics for bacterial infections, anti-inflammatory medications, or drainage of the abscess if present.

Sialadenitis can lead to complications such as abscess formation, cellulitis, and permanent damage to the salivary gland if left untreated. Therefore, it is important to seek medical attention if symptoms persist or worsen over time.

There are several causes of hypergammaglobulinemia, including:

1. Chronic infections: Prolonged infections can cause an increase in the production of immunoglobulins to fight off the infection.
2. Autoimmune disorders: Conditions such as rheumatoid arthritis, lupus, and multiple sclerosis can cause the immune system to produce excessive amounts of antibodies.
3. Cancer: Some types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause an increase in immunoglobulin production.
4. Genetic disorders: Certain genetic conditions, such as X-linked agammaglobulinemia, can lead to a deficiency or excess of immunoglobulins.
5. Medications: Certain medications, such as corticosteroids and chemotherapy drugs, can suppress the immune system and reduce the production of immunoglobulins.

Symptoms of hypergammaglobulinemia can include:

1. Infections: Recurring infections are a common symptom of hypergammaglobulinemia, as the excessive amount of antibodies can make it difficult for the body to fight off infections effectively.
2. Fatigue: Chronic infections and inflammation can cause fatigue and weakness.
3. Weight loss: Recurring infections and chronic inflammation can lead to weight loss and malnutrition.
4. Swollen lymph nodes: Enlarged lymph nodes are a common symptom of hypergammaglobulinemia, as the body tries to fight off infections.
5. Fever: Recurring fevers can be a symptom of hypergammaglobulinemia, as the body tries to fight off infections.
6. Night sweats: Excessive sweating at night can be a symptom of hypergammaglobulinemia.
7. Skin rashes: Certain types of skin rashes can be a symptom of hypergammaglobulinemia, such as a rash caused by allergic reactions to medications or infections.
8. Joint pain: Pain and stiffness in the joints can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the joints.
9. Headaches: Chronic headaches can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the brain or other parts of the body.
10. Swollen liver and spleen: Enlarged liver and spleen can be a symptom of hypergammaglobulinemia, as the body tries to filter out excess antibodies and fight off infections.

It is important to note that these symptoms can also be caused by other medical conditions, so it is essential to consult a healthcare professional for proper diagnosis and treatment. A healthcare professional may perform blood tests and other diagnostic procedures to determine the underlying cause of the symptoms and develop an appropriate treatment plan. Treatment for hypergammaglobulinemia typically involves addressing the underlying cause of the condition, such as infections, allergies, or autoimmune disorders, and may include medications to reduce inflammation and suppress the immune system.

The symptoms of toxoplasmosis can vary depending on the severity of the infection and the individual's overall health. In some cases, it may cause mild flu-like symptoms or no symptoms at all. However, in severe cases, it can lead to complications such as brain inflammation, eye infections, and pneumonia.

Toxoplasmosis is a significant public health concern due to its potential to affect anyone and its ability to cause serious complications, especially in certain populations such as pregnant women, people with weakened immune systems, and the elderly. It is important for individuals who may be at risk of contracting the disease to take preventive measures such as avoiding undercooked meat, washing hands frequently, and avoiding contact with cat feces.

Diagnosis of toxoplasmosis typically involves a combination of physical examination, laboratory tests, and imaging studies. Laboratory tests may include blood tests or polymerase chain reaction (PCR) to detect the parasite's DNA in the body. Imaging studies such as ultrasound or computerized tomography (CT) scans may be used to evaluate any complications of the disease.

Treatment for toxoplasmosis typically involves antibiotics to control the infection and manage symptoms. In severe cases, hospitalization may be necessary to monitor and treat any complications. Prevention is key to avoiding this disease, as there is no vaccine available to protect against it.

The term splenomegaly is used to describe any condition that results in an increase in the size of the spleen, regardless of the underlying cause. This can be caused by a variety of factors, such as infection, inflammation, cancer, or genetic disorders.

Splenomegaly can be diagnosed through a physical examination, where the doctor may feel the enlarged spleen during an abdominal palpation. Imaging tests, such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI), may also be used to confirm the diagnosis and evaluate the extent of the splenomegaly.

Treatment for splenomegaly depends on the underlying cause. For example, infections such as malaria or mononucleosis are treated with antibiotics, while cancerous conditions may require surgical intervention or chemotherapy. In some cases, the spleen may need to be removed, a procedure known as splenectomy.

In conclusion, splenomegaly is an abnormal enlargement of the spleen that can be caused by various factors and requires prompt medical attention for proper diagnosis and treatment.

Spondylitis, ankylosing can affect any part of the spine, but it most commonly affects the lower back (lumbar spine) and the neck (cervical spine). The condition can also affect other joints, such as the hips, shoulders, and feet.

The exact cause of spondylitis, ankylosing is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissue in the joints. Genetics may also play a role in the development of the condition.

Symptoms of spondylitis, ankylosing can include:

* Back pain and stiffness
* Pain and swelling in the joints
* Limited mobility and flexibility
* Redness and warmth in the affected area
* Fatigue

If you suspect that you or someone you know may have spondylitis, ankylosing, it is important to seek medical attention for proper diagnosis and treatment. A healthcare professional can perform a physical examination and order imaging tests, such as X-rays or MRIs, to confirm the diagnosis and rule out other conditions.

Treatment for spondylitis, ankylosing typically involves a combination of medications and physical therapy. Medications may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy can help improve mobility and flexibility, as well as strengthen the muscles supporting the affected joints.

In severe cases of spondylitis, ankylosing, surgery may be necessary to repair or replace damaged joints. In some cases, the condition may progress to the point where the joints become fused and immobile, a condition known as ankylosis.

While there is no cure for spondylitis, ankylosing, early diagnosis and appropriate treatment can help manage symptoms and slow the progression of the disease. With proper care and support, individuals with spondylitis, ankylosing can lead active and fulfilling lives.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

Examples of syndromes include:

1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21 that affects intellectual and physical development.
2. Turner syndrome: A genetic disorder caused by a missing or partially deleted X chromosome that affects physical growth and development in females.
3. Marfan syndrome: A genetic disorder affecting the body's connective tissue, causing tall stature, long limbs, and cardiovascular problems.
4. Alzheimer's disease: A neurodegenerative disorder characterized by memory loss, confusion, and changes in personality and behavior.
5. Parkinson's disease: A neurological disorder characterized by tremors, rigidity, and difficulty with movement.
6. Klinefelter syndrome: A genetic disorder caused by an extra X chromosome in males, leading to infertility and other physical characteristics.
7. Williams syndrome: A rare genetic disorder caused by a deletion of genetic material on chromosome 7, characterized by cardiovascular problems, developmental delays, and a distinctive facial appearance.
8. Fragile X syndrome: The most common form of inherited intellectual disability, caused by an expansion of a specific gene on the X chromosome.
9. Prader-Willi syndrome: A genetic disorder caused by a defect in the hypothalamus, leading to problems with appetite regulation and obesity.
10. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dry eyes and mouth.

Syndromes can be diagnosed through a combination of physical examination, medical history, laboratory tests, and imaging studies. Treatment for a syndrome depends on the underlying cause and the specific symptoms and signs presented by the patient.

... anti-Sm antibodies, anti-nRNP antibodies, anti-Scl-70 antibodies, anti-dsDNA antibodies, anti-histone antibodies, antibodies to ... Anti-nuclear ribonucleoprotein (anti-nRNP) antibodies, also known as anti-U1-RNP antibodies, are found in 30-40% of SLE. They ... Antinuclear antibodies (ANAs, also known as antinuclear factor or ANF) are autoantibodies that bind to contents of the cell ... This pattern is associated with anti-dsDNA antibodies, antibodies to nucleosomal components, and anti-histone antibodies. There ...
ANA) Antinuclear Antibodies". CARD in Libby, MT. Retrieved 2020-12-21. "LIBBY GROUND WATER CONTAMINATION Site Profile". United ...
Invernizzi P, Selmi C, Ranftler C, Podda M, Wesierska-Gadek J (2005). "Antinuclear antibodies in primary biliary cirrhosis". ... 2003). "Profile and clinical significance of anti-nuclear envelope antibodies found in patients with primary biliary cirrhosis ... Anti-p62 antibodies (AP62A) are found in a primary biliary cirrhosis. The p62 protein is also more frequent in Stage IV primary ...
Other auto-antibodies may be present: Antinuclear antibody measurements are not diagnostic for PBC because they are not ... Nesher G, Margalit R, Ashkenazi YJ (April 2001). "Anti-nuclear envelope antibodies: Clinical associations". Seminars in ... Anti-glycoprotein-210 antibodies, and to a lesser degree anti-p62 antibodies, correlate with the disease's progression toward ... Anti-gp210 antibodies are found in 47% of PBC patients. Anti-centromere antibodies often correlate with developing portal ...
"Antinuclear Antibody (ANA)". labtestsonline.org. Retrieved 14 April 2020. "Complete blood count (CBC)". www.mayoclinic.org. 19 ... A test used to identify abnormal proteins, known as antinuclear antibodies, produced when the body attacks its own tissues. It ... have shown an increase of antinuclear antibodies, a common biomarker for autoimmune diseases. This shows that there has been an ... "Increasing Prevalence of Antinuclear Antibodies in the United States". Arthritis & Rheumatology. 72 (6): 1026-1035. doi:10.1002 ...
Ehrenstein MR (August 1999). "Antinuclear antibodies and lupus: causes and consequences". Rheumatology. 38 (8): 691-3. doi: ... I. A clinical analysis of 55 anti-Yo antibody-positive patients". Neurology. 42 (10): 1931-7. doi:10.1212/wnl.42.10.1931. PMID ... Franceschini F, Cavazzana I (February 2005). "Anti-Ro/SSA and La/SSB antibodies". Autoimmunity. 38 (1): 55-63. doi:10.1080/ ... "Possible Source of Kawasaki Disease Found". Wisnieski JJ, Naff GB (September 1989). "Serum IgG antibodies to C1q in ...
... pattern of anti-nuclear antibody, and complement-fixing antibodies to DNA in sera from patients with systemic lupus ... These are known as anti-nuclear antibodies (ANA) and have also been observed in concert with multiple sclerosis as part of ... Barned S, Goodman AD, Mattson DH (February 1995). "Frequency of anti-nuclear antibodies in multiple sclerosis". Primary. ... Antibodies to certain types of chromatin organization, in particular, nucleosomes, have been associated with a number of ...
Two thirds of patients have positive anti nuclear antibodies. The IgM levels are usually low and a low IgA is common. There is ... The name is an acronym of "PLCG2-associated antibody deficiency and immune dysregulation". It is characterised by cold-induced ... The name is an acronym of PLCG2-associated antibody deficiency and immune dysregulation.[citation needed] Milner, JD (August ... PLAID syndrome is an inherited condition characterised by antibody deficiency and immune dysregulation, first described in 2012 ...
... antinuclear antibodies were negative and p-ANCA was reactive. Coagulation studies were within normal limits. There was an ...
In addition, he studied the relationship between juvenile idiopathic arthritis and uveitis to antinuclear antibodies (ANA), ... "Clinical correlates of antinuclear antibodies in juvenile rheumatoid arthritis". The Journal of Pediatrics. 83 (3): 386-389. ... His thesis was titled The significance of antibody affinity in immune complex disease. In 1976, Petty returned to Canada and ... the influence of maternal anti-IgA antibodies on the occurrence of IgA deficiency in the offspring. He and colleagues first ...
Of the antibodies, 90% have a detectable antinuclear antibody. Anticentromere antibody is more common in the limited form (80- ... and a normal antinuclear antibodies test result. No cure for scleroderma is known, though treatments exist for some of the ... It is most common in diffuse cutaneous scleroderma, and is often associated with antibodies against RNA polymerase (in 59% of ... The patient's white blood cells are destroyed with cyclophosphamide and rabbit antibodies against the white blood cells. Then, ...
... especially antinuclear antibodies (ANA). Around 80% of people with DM test positive for ANA and around 30% of people have ... anti-synthetase antibodies), including antibodies against histidine-tRNA ligase (also called Jo-1); antibodies to signal ... recognition particle (SRP); and anti-Mi-2 antibodies. Magnetic resonance imaging may be useful to guide muscle biopsy and to ... myositis-specific autoantibodies which include antibodies to aminoacyl-tRNA synthetases ( ...
Anti-double stranded DNA (Anti-dsDNA) antibodies are a group of anti-nuclear antibodies (ANA) the target antigen of which is ... Animal tissue was the first substrate for immunofluorescent detection of antinuclear antibodies and has been in use since the ... The first evidence for antinuclear antibodies arose in 1948 when Hargraves, Richmond and Morton discovered the LE cell. These ... Kumar Y, Bhatia A, Minz RW (2009). "Antinuclear antibodies and their detection methods in diagnosis of connective tissue ...
Antinuclear antibodies and anti-dsDNA antibodies may be positive. Biopsies show non specific inflammatory changes.[citation ...
Garcia-De La Torre, Ignacio (1993). "Autoimmune phenomena in leprosy, particularly antinuclear antibodies and rheumatoid factor ... It is defined as an antibody against the Fc portion of IgG and different RFs can recognize different parts of the IgG-Fc. RF ... Rheumatoid factor can also be a cryoglobulin (antibody that precipitates on cooling of a blood sample); it can be either type 2 ... Zhang Y, Liang Y, Feng L, Cui L. Diagnostic performance of 14-3-3η and anti-carbamylated protein antibodies in Rheumatoid ...
... is an anti-nuclear antibody. Anti-Jo1 has been associated with inflammatory myopathies such as polymyositis and ... "A dermatomyositis and scleroderma overlap syndrome with a remarkable high titer of anti-exosome antibodies" (PDF). Reumatismo. ... and anti-Jo-1 antibodies--an interesting association". Clinical and Diagnostic Laboratory Immunology. 4 (2): 236-40. doi: ...
"ANA (Antinuclear Antibody) Test: MedlinePlus Medical Test". medlineplus.gov. Retrieved 2022-11-18. "Joint Aspiration ( ... Doctors may perform some of the following tests to diagnose the condition ANA (Antinuclear Antibody) Test Joint Aspiration ... and may cause eye inflammation in girls with positive anti-nuclear antibodies (ANA). Girls younger than eight are more likely ... number of joints involved and the presence of certain antibodies in the blood. Polyarticular arthritis is the first type of ...
Unlike in SLE, an anti-nuclear antibody test is usually negative. Avoiding sun exposure and the use of sunscreens (not ...
"Antinuclear antibodies in patients with Raynaud's phenomenon: clinical significance of anticentromere antibodies". Annals of ... Cold sensitive antibodies (CSA) are antibodies sensitive to cold temperature. Some cold sensitive antibodies are pathological ... In cryoglobulinemia, antibodies accumulate and block blood vessels. In cold agglutinin disease, antibodies (different from ... Yet, the place where the hemolysis taking place differentiates between D-L antibodies and cold agglutinin. D-L antibodies ...
Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies (which are linked to SLE ... Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for ... These are most commonly anti-nuclear antibodies and they result in inflammation. Diagnosis can be difficult and is based on a ... which leads to the development of antinuclear antibodies. Monocytes isolated from whole blood of people with SLE show reduced ...
"Multiple nuclear dots antinuclear antibodies are not specific for primary biliary cirrhosis". Hepatology. 16 (1): 127-31. doi: ... antibodies to measles show expression in and localization to the nuclear bodies. In promyelocytic leukemia (PML), the oncogenic ...
Autoantibodies may be present including antinuclear, antiphospholipid, and anticardiolipin antibodies.[citation needed] The ...
"Antinuclear Autoantibodies in Health: Autoimmunity Is Not a Synonym of Autoimmune Disease". Antibodies. 10 (1): 9. doi:10.3390/ ... He studied antigen-antibody reactions and developed a "carrier" theory of antibody function. His award-winning development of ... Auto-antibodies and immunological theories: An analytical review". Clinical Immunology and Immunopathology. 4 (4): 453-466. doi ... Pierre Grabar spent several years simplifying Tiselius' methodology, modifying his method by introducing antibodies. In 1953 ...
Diagnostic testing includes screening for the positive antinuclear antibody.[citation needed] There is no current cure. The ... Vandergheynst F, Ocmant A, Sordet C, Humbel RL, Goetz J, Roufosse F, Cogan E, Sibilia J (2006). "Anti-pm/scl antibodies in ... Autoantibodies often found in these patients are the anti-PM/Scl (anti-exosome) antibodies. The symptoms that are seen most ... As of 2006 it is unclear which antibodies will best treat connective tissue diseases. One study from 2014 showed some potential ...
The antinuclear antibody (ANA) test is often ordered first. ANA is a marker of the autoimmune process - it is positive with a ... Many autoimmune diseases (notably lupus erythematosus) are associated with such antibodies. Antibodies are produced by B cells ... An autoantibody is an antibody (a type of protein) produced by the immune system that is directed against one or more of the ... Initially, one B cell produces one specific kind of antibody. In either case, the B cell is allowed to proliferate or is killed ...
Graus F, Cordon-Cardo C, Posner JB (1985). "Neuronal antinuclear antibody in sensory neuronopathy from lung cancer". Neurology ... Nearly all people with the condition have anti-Hu antibodies in their serum. The antibody is produced by the body as an immune ... However, the injection of the antibodies into mice did not produce any disease, and the deposition of antibody was often not at ... Pohley I, Roesler K, Wittstock M, Bitsch A, Benecke R, Wolters A (2015). "NMDA-receptor antibody and anti-Hu antibody positive ...
Permin H, Wiik A (October 1978). "The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus ... June 2010). "Antibodies specific for a segment of human membrane IgE deplete IgE-producing B cells in humanized mice". The ... In the second approach, antibodies specific for a domain of 52 amino acid residues, referred to as CεmX or M1' (M1 prime), ... Immunoglobulin E (IgE) is a type of antibody (or immunoglobulin (Ig) "isotype") that has been found only in mammals. IgE is ...
These are called anti-mitochondrial antibodies (AMA) and anti-nuclear antibodies (ANA), respectively. These antibodies are ... O'Brien C, Joshi S, Feld JJ, Guindi M, Dienes HP, Heathcote EJ (Aug 2008). "Long-term follow-up of antimitochondrial antibody- ... There is also evidence of anti-PDC-E2 antibodies in autoimmune hepatitis (AIH) patients. Pyruvate dehydrogenase deficiency (PDH ... "Catalytic domain of PDC-E2 contains epitopes recognized by antimitochondrial antibodies in primary biliary cirrhosis". World ...
"Antinuclear antibody, lupus anticoagulant, and anticardiolipin antibody in women with idiopathic habitual abortion. A ... They are a form of anti-mitochondrial antibody. In SLE, anti-DNA antibodies and anti-cardiolipin antibodies may be present ... Anti-cardiolipin antibodies (ACA) are antibodies often directed against cardiolipin and found in several diseases, including ... Only a subset of autoimmune anti-cardiolipin antibodies bind Apo-H, these anti-apolipoprotein antibodies are associated with ...
The appearance of anti-nuclear antibodies in autoimmune hepatitis was found to correlate with A1-B8-DR3. One of the problems ... Christian N, Smikle MF, DeCeulaer K, Daniels L, Walravens MJ, Barton EN (March 2007). "Antinuclear antibodies and HLA class II ... of these half had anti-transglutaminase antibodies, but few had endomysial antibody. This could indicate an association with ... DR3 is found to correlate with anti-Ro/La antibodies in SLE. HLA-DR3 has been consistently observed at high frequencies in ...
... is an anti-topoisomerase antibody-type of anti-nuclear autoantibodies, seen mainly in diffuse systemic scleroderma (with a ... Anti Scl-70 antibodies are associated with more severe scleroderma disease. The etymology of scl-70 consists of an abbreviation ... de Rooij DJ, Van de Putte LB, Habets WJ, Van Venrooij WJ (1989). "Marker antibodies in scleroderma and polymyositis: clinical ... of the antibodies. Guldner HH, Szostecki C, Vosberg HP, Lakomek HJ, Penner E, Bautz FA (1986). "Scl 70 autoantibodies from ...
In particular, IgA, IgE (in females only) and C-reactive protein have been shown to decrease whereas antinuclear antibodies ... in the C8 studies are decreased antibody response to vaccines, asthma, decreased mammary gland development, low birth weight (- ... PFAS exposure is linked to increased risk of decreased antibody response, dyslipidemia (abnormally high cholesterol), decreased ...
... antinuclear antibody, rheumatoid factor) and serology for infectious diseases (Syphilis, Toxoplasmosis, Tuberculosis). Major ...
... proteins are also the autoantigenic target for some anti-nuclear antibodies, such as anti-centromere antibodies. It ...
2011) was found to have antinuclear antibody, anti-dsDNA antibody titers, microglobulinemia, and hypogammaglobulinemia. Hermann ... "ACP5 Gene - GeneCards , PPA5 Protein , PPA5 Antibody". www.genecards.org. Retrieved 2022-10-23. "ACP5 gene: MedlinePlus ...
... an intermediate representation of programs in functional compilers Anti-nuclear antibody, or anti-nuclear factor in blood Array ...
Beside CD4+T cells to inflammation disorder contribute B cells by producing autoantibodies like antinuclear antibodies. The ...
In the 1990s and 2000s the roles of antibodies in the condition became more clear. SPS patients generally have GAD antibodies, ... Anti-thyroid, anti-intrinsic factor, anti-nuclear, anti-RNP, and anti-gliadin are also often present in blood tests. ... It is also unknown whether these antibodies are pathogenic. The amount of GAD antibody titers found in SPS patients does not ... Most SPS patients with high-titer GAD antibodies also have antibodies that inhibit GABA-receptor-associated protein (GABARAP). ...
... antibodies, antineutrophil cytoplasmic MeSH D12.776.377.715.548.114.323.204 - antibodies, antinuclear MeSH D12.776.377.715. ... antibodies MeSH D12.776.377.715.548.114.071 - antibodies, anti-idiotypic MeSH D12.776.377.715.548.114.107 - antibodies, ... antibodies, bispecific MeSH D12.776.377.715.548.114.143 - antibodies, blocking MeSH D12.776.377.715.548.114.167 - antibodies, ... antibodies, helminth MeSH D12.776.377.715.548.114.191 - antibodies, heterophile MeSH D12.776.377.715.548.114.224 - antibodies, ...
23 March - Hilda Murrell, 78-year-old rose grower and anti-nuclear campaigner, is found dead near her home in Shropshire, five ... in development and control of the immune system and the discovery of the principle for production of monoclonal antibodies". 11 ...
These might include: rheumatoid factor, antinuclear factor (ANF), extractable nuclear antigen, and specific antibodies.[ ... The drugs to treat rheumatoid arthritis (RA) range from corticosteroids to monoclonal antibodies given intravenously. Due to ...
... focused on the reproducible detections antinuclear antibodies (ANA) with fluorescein labeled antibodies to human IgG. Beutner ... of Microbiology - New York Academy of Sciences (1983) Code of Federal Regulations, Antinuclear antibody immunological test ... 682-688; Jordon, RE., Beutner, E.H. Witebsky E., Blumenthal B., Hale, W.L. & Lever, W.F. (1967) Basement Zone Antibodies in ... Lupus.2004;13(11):839-49 Beutner, E. H.; Jordon, R.E. (November 1964). "Demonstration of skin antibodies in sera of pemphigus ...
Tests for rheumatoid factor and anti-nuclear antibodies are usually negative and serum ferritin is markedly elevated. Patients ... The monoclonal anti-IL6 antibody tocilizumab is another treatment option as effective as anakinra. The condition "juvenile- ...
... thrombocytopenic purpura and is preferred over danazol or interferon alpha in those people with antinuclear antibodies. Chronic ...
The association with viral hepatitis was subsequently demonstrated and patients with antinuclear antibodies were more likely to ... Though, the association of A1 with autoimmune hepatitis with no anti-viral antibody was stronger than with chronic active ...
... antibodies, antineutrophil cytoplasmic MeSH D12.776.124.486.485.114.323.204 - antibodies, antinuclear MeSH D12.776.124.486. ... antibodies, antineutrophil cytoplasmic MeSH D12.776.124.790.651.114.323.204 - antibodies, antinuclear MeSH D12.776.124.790. ... antibodies MeSH D12.776.124.486.485.114.071 - antibodies, anti-idiotypic MeSH D12.776.124.486.485.114.089 - antibodies, ... antibodies, bispecific MeSH D12.776.124.486.485.114.143 - antibodies, blocking MeSH D12.776.124.486.485.114.167 - antibodies, ...
Additional, more specific tests include: Antinuclear antibody test can detect an underlying connective tissue disorder, ... Antineutrophil cytoplasmic antibody may suggest granulomatosis with polyangiitis, microscopic polyangiitis, eosinophilic ... Bosch X, Guilabert A, Espinosa G, Mirapeix E (2007). "Treatment of antineutrophil cytoplasmic antibody associated vasculitis: a ... A systematic review of antineutrophil cytoplasmic antibody-positive vasculitis identified best treatments depending on whether ...
Affimer Anti-mitochondrial antibodies Anti-nuclear antibodies Antibody mimetic Aptamer Colostrum ELISA Humoral immunity ... antibody Neutralizing antibody Optimer Ligand Secondary antibodies Single-domain antibody Slope spectroscopy Synthetic antibody ... Antibody fragments, such as Fab and nanobodies are not considered as antibody mimetics. Common advantages over antibodies are ... these antibodies are called monoclonal antibodies. Polyclonal and monoclonal antibodies are often purified using Protein A/G or ...
Antinuclear antibodies and anti-smooth muscle antibody are found in 20-50% of PSC patients, and likewise are not specific for ... An IgA isotype autoantibody to the pancreatic GP2 protein (anti-GP2 IgA antibody) is the first verified prognostic biomarker in ... Simtuzumab is a monoclonal antibody against the profibrotic enzyme LOXL2 that is being developed as a possible therapy for PSC ... Tornai D, Papp M (January 2021). "Editorial: serologic antibodies in primary sclerosing cholangitis - a tell-tale sign of ...
Brennan FM, Andrew EM, Williams DG, Maini RN (February 1988). "Anti-nRNP anti-nuclear antibody-secreting cells are represented ... Anti-nRNP is a type of antibody. They are autoantibodies against some ribonucleoproteins. Anti-nRNP antibodies can be elevated ... snRNP70 Migliorini P, Baldini C, Rocchi V, Bombardieri S (February 2005). "Anti-Sm and anti-RNP antibodies". Autoimmunity. 38 ( ... Satoh M, Richards HB, Hamilton KJ, Reeves WH (May 1997). "Human anti-nuclear ribonucleoprotein antigen autoimmune sera contain ...
Lewy, RI (1995). "Antinuclear Antibodies, Lipid Disturbances and Central Nervous System Imaging Abnormalities in Silicone ...
... and those with a positive anti-nuclear antibody (ANA). It usually follows the onset of arthritis or may be detected at the same ... as well as the presence of specific immune markers which may include anti-nuclear antibody, HLA-B27, rheumatoid factor and anti ... The anti-nuclear antigen (ANA) is positive in up to 80% of patients with oligoarthritis and is associated with a higher risk of ... protein antibody. These serological markers may be negative in children with JIA, and are often present in healthy children; as ...
The antinuclear antibody panel is a blood test that looks at antinuclear antibodies (ANA). ... Antinuclear antibodies (ANA). www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions/Antinuclear-Antibodies-ANA. ... The antinuclear antibody panel is a blood test that looks at antinuclear antibodies (ANA). ... The antinuclear antibody test looks for antibodies that bind to a part of the cell called the nucleus. ...
Information on antinuclear antibodies (ANA) and their role in rheumatic disease, how to test for them and what a positive ... Anti-nuclear antibodies (ANA) are possible signs of autoimmune diseases, such as lupus, scleroderma, Sjögrens syndrome, ... Sometimes, antibodies target normal proteins in our body by mistake. This can trigger inflammation that leads to joint or ... These antibodies are called autoantibodies. Everyone has small amounts of autoantibodies. ANAs are one type of autoantibody. A ...
... [Abstract Increasing Prevalence of Antinuclear Antibodies ... Synopsis Increasing Prevalence of Antinuclear Antibodies in the United States] [Story Increasing Prevalence of Antinuclear ... Antibodies in the United States] Dinse GE, Parks CG, Weinberg CR, Co CA, Wilkerson J, Zeldin DC, Chan EKL, Miller FW. June 2020 ...
Most of these antibodies are IgG, but IgM and IgA have also been detected. ... tests identify antibodies present in serum that bind to autoantigens present in the nuclei of mammalian cells. ... encoded search term (Antinuclear Antibody) and Antinuclear Antibody What to Read Next on Medscape ... Antinuclear antibody (ANA) tests identify antibodies present in serum that bind to autoantigens present in the nuclei of ...
... *Medical Editor: William C. Shiel Jr., MD, FACP, FACR ... Antinuclear antibodies (ANAs) are most commonly described in titers of dilution. That is, the highest dilution at which they ...
Complement-fixing antinuclear antibody (CFANA) titers were measured in 18 patients with lupus nephritis and were compared to ... Complement-fixing antinuclear antibody (CFANA) titers were measured in 18 patients with lupus nephritis and were compared to ... Comparison of the complement-fixing activity of antinuclear antibodies in lupus nephritis, mixed connective tissue disease, and ... among these patients with high titer ANA cannot be explained by differences in complement fixation by these antibodies. ...
The non-detection of hidden anti-nuclear antibodies by tissue sections in the absence of a splitting agent may be … ... Hidden anti-nuclear antibodies are demonstrated by immunofluorescence using smears of rat nuclei as substrate and rat liver ... Hidden anti-nuclear antibodies in rheumatic diseases P S Mach, D Piatier, A Le Go, F Delbarre ... Hidden anti-nuclear antibodies in rheumatic diseases P S Mach et al. Clin Exp Immunol. 1980 Feb. ...
The non-detection of hidden anti-nuclear antibodies by tissue sections in the absence of a splitting agent may be … ... Hidden anti-nuclear antibodies are demonstrated by immunofluorescence using smears of rat nuclei as substrate and rat liver ... Hidden anti-nuclear antibodies in rheumatic diseases P S Mach, D Piatier, A Le Go, F Delbarre ... Hidden anti-nuclear antibodies in rheumatic diseases P S Mach et al. Clin Exp Immunol. 1980 Feb. ...
Response to: Antinuclear antibodies: mitotic patterns and their clinical associations by Betancur and Gómez-Puerta ... Response to: Antinuclear antibodies: mitotic patterns and their clinical associations by Betancur and Gómez-Puerta ...
Book Antinuclear Antibodies Immunofluorescence Biopsy Tissue @Home at Best Prices at the slot of your choice. View details of ... An Antinuclear Antibodies (ANA) test measures the antinuclear antibodies present in the body. ... Antinuclear antibodies are also produced by our immune system that attacks and destroys the bodys normal tissues. They target ... If the ANA test results are positive it indicates the presence of antinuclear antibodies in the blood. A positive result can be ...
ten Berge, J., Groen, F., Rothova, A., & Schreurs, M. (2018). Antinuclear antibody profiling in uveitis. Acta Ophthalmologica, ... Antinuclear antibody profiling in uveitis. / ten Berge, Josianne; Groen, Fahriye; Rothova, Aniki et al. In: Acta ... ten Berge, J, Groen, F, Rothova, A & Schreurs, M 2018, Antinuclear antibody profiling in uveitis, Acta Ophthalmologica, vol. ... title = "Antinuclear antibody profiling in uveitis",. author = "{ten Berge}, Josianne and Fahriye Groen and Aniki Rothova and ...
... study were to detect serum anti-HMGB1 antibodies in patients with SLE and relate them to other types of antinuclear antibodies ... Levels of anti-HMGB1 antibodies correlated with anti-dsDNA antibody levels (r = 0.49; p < 0.001). Significant, but less ... Anti-HMGB1 antibodies occurred in 49 % of the IF-ANA positive SLE patients, and in 34 % of IF-ANA negative cases (p ... Anti-HMGB1 antibody levels were analysed in patient and control (n = 112) sera by an in-house ELISA using recombinant histidine ...
Book Anti Nuclear Antibody, EIA In New Delhi online from Tata 1mg Labs ( Tata 1mg Technologies Private Limited). View test ... Anti Nuclear Antibody, EIA. ?. The anti nuclear antibody (ANA) test is used to detect the presence of antinuclear antibodies ( ... Anti-dsDNA Antibody Test · Anti-Centromere Antibody Test · Anti-Histone Antibody Test · Anti-Smooth Muscle Antibody Test. ... Antibodies produced in an autoimmune disease are called autoantibodies.. Antinuclear antibodies (ANA) are autoantibodies that ...
Antinuclear antibody. Antinuclear antibody (ANA) results are negative in ankylosing spondylitis but positive in many patients ... What is the role of antinuclear antibody (ANA) testing in the workup of ophthalmologic manifestations of ankylosing spondylitis ... Treponemal tests such as the fluorescent treponemal antibody absorption (FTA-ABS) test should be performed to rule out syphilis ...
Antinuclear antibody (ANA) test is used as a primary test to help evaluate a person for autoimmune disorders that affect many ... Antinuclear antibody Titer and Pattern. $60.00. Antinuclear antibody (ANA) test is used as a primary test to help evaluate a ... Home / Lab Tests / Antinuclear antibody Titer and Pattern. Lab Tests. ...
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Antinuclear Antibodies (ANA) Level. CPT Code 86038 A lab test to analyze for the presence of antinuclear antibodies in the ... Analysis for antibody borrelia burgdorferi (lyme disease bacteria) (86618). *Measurement of antibody for rheumatoid arthritis ... serum (antibodies to the nucleus of a human cell) to screen for an autoimmune disorder. ...
Anti-Nuclear cap-binding protein subunit 1 Antibody Product Information Form: Lyophilized Stability & Storage: Use a manual ... Youre reviewing:ABH1 / Anti-Nuclear cap-binding protein subunit 1 Antibody. Your Rating. Rating. 1 star 2 stars 3 stars 4 ...
ANA-associated rheumatic disease; anti-DFS70 antibody; anti-nuclear antibody; dense fine speckled; diagnosis ... To investigate the relationship between the prevalence of antinuclear antibody (ANA) -associated rheumatic diseases (AARD) and ... The significance of dense fine speckled pattern in antinuclear antibody-associated rheumatic disease and coexisting ... The significance of dense fine speckled pattern in antinuclear antibody-associated rheumat ...
"Range of antinuclear antibodies in healthy individuals",. abstract = "Objective. To determine the range of antinuclear ... Range of antinuclear antibodies in healthy individuals. / Tan, E. M.; Feltkamp, T. E.W.; Smolen, J. S. et al. In: Arthritis ... Range of antinuclear antibodies in healthy individuals. E. M. Tan, T. E.W. Feltkamp, J. S. Smolen, B. Butcher, R. Dawkins, M ... Range of antinuclear antibodies in healthy individuals. Arthritis and Rheumatism. 1997 Sep;40(9):1601-1611. doi: 10.1002/art. ...
Antinuclear antibody. Anti-double stranded DNA. Anti-Ro antigen. Anti-Smith antigen ... or antibodies in serum and CSF. Only antibodies were found in this patient. However, viral antigen and RNA often are not ... Detection of viral antibodies in serum can be indicative of previous vaccination or exposure to a lyssavirus, but does not ... Antibodies to rabies virus were detected in specimens of the girls serum and cerebrospinal fluid (CSF) by indirect fluorescent ...
Antiglomerular basement membrane antibody test. *Antineutrophil cytoplasmic antibodies (ANCAs). *Antinuclear antibodies. *BUN ... that does not contain antibodies). Removing antibodies may reduce inflammation in the kidney tissues. ... The fluid part of the blood that contains antibodies is removed and replaced with intravenous fluids or donated plasma ( ... Membranoproliferative GN (form of glomerulonephritis due to abnormal buildup of antibodies in the kidneys) ...
Antiphospholipid antibodies * Enzyme-linked immunosorbent assay (ELISA) for toxoplasmosis, rubella, cytomegalovirus, herpes ...
... antinuclear antibodies; lipemia; icterus; systemic lupus erythematosus; rheumatoid arthritis; and positive results for ... Two-tiered antibody testing for Lyme disease with use of 2 enzyme immunoassays, a whole-cell sonicate enzyme immunoassay ... Evaluation of the intrathecal antibody response to Borrelia burgdorferi as a diagnostic test for Lyme neuroborreliosis. J ... Persistence of immunoglobulin M or immunoglobulin G antibody responses to Borrelia burgdorferi 10-20 years after active Lyme ...
Antinuclear antibodies (ANAs). Any antibody to nuclear components is an ANA. Most patients with ANAs do not have SLE, but most ... Antibodies to ENAs. ANTI-RO/la antibodies. Diagnosis. Antibodies to Ro(SS-A) and La(SS-B) are found in SLE and Sjogrens ... Range of antinuclear antibodies in "healthy" individuals [see comments]. Arthritis Rheum 1997;40:1601-11. ... dsDNA antibodies rise in active disease and in the evolution of lupus nephritis in most patients.51-55 dsDNA antibody assays ...
... anticardiolipin antibody; and antinuclear antibody. In contrast, people with ALPS often have abnormally low levels of HDL (high ...
... s list of labs providing Anti-Nuclear Antibody (ANA IFA) Test services in Gurgaon & book Anti-Nuclear Antibody (ANA IFA) Test ... Want to book affordable Anti-Nuclear Antibody (ANA IFA) Test online? Check out Flebo.in ... Anti-Nuclear Antibody (ANA IFA) Test In Gurgaon. () Starts from 475* An anti-nuclear antibody or ANA IFA test in Gurgaon is ... What does the Anti-Nuclear Antibody (ANA IFA) Test measure? In simple words, the antinuclear antibody test or the ANA IFA test ...
antinuclear antibody test (ANA). *rheumatoid factor (RF). *complement 3 (C3). *complement 4 (C4) ...
positive antinuclear. phosphokinase. antibody. increased bilirubin. increased liver. transaminases (AST [SGOT], ALT [SGPT]). ...
  • The authors conclude that no relationship could be established between chemical exposures and antinuclear antibody positivity. (cdc.gov)
  • What Is a Healthy Range of Antinuclear Antibodies (ANAs)? (medicinenet.com)
  • Antinuclear antibodies (ANAs) are most commonly described in titers of dilution. (medicinenet.com)
  • ANAs are antibodies that cause disease by attacking healthy cells and tissues. (1mg.com)
  • Antinuclear antibody (ANA) tests identify antibodies present in serum that bind to autoantigens present in the nuclei of mammalian cells. (medscape.com)
  • The IFA method used in most laboratories uses human tumor cell-line substrate (the HEp-2 cell line) to detect the presence of these antibodies in human serum. (medscape.com)
  • The main aims of this study were to detect serum anti-HMGB1 antibodies in patients with SLE and relate them to other types of antinuclear antibodies (ANA), and to disease activity. (biomedcentral.com)
  • Abnormally high serum levels of antinuclear antibodies (ANA) assessed by indirect immunofluorescence (IF) microscopy (IF-ANA) is one of the 11 classification criteria for systemic lupus erythematosus (SLE) according to the American College of Rheumatology (ACR) 1982 and the suggested update 1997 [ 1 , 2 ]. (biomedcentral.com)
  • A lab test to analyze for the presence of antinuclear antibodies in the serum (antibodies to the nucleus of a human cell) to screen for an autoimmune disorder. (nh.gov)
  • Antibodies to rabies virus were detected in specimens of the girl's serum and cerebrospinal fluid (CSF) by indirect fluorescent antibody test (IFA). (cdc.gov)
  • 24. Detection and identification of antinuclear antibodies (ANA) in a large and consecutive cohort of serum samples referred for ANA testing. (nih.gov)
  • These antibodies are called autoantibodies. (rheumatology.org)
  • Antibodies produced in an autoimmune disease are called autoantibodies. (1mg.com)
  • Antinuclear antibodies (ANA) are autoantibodies that are produced against protein markers present in the nucleus of certain cells of the body. (1mg.com)
  • The significance of dense fine speckled pattern in antinuclear antibody-associated rheumatic disease and coexisting autoantibodies: A propensity score-matched cohort study. (bvsalud.org)
  • The presence of anti-DFS70 antibodies and other common autoantibodies were detected using EUROLINE ANA Profile 23. (bvsalud.org)
  • Among the 33 patients with monospecific anti-DFS70 antibodies , five had a mixed pattern, and all patients with common autoantibodies had an isolated DFS pattern. (bvsalud.org)
  • Autoantibodies are antibodies that target one's own cells and tissues. (nih.gov)
  • Anti-nuclear antibodies (ANA) are possible signs of autoimmune diseases, such as lupus, scleroderma, Sjögren's syndrome, juvenile arthritis, or polymyositis and dermatomyositis. (rheumatology.org)
  • Hidden anti-nuclear antibodies are demonstrated by immunofluorescence using smears of rat nuclei as substrate and rat liver section technique when sera are incubated with penicillamine. (nih.gov)
  • The non-detection of hidden anti-nuclear antibodies by tissue sections in the absence of a splitting agent may be due to the formation of high molecular weight complexes between rheumatoid factors and anti-nuclear antibodies. (nih.gov)
  • These high molecular weight complexes containing anti-nuclear antibodies do not have access to tissue nuclear antigens, but can react directly with free nuclei. (nih.gov)
  • It is postulated that anti-nuclear antibodies may represent the early pathway of both rheumatoid arthritis and connective tissue diseases. (nih.gov)
  • The demonstration of hidden anti-nuclear antibodies in seropositive sera indicates that rheumatoid factors may have a protective effect. (nih.gov)
  • that's anti-nuclear antibodies. (curezone.com)
  • 31. Can an ELISA replace immunofluorescence for the detection of anti-nuclear antibodies? (nih.gov)
  • Systemic lupus erythematosus (SLE) is also a common autoimmune and inflammatory disease, which is characterized by complement activation, production of numerous auto-antibodies and damage to multiple organs and tissues. (spandidos-publications.com)
  • 4. Scl 70 antibody--a specific marker of systemic sclerosis. (nih.gov)
  • 5. [Anti-Scl-70 antibodies in systemic scleroderma]. (nih.gov)
  • 6. Antinuclear antibodies in the relatives of patients with systemic sclerosis. (nih.gov)
  • 7. Clinical significance of antinuclear antibodies in Japanese patients with systemic sclerosis. (nih.gov)
  • 10. Antinuclear antibodies in progressive systemic sclerosis. (nih.gov)
  • 15. Clinical and laboratory associations of anticentromere antibody in patients with progressive systemic sclerosis. (nih.gov)
  • 18. Association of anti-U1RNP- and anti-Scl-70-antibodies with neurological manifestations in systemic sclerosis (scleroderma). (nih.gov)
  • 19. Anti-Scl-70 antibodies detected by immunoblotting in progressive systemic sclerosis: specificity and clinical correlations. (nih.gov)
  • An antibody pattern is reported with a positive titer and gives an indication of the likely diagnosis (see the image below). (medscape.com)
  • Thus the striking differences in the prevalence of nephritis among these patients with high titer ANA cannot be explained by differences in complement fixation by these antibodies. (nih.gov)
  • 36. Utility of age, gender, ANA titer and pattern as predictors of anti-ENA and -dsDNA antibodies. (nih.gov)
  • Immunodiffusion (ID) detects high affinity antibodies, immunofluorescence (IIF) moderate and high affinity antibodies, and enzyme linked immunosorbent assay (ELISA) low and high affinity antibodies. (bmj.com)
  • 28. Enzyme-linked immunosorbent assay screening then indirect immunofluorescence confirmation of antinuclear antibodies: a statistical analysis. (nih.gov)
  • 33. [Comparison of indirect immunofluorescence assay and ELISA for detecting antinuclear antibodies and anti-double-stranded DNA antibodies]. (nih.gov)
  • 39. Detection of specific antinuclear reactivities in patients with negative anti-nuclear antibody immunofluorescence screening tests. (nih.gov)
  • The reference range for antinuclear antibody is negative by ELISA. (medscape.com)
  • Anti-HMGB1 antibody levels were analysed in patient and control (n = 112) sera by an in-house ELISA using recombinant histidine-tagged HMGB1. (biomedcentral.com)
  • Although anti-HMGB1 antibodies measured by ELISA often coincide with nuclear IF-ANA staining, our results indicate that anti-HMGB1 antibodies do not give rise to nuclear staining of the predominantly used commercial HEp-2 cell slides. (biomedcentral.com)
  • The Antinuclear Antibody Test can be performed either by Immunoassay method (ELISA) or Indirect Fluorescent Antibody (IFA) method to detect ANA in blood. (1mg.com)
  • Both these tests may be used by some laboratories together: the Immunoassay method (ELISA) screens for the presence of antinuclear antibodies, and IFA method subsequently confirms the positive or equivocal Immunoassay results. (1mg.com)
  • 21. [Detection of anti-SSA/Ro antibody by ELISA, double immunodiffusion, and immunoblotting: a comparative study]. (nih.gov)
  • 22. Screening tests for antinuclear antibodies (ANA): selective use of central nuclear antigens as a rational basis for screening by ELISA. (nih.gov)
  • What are Antiphospholipid Antibodies (APA)? (sharedjourney.com)
  • This is the case with antiphospholipid antibodies - they attack our own cells. (sharedjourney.com)
  • Antiphospholipid antibodies are proteins that circulate around in the bloodstream. (sharedjourney.com)
  • There are 21 different types of antiphospholipid antibodies. (sharedjourney.com)
  • Who Has Antiphospholipid Antibodies? (sharedjourney.com)
  • Though they can cause problems, surprisingly, 2% to 15% of the healthy population actually has antiphospholipid antibodies in their blood. (sharedjourney.com)
  • It is only when they are at high levels that the antiphospholipid antibodies begin to make trouble. (sharedjourney.com)
  • It is thought that antiphospholipid antibodies compromise the placenta which nourishes your baby. (sharedjourney.com)
  • To investigate the relationship between the prevalence of antinuclear antibody (ANA) -associated rheumatic diseases (AARD) and the presence of dense fine speckled (DFS) and homogeneous patterns in ANA tests. (bvsalud.org)
  • The DFS group had a significantly lower prevalence of AARD (3.4% vs. 16.9%, p = .008) and the subgroup with anti-DFS70 antibodies showed an even lower prevalence (2% vs. 20%, p = .002). (bvsalud.org)
  • Therefore, the information obtained from any test will reflect the types of antibody detected, the prevalence of the disease in the population being tested, and the question being asked of the test. (bmj.com)
  • Future study of why the prevalence of these antibodies has increased may help reveal the underlying causes of autoimmune diseases. (nih.gov)
  • Sera of positive cases were analyzed for additional classes of antinuclear antibodies associated with specific connective tissue diseases. (cdc.gov)
  • Sometimes, antibodies target normal proteins in our body by mistake. (rheumatology.org)
  • Antibodies are proteins produced by our immune system to fight against foreign substances such as bacterias and viruses. (practo.com)
  • ANA are antibodies produced by the immune system that bind to the body's own tissues. (medlineplus.gov)
  • Antinuclear antibodies are also produced by our immune system that attacks and destroys the body's normal tissues. (practo.com)
  • Antinuclear antibody (ANA) test is used as a primary test to help evaluate a person for autoimmune disorders that affect many tissues and organs throughout the body systemically. (drcelaya.com)
  • Removing antibodies may reduce inflammation in the kidney tissues. (nih.gov)
  • But to ensure there are no antinuclear antibodies within the bloodstream that can encourage the immunity system to attack its own body tissues, cells, or organs, an ANA IFA test is necessary. (flebo.in)
  • These antibodies are very harmful to the immune system as it starts fighting the inner parts of the body like cells, tissues, and organs as it fails to recognize them as their own. (flebo.in)
  • The antinuclear antibody panel is a blood test that looks at antinuclear antibodies (ANA). (medlineplus.gov)
  • The antinuclear antibody test looks for antibodies that bind to a part of the cell called the nucleus. (medlineplus.gov)
  • If the test is positive, a panel of tests may be done to identify specific antibodies. (medlineplus.gov)
  • Read our full medical article on antinuclear antibody test . (medicinenet.com)
  • An Antinuclear Antibodies (ANA) test measures the antinuclear antibodies present in the body. (practo.com)
  • If the ANA test results are positive it indicates the presence of antinuclear antibodies in the blood. (practo.com)
  • Normally, the test for antibodies is negative. (practo.com)
  • The anti nuclear antibody (ANA) test is used to detect the presence of antinuclear antibodies (ANA) in blood. (1mg.com)
  • Antinuclear antibody (ANA) test screens for the presence of ANA in blood. (1mg.com)
  • The Antinuclear Antibody Test can be affected by a number of factors including: · Certain medications like procainamide, hydralazine, phenytoin, etc. (1mg.com)
  • Importantly, the methods for detecting these antibodies are not specified by the ARA, and this article aims to highlight the fact that the particular assay used will crucially influence the interpretation of the test (table 2). (bmj.com)
  • No test or test panel can currently perform all these tasks because increases in specificity usually lead to reciprocal decreases in sensitivity, and because some of the clinical features of SLE are not antibody mediated. (bmj.com)
  • An anti-nuclear antibody or ANA IFA test in Gurgaon is conducted to test the presence of antinuclear antibodies in the bloodstream. (flebo.in)
  • Why is Anti-Nuclear Antibody (ANA IFA) Test done? (flebo.in)
  • What does the Anti-Nuclear Antibody (ANA IFA) Test measure? (flebo.in)
  • In simple words, the antinuclear antibody test or the ANA IFA test measures the absence or presence of antinuclear antibodies in the bloodstream. (flebo.in)
  • The anti-phospholid antibody screen is a popular test, especially among women who have experienced recurrent miscarriage and continued implantation failure. (sharedjourney.com)
  • Complement-fixing antinuclear antibody (CFANA) titers were measured in 18 patients with lupus nephritis and were compared to titers in 22 patients with scleroderma and mixed connective tissue disease (MCTD) who had comparable ANA titers but lacked nephritis. (nih.gov)
  • rather it compliments clinical signs and symptoms, specific antibody tests, and histopathologic and radiographic findings. (medscape.com)
  • In all six survivors, rabies was diagnosed based on exposure history, compatible clinical symptoms, and detection of rabies virus-neutralizing antibodies (VNA). (cdc.gov)
  • Different assays detect particular antibody properties, which are often quite different, and the clinical importance of this for pathogenesis or diagnosis is rarely fully understood. (bmj.com)
  • 35. Comparison of the analytical and clinical performances of two different routine testing protocols for antinuclear antibody screening. (nih.gov)
  • 16. Anticentromere antibodies--clinical correlates. (nih.gov)
  • Thus, antibodies against double-stranded (ds) DNA, histones and DNA-histone complexes typically produce a homogeneous nuclear staining pattern on non-dividing cells, and staining of the condensed chromatin-associated antigens in mitotic cells. (biomedcentral.com)
  • 12. Anticentromere antibody in localized scleroderma. (nih.gov)
  • 14. Anticentromere antibody and immunoglobulin allotypes in scleroderma. (nih.gov)
  • White blood cells in the body's immune system make antibodies to spot and attack foreign agents that cause infections or disease. (rheumatology.org)
  • Monoclonal HMGB1-targeting antibodies can ameliorate murine polyarthritis and lupus-like disease. (biomedcentral.com)
  • A fluorescent-labeled antibody adheres to this antigen-antibody complex and allows visualization of the pattern. (medscape.com)
  • However, an isolated DFS pattern in ANA testing does not necessarily indicate the presence of monospecific anti-DFS70 antibodies or AARD. (bvsalud.org)
  • Many women with unexplained infertility actually have antibodies in their bloodstream which are working against conception. (sharedjourney.com)
  • To quantify antibodies to double-stranded DNA, a fluoroenzyme-immunoassay was employed. (biomedcentral.com)
  • 26. Comparison of antinuclear antibody profiles obtained using line immunoassay and fluorescence enzyme immunoassay. (nih.gov)
  • When the immune system identifies a cell as foreign or 'non-self', it produces antibodies against these cells to destroy them. (1mg.com)
  • These disorders are known to be highly risky as they encourage the immune system to attack the body by creating antinuclear antibodies. (flebo.in)
  • Antibodies are molecules made by the immune system-for example, in response to infections. (nih.gov)
  • A doctor will view antibodies under a microscope and look for certain patterns and intensity. (rheumatology.org)
  • Average anti-HMGB1 antibody levels were significantly higher among patients with homogenous ± other IF-ANA staining patterns (median 180 AU) compared to IF-ANA negative cases (median 83 AU) (p = 0.004). (biomedcentral.com)
  • Mercury Exposure and Antinuclear Antibodies among Females of Reproductive Age in the United States: NHANES. (nih.gov)
  • They target the nucleus of the cells and hence called antinuclear antibodies. (practo.com)
  • These antibodies are called "antinuclear" because they target the nucleus-the large organelle that contains our chromosomes-of healthy cells. (nih.gov)
  • Your health care provider can run a series of tests to determine if you have large amounts of such antibodies in your blood. (sharedjourney.com)
  • Many healthy individuals may also have antinuclear antibodies in their blood. (practo.com)
  • The fluid part of the blood that contains antibodies is removed and replaced with intravenous fluids or donated plasma (that does not contain antibodies). (nih.gov)
  • Autoimmunity may be on the rise, based on a study of antinuclear antibodies in blood samples collected nationwide from 1988-2012. (nih.gov)
  • The presence of antinuclear antibodies (ANA) in the blood is the most common biomarker of autoimmunity. (nih.gov)
  • Blood samples showed that five of the 51 workers in the study population had antinuclear antibodies detected in their blood. (cdc.gov)
  • The presence of these antibodies is considered to be very harmful as they increase the chances of getting targeted by autoimmune diseases. (flebo.in)
  • At inclusion, 23 % of the SLE patients were anti-HMGB1 antibody positive compared to 5 % of the controls. (biomedcentral.com)
  • Anti-HMGB1 antibodies occurred in 49 % of the IF-ANA positive SLE patients, and in 34 % of IF-ANA negative cases (p = 0.004). (biomedcentral.com)
  • We confirm that anti-HMGB1 antibodies are common in SLE and correlate with disease activity variables. (biomedcentral.com)
  • In the general population, women, older adults, and individuals exposed to certain drugs and chemicals are more likely to have the antibodies. (nih.gov)
  • Antibodies are special cells that are supposed to help our bodies attack foreign invaders, like bacteria from colds and infections. (sharedjourney.com)
  • There are a number of complications associated with high levels of antiphospholipid antibody. (sharedjourney.com)
  • Rabbit anti-HMGB1 antibodies gave rise to cytoplasmic, but not nuclear, staining of HEp-2 cells. (biomedcentral.com)