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.
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.
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).
An antiphospholipid antibody 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. In vitro, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis mainly in the larger veins and arteries. It further causes obstetrical complications, including fetal death and spontaneous abortion, as well as a variety of hematologic and neurologic complications.
A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.
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.
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.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
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.
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.
Three or more consecutive spontaneous abortions.
Antibodies produced by a single clone of cells.
Immunoglobulins produced in response to VIRAL ANTIGENS.
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.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
Formation and development of a thrombus or blood clot in the blood vessel.
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.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
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.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.
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 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.
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.
A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
Laboratory tests for evaluating the individual's clotting mechanism.
Sites on an antigen that interact with specific antibodies.
Serological reactions in which an antiserum against one antigen reacts with a non-identical but closely related antigen.
Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies.
Central nervous system vasculitis that is associated with SYSTEMIC LUPUS ERYTHEMATOSUS. Clinical manifestations may include DEMENTIA; SEIZURES; CRANIAL NERVE DISEASES; HEMIPARESIS; BLINDNESS; DYSPHASIA; and other neurological disorders.
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.
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.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
A subnormal level of BLOOD PLATELETS.
The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.
Antibodies reactive with HIV ANTIGENS.
A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.
An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)
The co-occurrence of pregnancy and a blood disease (HEMATOLOGIC DISEASES) which involves BLOOD CELLS or COAGULATION FACTORS. The hematologic disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.
Immunoglobulins induced by antigens specific for tumors other than the normally occurring HISTOCOMPATIBILITY ANTIGENS.
Immunoglobulins produced in a response to PROTOZOAN ANTIGENS.
Ulceration of the skin and underlying structures of the lower extremity. About 90% of the cases are due to venous insufficiency (VARICOSE ULCER), 5% to arterial disease, and the remaining 5% to other causes.
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.
Condition of induced systemic hypersensitivity in which tissues respond to appropriate challenging agents with a sudden local calcification.
Expulsion of the product of FERTILIZATION before completing the term of GESTATION and without deliberate interference.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
Conditions or pathological processes associated with pregnancy. They can occur during or after pregnancy, and range from minor discomforts to serious diseases that require medical interventions. They include diseases in pregnant females, and pregnancies in females with diseases.
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.
The formation or presence of a blood clot (THROMBUS) within a vein.
Agents that prevent clotting.
A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.
Immunoglobulins produced in a response to FUNGAL ANTIGENS.
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.
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).
Transfer of immunity from immunized to non-immune host by administration of serum antibodies, or transplantation of lymphocytes (ADOPTIVE TRANSFER).
Death of the developing young in utero. BIRTH of a dead FETUS is STILLBIRTH.
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).
A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
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.
Techniques for removal by adsorption and subsequent elution of a specific antibody or antigen using an immunosorbent containing the homologous antigen or antibody.
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.
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.
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.
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)
Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.
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.
Rare chronic inflammatory disease involving the small blood vessels. It is of unknown etiology and characterized by mucocutaneous ulceration in the mouth and genital region and uveitis with hypopyon. The neuro-ocular form may cause blindness and death. SYNOVITIS; THROMBOPHLEBITIS; gastrointestinal ulcerations; RETINAL VASCULITIS; and OPTIC ATROPHY may occur as well.
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).
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.
A contagious venereal disease caused by the spirochete TREPONEMA PALLIDUM.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
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.
Antibodies that can catalyze a wide variety of chemical reactions. They are characterized by high substrate specificity and share many mechanistic features with enzymes.
Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a serine moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and serine and 2 moles of fatty acids.
Diminished or absent ability of a female to achieve conception.
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.
The formation of an area of NECROSIS in the CEREBRUM caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., INFARCTION, ANTERIOR CEREBRAL ARTERY), and etiology (e.g., embolic infarction).

Antibodies against phospholipids and oxidized LDL in alcoholic patients. (1/381)

Antiphospholipid antibodies (APA) are a generic term describing antibodies that recognize various phospholipids. Hepatocyte damage is a cardinal event in the course of alcoholic liver injury and autoantibodies against phospholipids could play an important role in this process. APA in alcoholic patients seem to reflect membrane lesions, impairment of immunological reactivity, liver disease progression and they correlate significantly with disease severity. LDL oxidation is supposed to be one of the most important pathogenic mechanisms of atherosclerosis and antibodies against oxidized low-density lipoprotein (oxLDL) are some kind of an epiphenomenon of this process. The scope of our study was to determine some autoantibodies (IgG-oxLDL and antiphospholipid antibodies) and their possible changes in alcoholic patients. We studied IgG-oxLDL and four APA - anticardiolipin antibodies (ACA), antiphosphatidylserine antibodies (APSA) antiphosphatidylethanolamine antibodies (APE) and antiphosphatidylcholine antibodies (APCA) in 35 alcoholic patients with mildly affected liver function at the beginning of the abuse treatment. The control group consisted of 60 healthy blood donors. In the studied group, we obtained positive results concerning total ACA in 17.1 % of alcoholic patients (8.3 % in the control group), 11.4 % IgG-ACA (6.7 %), 8.6 % IgM-ACA (3.3 %), 14.3 % total APE (6.7 %), 14.3 % total APCA (8.3 %) and 20 % total APSA (8.3 % in the control group). The IgG-oxLDL (406.4+/-52.5 vs 499.9+/-52.5 mU/ml) was not affected in alcoholic patients. We conclude that the autoantibodies against oxLDL are present in sera of alcoholics and healthy blood donors. Based on our results which revealed a wide range of IgG-oxLDL titres in the healthy population, this parameter does not appear to be very promising for the evaluation of the risk of atherosclerosis. Alcoholics with only mild affection of liver functions did not exhibit a significantly higher prevalence of all studied antiphospholipid antibodies (ACA, APSA, APE, APCA) which could lead to membrane lesions in these patients.  (+info)

Cerebral vasculopathy in HIV infection revealed by transcranial Doppler: A pilot study. (2/381)

BACKGROUND AND PURPOSE: There is growing evidence for affection of cerebral vessels during human immunodeficiency virus (HIV) infection. We prospectively evaluated cerebrovascular reserve capacity (CRC) in HIV-seropositive patients by transcranial Doppler sonography (TCD) after systemic administration of acetazolamide. We hypothesized that a disturbed vasoreactivity would reflect the cerebral arteries' involvement in HIV infection. METHODS: We assessed the mean blood flow velocity (BFV) of the middle cerebral artery and its increase after intravenous administration of 1 g acetazolamide (CRC) in 31 HIV-infected individuals without symptoms of cerebrovascular disease (mean+/-SD age, 39+/-11 years). Stenotic or occlusive lesions of the large brain-supplying arteries were excluded by color-coded duplex and transcranial imaging. BFV and CRC were also measured in an age-matched group of 10 healthy control subjects. Patients were classified according to clinical, laboratory, and neurophysiological parameters. We also performed cerebral MRI (n=25) and rheumatological blood tests (n=26). RESULTS: Baseline BFV and CRC both were significantly reduced in HIV-infected patients as compared with control subjects (P<0.05, Student's t test). These findings did not correlate with duration of seropositivity, helper cell count, or other clinical, rheumatological, and neuroradiological findings. CONCLUSIONS: Our findings support the hypothesis of a cerebral vasculopathy etiologically associated with HIV infection.  (+info)

Anti-phospholipid antibodies and CD5+ B cells in HIV infection. (3/381)

This cross-sectional study evaluates the correlation between anti-phospholipid antibodies and CD5+ B cells in 110 patients infected with HIV-1. There were 89.1% of the patients who had IgG antibodies against cardiolipin and phosphatidylserine. The prevalence of IgM and IgA antibodies was < 22%. AIDS was associated with lower frequencies of IgM antibodies against cardiolipin (P = 0.05) and IgG-antibodies against cardiolipin and phosphatidylserine (P = 0.011). Drug users had higher IgM antibodies against phospholipids than patients from other risk groups (P = 0.02). A history of thromboembolic events was not accompanied by higher levels of anti-phospholipid antibodies (P > 0.2). No correlation between anti-phospholipid antibodies and CD5+ B cells was detected. Percentage part of CD5+ B lymphocytes was elevated in all patients and absolute CD4+ T lymphocyte counts and HIV p24 antigen were inversely correlated. In advanced disease a significant reduction of anti-phospholipid antibodies was contrasted with persistent elevation of CD5+ B lymphocytes. These observations may reflect immunological dysfunction involving apoptosis and endothelial damage rather than polyclonal B cell hyperstimulation. A possible explanation would be that in HIV infection an increased rate of spontaneous apoptosis in peripheral blood lymphocytes is accompanied by functional and structural changes of mitochondria. Therefore, structurally altered mitochondrial phospholipids could serve as antigen to induce specific humoral immune responses.  (+info)

Antibodies to adult human endothelial cells cross-react with oxidized low-density lipoprotein and beta 2-glycoprotein I (beta 2-GPI) in systemic lupus erythematosus. (4/381)

Cardiovascular manifestations are common in systemic lupus erythematosus (SLE). Oxidized low-density lipoprotein (oxLDL) is implicated in cardiovascular disease, especially atherosclerosis, and cross-reacts with antibodies to cardiolipin (aCL). beta 2-GPI is a plasma protein participating in the coagulating cascade, and is also cofactor for aCL, and some aCL have been shown to be directed against beta 2-GPI and/or complexes between beta 2-GPI and phospholipids. Lysophosphatidylcholine (LPC) is a phospholipid present both in oxLDL and in damaged endothelium, and we recently showed that LPC is involved in the antigenicity of oxLDL. Antibodies to endothelial cells (aEC) correlate with diseases activity in SLE and vasculitis, and we recently showed that aEC are enhanced in cardiovascular disease such as borderline hypertension and early atherosclerosis. aEC were determined using EC from adult V. Saphena Magna. Antibody levels were determined by ELISA. aEC of IgG type were enhanced in 184 patients with SLE compared with 85 healthy controls. There was a close correlation between aoxLDL, aCL, aLPC, a beta 2-GPI and aEC. Binding of sera to EC was competitively inhibited by beta 2-GPI, LPC and oxLDL. Taken together, the data indicate that EC share antigenic epitopes with beta 2-GPI and with oxLDL, especially LPC. Phospholipids in EC membranes may thus be antigenic epitopes. beta 2-GPI may bind to these phospholipids, and become an autoantigen. LPC is formed by oxidation of phospholipids and/or proinflammatory factors leading to activation of phospholipase A2, and the findings indicate the potential role of both lipid oxidation and phospholipase A2 in SLE.  (+info)

Conformationally altered beta 2-glycoprotein I is the antigen for anti-cardiolipin autoantibodies. (5/381)

Anti-cardiolipin autoantibodies (aCL) induce thrombosis and recurrent fetal death. These antibodies require a 'cofactor', identified as beta 2-glycoprotein I (beta 2-GPI), to bind phospholipids. We show here that aCL can bind beta 2-GPI in the absence of phospholipid. Binding of aCL to beta 2-GPI is dependent upon the beta 2-GPI being immobilized on an appropriate surface including cardiolipin, irradiated polystyrene and nitrocellulose membrane. This effect cannot be explained by increased antigen density of beta 2-GPI immobilized on these surfaces. Rather, conformational changes that occur following the interaction of beta 2-GPI with phospholipid render this protein antigenic to aCL. Liquid-phase beta 2-GPI was not antigenic for aCL. Thus, aCL cannot bind circulating beta 2-GPI. These findings may explain why patients with aCL can remain healthy for many years but then undergo episodes of thrombosis or fetal loss without changes in their circulating aCL profile, as the triggering event for these pathologies can be predicted to be one that renders beta 2-GPI antigenic for aCL.  (+info)

A prospective analysis of cognitive function and anticardiolipin antibodies in systemic lupus erythematosus. (6/381)

OBJECTIVE: To prospectively analyze the association between changes in cognitive function and circulating anticardiolipin antibodies (aCL) over a period of 5 years in patients with systemic lupus erythematosus (SLE). METHODS: Cognitive function was assessed in 51 unselected female SLE patients at baseline and after a mean followup of 64.5 months (range 52-71 months), using standardized tests of cognitive function, i.e., the Wechsler Adult Intelligence Scale-Revised, the Wechsler Memory Scale-Revised, and the California Verbal Learning Test. Circulating IgG, IgA, and IgM aCL and anti-double-stranded DNA (anti-dsDNA) antibody levels were determined by enzyme-linked immunosorbent assay on 4-7 occasions over the same time period. Persistent antibody reactivity was defined as levels more than 2 standard deviations (moderately positive) and more than 5 standard deviations (highly positive) above the mean for normal controls over the duration of the study. Changes in overall cognitive performance and in raw scores on individual cognitive tests were compared in patients who were persistently positive or negative for aCL. RESULTS: At baseline 11 patients (22%) were cognitively impaired, compared with 7 (14%) at followup. Between 16% and 37% of patients had persistently elevated aCL levels of different isotypes. There was no significant difference in the prevalence of overall cognitive impairment in patients who were persistently positive for aCL compared with those who were not. In contrast, over the period of study, patients who had persistent IgG aCL positivity had a reduction in psychomotor speed, and patients who had persistent IgA aCL positivity had a reduction in conceptual reasoning and executive ability. Similar associations with anti-dsDNA antibodies were not found. CONCLUSION: These results suggest that IgG and IgA aCL may be responsible for long-term subtle deterioration in cognitive function in patients with SLE.  (+info)

A longitudinal study of anticardiolipin antibody levels and cognitive functioning in systemic lupus erythematosus. (7/381)

OBJECTIVE: To determine the relationship between persistently raised anticardiolipin antibody (aCL) levels and neuropsychological performance in patients with systemic lupus erythematosus (SLE). METHODS: Forty-five patients with SLE underwent a detailed neuropsychological assessment on 2 occasions 12-18 months apart. Serum samples stored since the time of previous assessments as well as samples obtained 6 months to 2 years before the first neuropsychological assessment were tested for IgG aCL levels. Patients were divided into 4 groups according to the number of times their aCL levels were elevated (never, once, twice, 3 times). A wide-ranging battery of new neuropsychological tests was utilized, and the results were compared with double-stranded DNA (dsDNA) antibody levels, C3 levels, and results of magnetic resonance imaging (MRI). RESULTS: Analysis of variance revealed that the group with persistently elevated aCL levels performed less well than the other groups. At the first neuropsychological assessment, poorer performance by this group was noted for letter cancellation (P = 0.02), trail making task B (P = 0.04), and digit span (P = 0.03). At the second assessment, letter cancellation (P = 0.01), trail making task A (P = 0.03), trail making task B (P = 0.01), word fluency (P = 0.01), and reaction time (P = 0.05) were impaired. In contrast, no significant differences in neuropsychological test results were identified with respect to DNA antibody or C3 levels. MRI abnormalities were associated with both persistent elevation of aCL levels and low C3 levels. CONCLUSION: Levels of IgG aCL that were persistently elevated over a 2-3-year period (as opposed to never or occasionally elevated) were associated with significantly poorer performance in cognitive function by patients with SLE. Tasks requiring speed of attention and concentration appear to be particularly affected.  (+info)

A possible role for activated protein C resistance in patients with first and second trimester pregnancy failure. (8/381)

Thrombophilia was recently suggested as a possible factor in recurrent pregnancy losses. We studied prospectively 125 patients (mean age 31.4 +/- 5.6 years) with one or more first or second trimester pregnancy losses for the prevalence of activated protein C resistance (APCR). Proteins C and S antigens, antithrombin III, anticardiolipin, and lupus anti-coagulant were also evaluated. Patients with uterine malformations, hormonal abnormalities, chromosomal translocations and infectious causes were excluded. A control group of 125 women with no past fetal loss were matched with the study group. Whenever the APC-sensitivity ratio (APC-SR) was +info)

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.

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.

A condition in which spontaneous abortions occur repeatedly, often due to an underlying cause such as a uterine anomaly or infection. Also called recurrent spontaneous abortion.

Synonym(s): habitual abortion, recurrent abortion, spontaneous abortion.

Antonym(s): multiple pregnancy, retained placenta.

Example Sentence: "The patient had experienced four habitual abortions in the past year and was concerned about her ability to carry a pregnancy to term."

There are several types of thrombosis, including:

1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.

The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:

1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic

Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.

There are several types of thrombophilia, including:

1. Factor V Leiden: This is the most common inherited thrombophilia and is caused by a mutation in the Factor V gene.
2. Prothrombin G20210A: This is another inherited thrombophilia that is caused by a mutation in the Prothrombin gene.
3. Protein C and S deficiency: These are acquired deficiencies of protein C and S, which are important proteins that help to prevent blood clots.
4. Antiphospholipid syndrome: This is an autoimmune disorder that causes the body to produce antibodies against phospholipids, which can lead to blood clots.
5. Cancer-associated thrombophilia: This is a condition where cancer patients are at a higher risk of developing blood clots due to their cancer and its treatment.
6. Hormone-related thrombophilia: This is a condition where hormonal changes, such as those that occur during pregnancy or with the use of hormone replacement therapy, increase the risk of blood clots.
7. Inherited platelet disorders: These are rare conditions that affect the way platelets function and can increase the risk of blood clots.
8. Anti-cardiolipin antibodies: These are autoantibodies that can cause blood clots.
9. Lupus anticoagulant: This is an autoantibody that can cause blood clots.
10. Combined genetic and acquired risk factors: Some people may have a combination of inherited and acquired risk factors for thrombophilia.

Thrombophilia can be diagnosed through various tests, including:

1. Blood tests: These tests measure the levels of certain proteins in the blood that are associated with an increased risk of blood clots.
2. Genetic testing: This can help identify inherited risk factors for thrombophilia.
3. Imaging tests: These tests, such as ultrasound and venography, can help doctors visualize the blood vessels and look for signs of blood clots.
4. Thrombin generation assay: This test measures the body's ability to produce thrombin, a protein that helps form blood clots.
5. Platelet function tests: These tests assess how well platelets work and whether they are contributing to the development of blood clots.

Treatment for thrombophilia usually involves medications to prevent or dissolve blood clots, as well as measures to reduce the risk of developing new clots. These may include:

1. Anticoagulant drugs: These medications, such as warfarin and heparin, are used to prevent blood clots from forming.
2. Thrombolytic drugs: These medications are used to dissolve blood clots that have already formed.
3. Compression stockings: These stockings can help reduce swelling and improve blood flow in the affected limb.
4. Elevating the affected limb: This can help reduce swelling and improve blood flow.
5. Avoiding long periods of immobility: This can help reduce the risk of developing blood clots.

In some cases, surgery may be necessary to remove a blood clot or repair a damaged blood vessel. In addition, people with thrombophilia may need to make lifestyle changes, such as avoiding long periods of immobility and taking regular breaks to move around, to reduce their risk of developing blood clots.

Overall, the prognosis for thrombophilia is generally good if the condition is properly diagnosed and treated. However, if left untreated, thrombophilia can lead to serious complications, such as pulmonary embolism or stroke, which can be life-threatening. It is important for people with thrombophilia to work closely with their healthcare provider to manage the condition and reduce the risk of complications.

Symptoms of CNS lupus vasculitis can include headaches, seizures, confusion, weakness or paralysis, vision problems, and changes in personality or behavior. The condition can be difficult to diagnose, as it may mimic other conditions such as stroke, infection, or tumors.

Treatment of CNS lupus vasculitis typically involves high doses of corticosteroids to reduce inflammation and prevent further damage. In severe cases, intravenous immunoglobulin (IVIG) or plasmapheresis may be used to remove harmful antibodies from the blood. Anticoagulation therapy may also be prescribed to prevent blood clots.

While CNS lupus vasculitis can be a life-threatening condition, early diagnosis and aggressive treatment can improve outcomes. However, long-term follow-up is essential to monitor for recurrences of the disease and manage any ongoing neurological symptoms.

There are several possible causes of thrombocytopenia, including:

1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.

Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.

In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.

APC resistance can be caused by genetic or acquired factors and can lead to a range of clinical presentations, including:

1. Hereditary bleeding disorders: Familial APC resistance is caused by mutations in the APC gene and can result in severe bleeding, especially during childhood.
2. Acquired APC resistance: This can occur due to certain medical conditions, such as liver disease, sepsis, or cancer, which can impair APC function.
3. Drug-induced APC resistance: Certain medications, like anticoagulants, can reduce APC activity and lead to APC resistance.

Diagnosis of APC resistance typically involves testing for APC activity in the blood, as well as genetic analysis to identify mutations in the APC gene. Treatment options for APC resistance depend on the underlying cause and may include:

1. Fresh frozen plasma (FFP): FFP can be used to replace missing or deficient APC in the blood.
2. Recombinant APC: This is a synthetic version of APC that can be used to replace missing or deficient APC.
3. Anticoagulants: These medications can help prevent blood clots and reduce the risk of thrombotic events.
4. Platelet inhibitors: These medications can help prevent platelet aggregation, which can contribute to bleeding.

Overall, APC resistance is a rare but important condition that can affect blood coagulation and increase the risk of bleeding or thrombotic events. Prompt diagnosis and appropriate treatment are essential to manage the condition effectively and prevent complications.

Protein S is a vitamin K-dependent protein that is produced in the liver and circulates in the blood. It works by inhibiting the activity of thrombin, a clotting factor that helps to form blood clots. In people with protein S deficiency, there may be an overactivation of thrombin, leading to an increased risk of blood clots forming.

Protein S deficiency can be caused by several factors, including genetic mutations, vitamin K deficiency, and certain medical conditions such as liver disease or cancer. It is usually diagnosed through a combination of clinical evaluation, laboratory tests, and imaging studies.

Treatment for protein S deficiency typically involves replacing the missing protein with intravenous immune globulin (IVIG) or recombinant human protein S. In some cases, medications that inhibit thrombin activity, such as heparins or direct thrombin inhibitors, may also be used to reduce the risk of blood clots forming.

Preventing protein S deficiency involves ensuring adequate intake of vitamin K through dietary sources or supplements, managing underlying medical conditions, and avoiding factors that can increase the risk of bleeding or thrombosis, such as smoking, obesity, and inactivity.

In summary, protein S deficiency is a condition characterized by low levels of protein S, which increases the risk of developing blood clots. It can be caused by several factors and treated with replacement therapy or medications that inhibit thrombin activity. Prevention involves ensuring adequate vitamin K intake and managing underlying medical conditions.

1. Iron deficiency anemia: This is the most common hematologic complication of pregnancy, caused by the increased demand for iron and the potential for poor dietary intake or gastrointestinal blood loss.
2. Thrombocytopenia: A decrease in platelet count, which can be mild and resolve spontaneously or severe and require treatment.
3. Leukemia: Rare but potentially serious, leukemia can occur during pregnancy and may require prompt intervention to ensure the health of both the mother and the fetus.
4. Thrombosis: The formation of a blood clot in a blood vessel, which can be life-threatening for both the mother and the baby if left untreated.
5. Hemorrhage: Excessive bleeding during pregnancy, which can be caused by various factors such as placenta previa or abruption.
6. Preeclampsia: A condition characterized by high blood pressure and damage to organs such as the kidneys and liver, which can increase the risk of hemorrhage and other complications.
7. Ectopic pregnancy: A pregnancy that develops outside of the uterus, often in the fallopian tube, which can cause severe bleeding and be life-threatening if left untreated.

Symptoms of leg ulcers may include:

* Pain or tenderness in the affected area
* Redness or swelling around the wound
* Discharge or oozing of fluid from the wound
* A foul odor emanating from the wound
* Thickening or hardening of the skin around the wound

Causes and risk factors for leg ulcers include:

* Poor circulation, which can be due to conditions such as peripheral artery disease or diabetes
* Injury or trauma to the lower leg
* Infection, such as cellulitis or abscesses
* Skin conditions such as eczema or psoriasis
* Poorly fitting or compression garments
* Smoking and other lifestyle factors that can impair healing

Diagnosis of a leg ulcer typically involves a physical examination and imaging tests, such as X-rays or ultrasound, to rule out other conditions. Treatment may involve debridement (removal of dead tissue), antibiotics for infection, and dressing changes to promote healing. In some cases, surgery may be necessary to remove infected tissue or repair damaged blood vessels.

Prevention is key in managing leg ulcers. This includes maintaining good circulation, protecting the skin from injury, and managing underlying conditions such as diabetes or peripheral artery disease. Compression stockings and bandages can also be used to help reduce swelling and promote healing.

Prognosis for leg ulcers varies depending on the severity of the wound and underlying conditions. With proper treatment and care, many leg ulcers can heal within a few weeks to months. However, some may take longer to heal or may recur, and in severe cases, amputation may be necessary.

Overall, managing leg ulcers requires a comprehensive approach that includes wound care, debridement, antibiotics, and addressing underlying conditions. With proper treatment and care, many leg ulcers can heal and improve quality of life for those affected.

The condition is often seen in patients with long-standing ESRD, particularly those on hemodialysis. The exact cause of calciphylaxis is not well understood, but it is thought to be related to abnormal mineral metabolism, vascular inflammation, and oxidative stress.

The symptoms of calciphylaxis can vary depending on the severity of the condition, but may include:

* Skin lesions or ulcers
* Painful muscle weakness
* Difficulty moving or contracting muscles
* Numbness or tingling in the affected areas
* Decreased blood flow to organs and tissues

Calciphylaxis can be diagnosed through a combination of physical examination, laboratory tests, and imaging studies such as X-rays or CT scans. Treatment is primarily focused on managing the underlying causes of the condition, such as controlling blood pressure, correcting mineral imbalances, and addressing any infections or inflammation. In severe cases, surgical interventions such as bypass grafting or angioplasty may be necessary.

Overall, calciphylaxis is a rare and debilitating condition that can significantly impact the quality of life of patients with ESRD. Early detection and aggressive management are critical to preventing complications and improving outcomes.

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.

1. Preeclampsia: A condition characterized by high blood pressure during pregnancy, which can lead to complications such as stroke or premature birth.
2. Gestational diabetes: A type of diabetes that develops during pregnancy, which can cause complications for both the mother and the baby if left untreated.
3. Placenta previa: A condition in which the placenta is located low in the uterus, covering the cervix, which can cause bleeding and other complications.
4. Premature labor: Labor that occurs before 37 weeks of gestation, which can increase the risk of health problems for the baby.
5. Fetal distress: A condition in which the fetus is not getting enough oxygen, which can lead to serious health problems or even death.
6. Postpartum hemorrhage: Excessive bleeding after delivery, which can be life-threatening if left untreated.
7. Cesarean section (C-section) complications: Complications that may arise during a C-section, such as infection or bleeding.
8. Maternal infections: Infections that the mother may contract during pregnancy or childbirth, such as group B strep or urinary tract infections.
9. Preterm birth: Birth that occurs before 37 weeks of gestation, which can increase the risk of health problems for the baby.
10. Chromosomal abnormalities: Genetic disorders that may affect the baby's growth and development, such as Down syndrome or Turner syndrome.

It is important for pregnant women to receive regular prenatal care to monitor for any potential complications and ensure a healthy pregnancy outcome. In some cases, pregnancy complications may require medical interventions, such as hospitalization or surgery, to ensure the safety of both the mother and the baby.

Symptoms of venous thrombosis may include pain, swelling, warmth, and redness in the affected limb. In some cases, the clot can break loose and travel to the lungs, causing a potentially life-threatening condition called Pulmonary Embolism (PE).

Treatment for venous thrombosis typically involves anticoagulant medications to prevent the clot from growing and to prevent new clots from forming. In some cases, a filter may be placed in the vena cava, the large vein that carries blood from the lower body to the heart, to prevent clots from traveling to the lungs.

Prevention of venous thrombosis includes encouraging movement and exercise, avoiding long periods of immobility, and wearing compression stockings or sleeves to compress the veins and improve blood flow.

There are different types of fetal death, including:

1. Stillbirth: This refers to the death of a fetus after the 20th week of gestation. It can be caused by various factors, such as infections, placental problems, or umbilical cord compression.
2. Miscarriage: This occurs before the 20th week of gestation and is usually due to chromosomal abnormalities or hormonal imbalances.
3. Ectopic pregnancy: This is a rare condition where the fertilized egg implants outside the uterus, usually in the fallopian tube. It can cause fetal death and is often diagnosed in the early stages of pregnancy.
4. Intrafamilial stillbirth: This refers to the death of two or more fetuses in a multiple pregnancy, usually due to genetic abnormalities or placental problems.

The diagnosis of fetal death is typically made through ultrasound examination or other imaging tests, such as MRI or CT scans. In some cases, the cause of fetal death may be unknown, and further testing and investigation may be required to determine the underlying cause.

There are various ways to manage fetal death, depending on the stage of pregnancy and the cause of the death. In some cases, a vaginal delivery may be necessary, while in others, a cesarean section may be performed. In cases where the fetus has died due to a genetic abnormality, couples may choose to undergo genetic counseling and testing to assess their risk of having another affected pregnancy.

Overall, fetal death is a tragic event that can have significant emotional and psychological impact on parents and families. It is essential to provide compassionate support and care to those affected by this loss, while also ensuring appropriate medical management and follow-up.

The symptoms of Behcet syndrome can vary widely, but may include:

* Skin lesions, such as ulcers or rashes
* Eye inflammation (uveitis)
* Joint pain and swelling
* Digestive problems such as diarrhea and abdominal pain
* Nervous system problems such as seizures and headaches
* Inflammation of the blood vessels, which can lead to aneurysms or blood clots

The exact cause of Behcet syndrome is not known, but it is believed to be related to a combination of genetic and environmental factors. There is no cure for the disease, but various treatments are available to manage the symptoms and prevent complications. These may include medications such as corticosteroids, immunosuppressive drugs, and antibiotics, as well as lifestyle modifications such as avoiding triggers like spicy foods or stress.

Behcet syndrome is rare in the United States, but it is more common in certain parts of the world, including Turkey, Japan, and other countries with high prevalence of autoimmune disorders. It affects both men and women equally, and typically begins during adulthood, although it can sometimes begin in childhood or adolescence.

Overall, Behcet syndrome is a complex and multifaceted disease that requires careful management by a healthcare team to prevent complications and improve quality of life for patients.

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.

There are three stages of syphilis:

1. Primary stage: A small, painless sore or ulcer (called a chancre) appears at the site of infection, usually on the genitals, rectum, or mouth. This sore heals on its own within 2-6 weeks, but the infection remains in the body.
2. Secondary stage: A rash and other symptoms can appear weeks to months after the primary stage. The rash can be accompanied by fever, fatigue, and swollen lymph nodes.
3. Latent stage: After the secondary stage, the infection can enter a latent (hidden) phase, during which there are no visible symptoms but the infection remains in the body. If left untreated, syphilis can progress to the tertiary stage, which can cause serious complications such as damage to the heart, brain, and other organs.

Syphilis is diagnosed through a physical examination, blood tests, and/or a lumbar puncture (spinal tap). Treatment typically involves antibiotics, and early treatment can cure the infection and prevent long-term complications.

Prevention measures include safe sex practices such as using condoms and dental dams, avoiding sexual contact with someone who has syphilis, and getting regularly tested for STIs. It is important to seek medical attention if symptoms of syphilis are present, as early treatment can prevent long-term complications.

Causes of Female Infertility

There are several potential causes of female infertility, including:

1. Hormonal imbalances: Disorders such as polycystic ovary syndrome (PCOS), thyroid dysfunction, and premature ovarian failure can affect hormone levels and ovulation.
2. Ovulatory disorders: Problems with ovulation, such as anovulation or oligoovulation, can make it difficult to conceive.
3. Tubal damage: Damage to the fallopian tubes due to pelvic inflammatory disease, ectopic pregnancy, or surgery can prevent the egg from traveling through the tube and being fertilized.
4. Endometriosis: This condition occurs when tissue similar to the lining of the uterus grows outside of the uterus, causing inflammation and scarring that can lead to infertility.
5. Fibroids: Noncancerous growths in the uterus can interfere with implantation of a fertilized egg or disrupt ovulation.
6. Pelvic adhesions: Scar tissue in the pelvis can cause fallopian tubes to become damaged or blocked, making it difficult for an egg to travel through the tube and be fertilized.
7. Uterine or cervical abnormalities: Abnormalities such as a bicornuate uterus or a narrow cervix can make it difficult for a fertilized egg to implant in the uterus.
8. Age: A woman's age can affect her fertility, as the quality and quantity of her eggs decline with age.
9. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and being overweight or underweight can affect fertility.
10. Stress: Chronic stress can disrupt hormone levels and ovulation, making it more difficult to conceive.

It's important to note that many of these factors can be treated with medical assistance, such as medication, surgery, or assisted reproductive technology (ART) like in vitro fertilization (IVF). If you are experiencing difficulty getting pregnant, it is recommended that you speak with a healthcare provider to determine the cause of your infertility and discuss potential treatment options.

1. Stroke: A stroke occurs when the blood supply to the brain is interrupted, either due to a blockage or a rupture of the blood vessels. This can lead to cell death and permanent brain damage.
2. Cerebral vasospasm: Vasospasm is a temporary constriction of the blood vessels in the brain, which can occur after a subarachnoid hemorrhage (bleeding in the space surrounding the brain).
3. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches. It can lead to recurrent transient ischemic attacks (TIs) or stroke.
4. Cerebral amyloid angiopathy: This is a condition where abnormal protein deposits accumulate in the blood vessels of the brain, leading to inflammation and bleeding.
5. Cavernous malformations: These are abnormal collections of blood vessels in the brain that can cause seizures, headaches, and other symptoms.
6. Carotid artery disease: Atherosclerosis (hardening) of the carotid arteries can lead to a stroke or TIAs.
7. Vertebrobasilar insufficiency: This is a condition where the blood flow to the brain is reduced due to narrowing or blockage of the vertebral and basilar arteries.
8. Temporal lobe dementia: This is a type of dementia that affects the temporal lobe of the brain, leading to memory loss and other cognitive symptoms.
9. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL): This is a rare genetic disorder that affects the blood vessels in the brain, leading to recurrent stroke-like events.
10. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to decreased blood flow to the brain and increased risk of stroke.

It's important to note that this list is not exhaustive and there may be other causes of stroke and TIAs that are not included here. A proper diagnosis can only be made by a qualified medical professional after conducting a thorough examination and reviewing the individual's medical history.

Cerebral infarction can result in a range of symptoms, including sudden weakness or numbness in the face, arm, or leg on one side of the body, difficulty speaking or understanding speech, sudden vision loss, dizziness, and confusion. Depending on the location and severity of the infarction, it can lead to long-term disability or even death.

There are several types of cerebral infarction, including:

1. Ischemic stroke: This is the most common type of cerebral infarction, accounting for around 87% of all cases. It occurs when a blood clot blocks the flow of blood to the brain, leading to cell death and tissue damage.
2. Hemorrhagic stroke: This type of cerebral infarction occurs when a blood vessel in the brain ruptures, leading to bleeding and cell death.
3. Lacunar infarction: This type of cerebral infarction affects the deep structures of the brain, particularly the basal ganglia, and is often caused by small blockages or stenosis (narrowing) in the blood vessels.
4. Territorial infarction: This type of cerebral infarction occurs when there is a complete blockage of a blood vessel that supplies a specific area of the brain, leading to cell death and tissue damage in that area.

Diagnosis of cerebral infarction typically involves a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Treatment options vary depending on the cause and location of the infarction, but may include medication to dissolve blood clots, surgery to remove blockages, or supportive care to manage symptoms and prevent complications.

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The presence of anticardiolipin antibodies is a more serious risk factor for the disease, as well as the presence of more ... Anti-RNP antibodies in elevated levels, especially antibodies against protein 68 kD. Absence of severe renal or CNS disease. ... SLE, scleroderma, and in MCTD have antibodies against anti-U1-snRNP at differing percentages. These antibodies are in most MCTD ... Distinguishing laboratory characteristics are a positive, speckled anti-nuclear antibody and an anti-U1-RNP antibody. After the ...
... with all types of antiphospholipid antibody (lupus anticoagulant, anticardiolipin antibody and anti-β2 glycoprotein I antibody ... to detect anti-cardiolipin antibodies or anti-apolipoprotein antibodies.[citation needed] Genetic thrombophilia is part of the ... anti-apolipoprotein antibodies, or anti-cardiolipin antibodies. Antiphospholipid syndrome can be primary or secondary. Primary ... "antiphospholipid antibodies" (anticardiolipin antibodies and lupus anticoagulant) react against proteins that bind to anionic ...
"Identification of a region of β2-glycoprotein I critical for lipid binding and anti-cardiolipin antibody cofactor activity" ( ... "A phospholipid-beta 2-glycoprotein I complex is an antigen for anticardiolipin antibodies occurring in autoimmune disease but ... and a region recognized by anticardiolipin antibodies" (1994) Journal of Immunology, 152 (2), pp. 653-659. Cited 195 times. ... McNeil, H.P., Chesterman, C.N., Krilis, S.A. "Immunology and clinical importance of antiphospholipid antibodies" (1991) ...
Aortic dissection Anti-cardiolipin antibodies CMV infection Herpetic infection Hyperglycemia Hypersensitivity to broad-spectrum ...
... syndrome Polycythemia Hypercoagulability Protein C deficiency Antiphospholipid antibodies Anticardiolipin antibodies Lupus ... "Amaurosis fugax associated with antiphospholipid antibodies". Annals of Neurology. 25 (3): 228-32. doi:10.1002/ana.410250304. ...
... anti-cardiolipin antibodies, and anti-β2-glycoprotein 1 antibodies; it is therefore regarded as an autoimmune disease. In some ... The risk is determined by the subtype of antibody detected, by the antibody titer (amount of antibodies), whether multiple ... anti-cardiolipin antibody, anti-β2 glycoprotein 1 antibody, activated protein C resistance, fibrinogen tests, factor V Leiden ... Recurrent miscarriage is an indication for thrombophilia screening, particularly antiphospholipid antibodies (anti-cardiolipin ...
... is an acronym that may refer to: Anti-cardiolipin antibodies Allegheny County Library Association, a library association ...
... threonine Advisory Committee for Aeronautics Anterior cerebral artery Anti-cardiolipin antibodies Anti-centromere antibodies ...
... the other component being the serological testing for anticardiolipin antibodies and anti-β2 glycoprotein-I antibodies using ... Antiphospholipid antibody syndrome is an important marker for recurrent thrombosis, and often warrants indefinite anticoagulant ... This makes the test sensitive to the presence of lupus anticoagulants, because these antibodies interfere with the clot- ... The dRVVT is one component of a workup of a suspected antiphospholipid antibody, ...
... lupus anticoagulant is generally tested in conjunction with anti-apolipoprotein antibodies and anti-cardiolipin antibodies, and ... In vivo, the antibodies are thought to interact with platelet membrane phospholipids, increasing adhesion and aggregation of ... Its name is a partial misnomer, as it is actually a prothrombotic antibody in vivo. Lupus anticoagulant in living systems ... The name derives from their properties in vitro, as these antibodies increase coagulation times in laboratory tests such as the ...
... a common occurrence among participants of several sports Anti-cardiolipin antibodies ATP citrate lyase, aka ATP citrate ...
... and anticardiolipin antibodies. Neonatal lupus is the occurrence of lupus symptoms in an infant born from a mother with lupus, ... Women pregnant and known to have anti-Ro (SSA) or anti-La antibodies (SSB) often have echocardiograms during the 16th and 30th ... are recommended to be screened for antiphospholipid antibodies, both the lupus anticoagulant (the RVVT and sensitive PTT are ...
... antibodies, antiphospholipid MeSH D12.776.377.715.548.114.323.210.100 - antibodies, anticardiolipin 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, ...
... antibodies, antiphospholipid MeSH D12.776.124.486.485.114.323.210.100 - antibodies, anticardiolipin MeSH D12.776.124.486. ... antibodies, antiphospholipid MeSH D12.776.124.790.651.114.323.210.100 - antibodies, anticardiolipin 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, ...
The presence of the autoantibodies anti-dsDNA, anti-Sm, and anti-cardiolipin has been shown to correlate with the development ... antibodies. It is estimated that up to 25 percent of people with systemic autoimmune disease could be considered to have UCTD. ...
... Daboubi, M.K.. ... Anticardiolipin antibodies in women with recurrent abortion. EN. dc.relation.ispartofjournal. EMHJ - Eastern Mediterranean ... A high level of anticardiolipin antibody activity was detected among 19.23% of the habitual aborters but in none of the ... Enzyme-linked immunosorbent assay was used for detection of anticardiolipin antibodies in a group of 26 patients defined as ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
... this study shows that anticardiolipin IgM antibody was associated with preeclampsia. The level of this anticardiolipin IgM ... Association of anticardiolipin IgM antibody with preeclampsia Authors. * Sharmin Khanam Department of Obstetrics and Gynecology ... Anticardiolipin IgM antibody, Blood pressure, Preeclampsia Abstract. The objective of this study was to evaluate association of ... The level of anticardiolipin IgM antibody was significantly higher in preeclamptic women than in normal pregnant (mean 8.7 vs ...
Find Anti Cardiolipin Antibody [IgM] test cost Delhi NCR & Get upto 50% off at HOD Centres. Accurate, timely & quality reports ... This test measures the levels of Anti Cardiolipin Antibody (IgM) in the blood. AGL IgM test is done in cases like blood ...
The Rabbit Anti- cardiolipin antibody IgG(ACA-IgG) ELISA Kit is a ready to use kit manufactured by using high quality ... The IgG antibody has 2 antigen binding sites. They represent 70% or more of serum antibodies. This antibody can be antigen ... Small volumes from the liquid components of the Anti- cardiolipin antibody IgG(ACA-IgG) EIA kit may get caught on the walls and ... This EIA test for Rabbit Rabbit Anti- cardiolipin antibody IgG(ACA-IgG) will yield accurate and reproducible results. The ...
A rare case of carotid stroke in young due to Takayasu Arteritis with positive anti- cardiolipin antibodies � A case report. ... A rare case of carotid stroke in young due to Takayasu Arteritis with positive anti- cardiolipin antibodies � A case report. ... high Blood Pressure recordings and positive anti- cardiolipin antibodies. Imaging studies revealed Occluded right Common ...
Syndromes of circulating antiphospholipid (anticardiolipin) antibodies * Radiation nephritis * Nephropathy associated with bone ... Three nephritic antibodies are described in MPGN that play a role in the development of hypocomplementemia [5, 6] : (1) ... The reason for genesis of nephritic antibodies is not known. These autoantibodies are not specific for MPGN and are also seen ... The classic pathway is activated by the interaction of C1 with an antigen-antibody complex. This interaction results in the ...
Anticardiolipin antibody tests. *Antibodies to beta-2-glypoprotein I (Beta2-GPI). Your health care provider will diagnose ... ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS). In general, you will need treatment with a blood thinner for a long time if you have ... You may not have any symptoms, even though you have the antibodies. Symptoms that may occur include:. *Blood clots in the legs ... Some people carry the antibodies mentioned above, but do not have APS. Certain triggers may cause these people to have a blood ...
The present study sought to determine whether the level of anticardiolipin antibodies in women with recurrent abortion differed ...
Titers of PL antibodies had declined (IgM anticardiolipin, negative; IgG anticardiolipin, 54; IgG antibody against β2GPI 90). ... Anticardiolipin antibodies and, less frequently, β2GPI antibodies also have been found in patients with chronic HIV infection, ... Martinez V, Diemert MC, Braibant M, Potard V, Charuel JL, Barin F, Anticardiolipin antibodies in HIV infection are ... In HIV-infected patients, PL antibodies and β2GPI antibodies have been strongly linked with level of viral replication (9). In ...
Antiphospholipid and anticardiolipin antibodies should be obtained to evaluate for antiphospholipid syndrome. Other tests that ... If levels are elevated, further evaluation, including of complement levels, anti-deoxyribonucleic acid (DNA) antibodies, and ... Erythrocyte sedimentation rate and antinuclear antibody studies should be performed to screen for systemic lupus erythematosus ...
Antinuclear antibody, rheumatoid factor, anti-cyclic citrullinated peptide, anti-cardiolipin, and creatine phosphokinase ... Antinuclear antibody, rheumatoid factor, anti-cyclic citrullinated peptide, anti-cardiolipin, and creatine phosphokinase ... For information about antibody testing, see Using Antibody Tests for COVID-19. Healthcare professionals should also consider ... or because of waning antibody levels or false-negative antibody testing during follow up. ...
According to the USDHHS, one-third to one-half of women with lupus have an anticardiolipin antibody and lupus anticoagulant [2] ... Antiphospholipid antibody (APL). Autoantibodies that react with phospholipid; includes anticardiolipin; present in 30% to 40% ... Antiphospholipid antibody: antibodies to a constituent of cell membranes seen in approximately one-third of those with lupus. ... Anti-Sm: anti-Smith antibody; found only in lupus.. Anti-SSA antibody: associated with Sjögren syndrome, sun sensitivity, ...
Association of anticardiolipin antibodies and abnormal nailfold capillaroscopy in patients with systemic lupus erythematosus. ...
The Role of Mycoplasmal Infection and Anticardiolipin Antibodies as Autoimmune Parameters in Pregnancy Loss. Faten S. Bayoumi ...
This is often due to the presence of high levels of antiphospholipid antibodies (APA) and anticardiolipin antibodies ...
However, there were significant differences in mean anticardiolipin IgG antibody levels. Aspirin alone or in combination with ... and anticardiolipin antibodies (aCL)-the so-called antiphospholipid antibodies (aPL). APS was first described in the early ... Antiphospholipid antibodies: anticardiolipin and the lupus anticoagulant in systemic lupus erythematosus (SLE) and in non-SLE ... However, there were significant differences in mean anticardiolipin IgG antibody levels. Aspirin alone or in combination with ...
Antiphospholipid antibodies. Anticardiolipin antibodies (ACAs) of all isotypes are seen in 16-60% of patients with SLE. IgG ... Antibodies to ENAs. ANTI-RO/la antibodies. Diagnosis. Antibodies to Ro(SS-A) and La(SS-B) are found in SLE and Sjogrens ... The relationship of anticardiolipin antibodies to disease activity in systemic lupus erythematosus. Br J Rheumatol 1989;28:379- ... Association of anticardiolipin antibodies with intraglomerular thrombi and renal dysfunction in lupus nephritis. Q J Med 1998; ...
Antiphospholipid antibodies such as lupus anticoagulant, anticardiolipin and antiphosphatidylserine antibodies are highly ... Antiphospholipid antibodies, proteins C and S, and coagulation changes in sickle cell disease. J Lab Clin Med. 1999;134(4):352- ... The production of these auto-antibodies is thought to result from structural changes in sickled red cell membrane [37]. Genetic ...
... and antiphospholipid or anticardiolipin antibodies.40,58 In addition, auto-immune disease systemic lupus erythematosus (SLE) is ... Antibodies • Antiphospholipid antibodies: detectable in many HD patients, significance not clear 21. • Increased ↑ prevalence ... Platelets in early antibody-mediated rejection of renal transplants. J Am Soc Nephrol. 2015;26:855-863.. * Cited Here , ... A vast amount of SLE patients have antiphospholipid antibodies, also called lupus anticoagulant (LA), which increases the risk ...
Correlation with thrombocytopenia and anticardiolipin antibodies. Fanelli, A; Bergamini, C; Rapi, S; Caldini, A; Spinelli, A; ...
8.1.5. detection of H.pylori: (+) antibodies in serum, rapid urease test of antral biopsy, urea breath test to confirm ... anticardiolipin, lupus anticoagulant, urinalysis ... presence of ANA (not specific), antibodies to dsDNA, ssDNA, Sm ...
It is recommended for the aPL antibody report to include the antibodies for aCL and aβ2GPI IgG and IgM antibodies in numerical ... IgG and/or IgM anticardiolipin [aCL], IgG and/or IgM anti-beta2 glycoprotein I [aβ2GPI]). Thrombosis and obstetric ... The recognition that certain aPL antibody types, the number of positive aPL antibodies, or combination of aPL antibodies may be ... IgG isotype antibodies have higher risk for APS compared to IgM.. While laboratory investigation of aPL antibodies is method- ...
Anti Nuclear Antibody (ANA) IFA Titres Rs. 1485 Rs. 1650 View Details ...
ANTI CARDIOLIPIN IGG/IGM. ₹1,740.00. Add to cart * ANTI CCP ANTIBODY. ₹1,200.00. Add to cart ...
... have antiphospholipid antibodies such as anticardiolipin antibodies in their blood tests. There are more specific antibodies to ... The testing of the antinuclear antibody titer, or ANA titer for short, is one of the most reliable diagnostic tests for lupus. ... A more specialized test, antibodies to double stranded DNA, can be found in less than 50% of lupus patients. ... probably because they all involve autoimmune antibodies (the other ones are rheumatoid arthritis, scleroderma, polymyositis, ...
Anti-cardiolipin antibodies are acquired auto-antibodies produced against cardiolipins and are found in the immunoglobulin ... What is Anti-cardiolipin antibodies?. Anti-cardiolipin antibodies are acquired auto-antibodies produced against cardiolipins ... Anti-cardiolipin antibodies have been found in some cerebrovascular insufficiency, cerebral ischemia and in myocardial ... The presence of anti-cardiolipin antibodies in systemic lupus erythematosus can be related to the development of thrombosis. ...
  • Antiphospholipid antibody syndrome (APS) is a disorder characterized by the presence of medium to high levels of lupus anticoagulant antibodies (LAC) and anticardiolipin antibodies (aCL)-the so-called antiphospholipid antibodies (aPL). (
  • At this point, we don't know if this is a "typical" miscarriage or one caused by Antiphospholipid Antibody Syndrome. (
  • Antiphospholipid antibody syndrome (commonly referred to as APS) is a systemic autoimmune disease characterized by the presence of antiphospholipid (aPL) antibodies in association with thrombosis and/or specific pregnancy-related morbidities. (
  • This test measures the levels of Anti Cardiolipin Antibody (IgM) in the blood. (
  • Small volumes from the liquid components of the Anti- cardiolipin antibody IgG(ACA-IgG) EIA kit may get caught on the walls and lid of the vials. (
  • The Rabbit Anti- cardiolipin antibody IgG(ACA-IgG) ELISA Kit is a ready to use kit manufactured by using high quality antibodies sets, plates, solutions and detection molecules. (
  • This EIA test for Rabbit Rabbit Anti- cardiolipin antibody IgG(ACA-IgG) will yield accurate and reproducible results. (
  • Store all components and reagents of the Anti- cardiolipin antibody IgG(ACA-IgG) ELISA Kit refrigerated and +4 degrees Celcius. (
  • Anticardiolipin antibodies in systemic lupus erythematous. (
  • Antibodies against PLs have been commonly found in patients with autoimmune diseases such as systemic lupus erythematosus and primary antiphospholipid syndrome, in which clinical manifestations (mainly thrombotic events) have been directly attributed to antibodies against PLs. (
  • Erythrocyte sedimentation rate and antinuclear antibody studies should be performed to screen for systemic lupus erythematosus, Wegener granulomatosis, and temporal arteritis. (
  • 7. Prevalence and clinical significance of antiprothrombin antibodies in patients with systemic lupus erythematosus or with primary antiphospholipid syndrome. (
  • 11. Association of lupus anticoagulant and anticardiolipin antibodies with thrombosis in patients with systemic lupus erythematosus, primary antiphospholipid syndrome and other disorders. (
  • The presence of anti-cardiolipin antibodies in systemic lupus erythematosus can be related to the development of thrombosis. (
  • and antinuclear antibody. (
  • Correlation with thrombocytopenia and anticardiolipin antibodies. (
  • Antibody levels were estimated on ELISA reader. (
  • Immunodiffusion (ID) detects high affinity antibodies, immunofluorescence (IIF) moderate and high affinity antibodies, and enzyme linked immunosorbent assay (ELISA) low and high affinity antibodies. (
  • The IgG antibody has 2 antigen binding sites. (
  • This antibody can be antigen purified or protein A or G purified. (
  • The classic pathway is activated by the interaction of C1 with an antigen-antibody complex. (
  • The antibodies are detected by solid-phase IMMUNOASSAY employing the purified phospholipid antigen CARDIOLIPIN . (
  • 1 patient had posi- non-central nervous system thrombotic events (e.g., tive antiphospholipid antibodies. (
  • 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. (
  • Immunoglobulin gamma, IgG, mouse monoclonal H&L chain clones or rabbit, goat polyclonal antibodies have 4 parts. (
  • Anti-cardiolipin antibodies are acquired auto-antibodies produced against cardiolipins and are found in the immunoglobulin classes- IgG, IgM and/or IgA. (
  • Present study was conducted to evaluate the association of IgG anticardiolipin antibodies with instent restenosis in patients having undergone percutaneous intervention with bare metal or drug eluting stents. (
  • Enzyme-linked immunosorbent assay was used for detection of anticardiolipin antibodies in a group of 26 patients defined as habitual aborters [‎at least three consecutive spontaneous abortions]‎, and in a control group of 26 patients each of whom had had at least one live birth without pregnancy wastage. (
  • For a long term storage the kit's components may be frozen at -20 but cycles of freezing and thawing should be strictly avoided as they denaturate the polypeptide chains in the antibodies and controlls, thus causing a reduction in the kit's detection ability and specificity which changes will lead to inconsistant results. (
  • The 2006 revised Sapporo laboratory criteria for APS as previously mentioned includes the lupus anticoagulant tests as well as immunoassays for the detection of IgG and IgM antibodies to cardiolipin (CL) and β2GPI. (
  • I will be addressing the rationale for these suggestions during the course of this presentation with a focus on the immunoassays for the detection of IgG and IgM antibodies to CL and β2GPI. (
  • 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. (
  • The objective of this study was to evaluate association of anticardiolipin IgM antibody with preeclampsia among the 70 pregnant women having preeclampsia from March 2016 to February 2017. (
  • IMSEAR at SEARO: Association of anticardiolipin antibodies levels with instent restenosis in patients with coronary artery disease. (
  • 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). (
  • Autoimmune disorders occur when your body's immune system makes antibodies that attack and damage your own tissues or cells. (
  • however, aPL antibodies are thought to occur in 2-5% of the general population. (
  • The presence of these antibodies can cause problems with blood flow and lead to dangerous clots in blood vessels throughout the body. (
  • Western blot assay confirmed the presence of antibodies to p24, gp41, and gp120/160. (
  • Additionally, 5% to 10% of patients with SLE retinopathy will develop large vessel disease and the presence of anti-phospholipid antibodies, anticardiolipin antibodies. (
  • therefore, the presence of aPL antibody is an absolute requirement for the appropriate diagnosis of this disease. (
  • However, there were significant differences in mean anticardiolipin IgG antibody levels. (
  • The mean (±SD) anticardiolipin antibodies levels in cases and controls were 11.8±5.1 GPL/U/ml and 14.3±10.2 GPL/U/ml, respectively. (
  • If levels are elevated, further evaluation, including of complement levels, anti-deoxyribonucleic acid (DNA) antibodies, and neutrophil cytoplasmic antibodies (ANCA), could be considered. (
  • High levels of APS antibodies raise the risk of blood clots. (
  • High levels of APS antibodies in the blood raise the risk of health problems, but some people will never develop blood clots. (
  • You may not have any symptoms, even though you have the antibodies. (
  • Anti-cardiolipin antibodies (aCL) and lupus anticoagulant (LA) should be tested in patients with LPh because this may have therapeutic implications. (
  • In these patients, antibodies against PLs are specific for a neoepitope constituted by the union of β 2 GPI, a lipid-binding coagulation inhibitor, to the cellular membrane phospholipids ( 2 ). (
  • Tests for antiphospholipid antibodies (aPL) will also be done. (
  • The blood tests look for the three APS antibodies in your blood: anticardiolipin, beta-2 glycoprotein I (β2GPI), and lupus anticoagulant. (
  • These are generally referred to as 'criteria' aPL antibody tests. (
  • Moreover, the anticardiolipin test assists in the diagnosis of antiphospholipid syndrome. (
  • 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. (
  • Even in categorical distribution when the value was considered as positive by assessing a cut-off, cases had three times more chance to have positive level of anticardiolipin IgM antibody than controls (OR=3.3, 95% CI=1.1-9.6, p=0.046). (
  • Pearson's correlation test revealed that both systolic and diastolic blood pressure had a positive correlation with the level of anticardiolipin IgM antibody. (
  • For aCL IgG and IgM determinations, antibody cut-off values greater than 40 GPL or MPL units or more than the 99th percentile for the testing laboratory's population were recommended to be positive. (
  • In the case of a β2GPI IgG and IgM antibodies, cut-off values greater than 99th percentile for the laboratory's population was recommended to determine positive results. (
  • The antiphospholipid antibodies (aPL) cause the test to be abnormal in the laboratory. (
  • The present study sought to determine whether the level of anticardiolipin antibodies in women with recurrent abortion differed from that in the general population. (
  • Some people carry the antibodies mentioned above, but do not have APS. (
  • In fact, 20% to 30% of people with lupus have antiphospholipid antibodies. (
  • This antibody needs to be stored at + 4°C in a fridge short term in a concentrated dilution. (
  • Anti-cardiolipin antibodies have been found in some cerebrovascular insufficiency, cerebral ischemia and in myocardial infarction. (
  • To be diagnosed with APS, you must have APS antibodies and a history of health problems related to the disorder. (
  • The specific antibodies in APS are called "antiphospholipids" because they attack and damage parts of cells called phospholipids. (
  • Freeze thaw will destroy a percentage in every cycle and should be avoided.Antibody for research use. (
  • In conclusion, this study shows that anticardiolipin IgM antibody was associated with preeclampsia. (
  • The level of this anticardiolipin IgM antibody is directly proportional to the severity of preeclampsia and both systolic and diastolic blood pressure. (
  • One GPL/MPL unit is defined as the cardiolipin-binding activity of 1 g/ml of affinity-purified IgG or IgM aCL antibody. (
  • For storage sodium azide is added or you can call us to request azide free antibody preparations. (
  • HIV, hepatitis C, and the bacteria that causes Lyme disease can increase your risk of making APS antibodies or trigger APS. (

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