Antibodies, Antinuclear
Antibodies
Antibody Specificity
Autoantibodies
Lupus Erythematosus, Systemic
Fluorescent Antibody Technique
Antibody Formation
Antibodies, Neutralizing
Connective Tissue Diseases
Rheumatoid Factor
Fluorescent Antibody Technique, Indirect
Antibodies, Anti-Idiotypic
Autoimmune Diseases
Antibody Affinity
Immunoglobulin M
Immunoglobulin G
Binding Sites, Antibody
Scleroderma, Systemic
Cross Reactions
Antibodies, Neoplasm
Rheumatic Diseases
Sjogren's Syndrome
Hepatitis, Autoimmune
Enzyme-Linked Immunosorbent Assay
Autoantigens
Raynaud Disease
Antigen-Antibody Complex
Arthritis, Juvenile
Iritis
Antibodies, Antiphospholipid
Mixed Connective Tissue Disease
Antibodies, Antineutrophil Cytoplasmic
Immunoglobulin A
Scleroderma, Localized
Liver Cirrhosis, Biliary
Lupus Nephritis
Neutralization Tests
Antigen-Antibody Reactions
Antibodies, Bispecific
Molecular Sequence Data
Immunoglobulins
DNA
Single-Chain Antibodies
snRNP Core Proteins
Immunoenzyme Techniques
Antibodies, Blocking
Immunoassay
Autoimmunity
Amino Acid Sequence
Rabbits
Immunoglobulin Fab Fragments
Antibodies, Anticardiolipin
Antibodies, Heterophile
Antibodies, Catalytic
Immunodiffusion
Sensitivity and Specificity
Lupus Erythematosus, Cutaneous
B-Lymphocytes
Arthritis, Rheumatoid
Complement System Proteins
Immunoblotting
Antibodies, Monoclonal, Humanized
Lupus Vulgaris
Crithidia
Hybridomas
Immune Sera
Lupus Erythematosus, Discoid
Complement C4
Epitope Mapping
Glomerulonephritis
Immunization
RNA, Small Cytoplasmic
Mice, Inbred Strains
False Positive Reactions
Dermatomyositis
Biological Markers
Antigens, Surface
Cardiolipins
Immunization, Passive
Antiphospholipid Syndrome
T-Lymphocytes
Blotting, Western
Vasculitis
gamma-Globulins
HLA-DR5 Antigen
Immunoglobulin Fragments
Immunohistochemistry
Kidney Glomerulus
Ribonucleoproteins, Small Nuclear
Salivary Glands
Radioimmunoassay
Cells, Cultured
Immune Complex Diseases
HLA Antigens
Electrophoresis, Polyacrylamide Gel
Complement C3
Cell Nucleolus
Complement Fixation Tests
Disease Models, Animal
Hemagglutination Tests
Hemagglutination Inhibition Tests
Immunoglobulin Variable Region
Seroepidemiologic Studies
Lymphocyte Activation
Reagent Kits, Diagnostic
Sialadenitis
Hypergammaglobulinemia
Immunoglobulin Idiotypes
Immunologic Techniques
Lymphocytes
Mice, Congenic
Antigens, Neoplasm
Base Sequence
Immunosorbent Techniques
Haptens
Kidney
Mice, Inbred MRL lpr
Antibody Diversity
Cattle
Peptide Library
Biopsy
Hepatitis C Antibodies
Isoantibodies
Immunoglobulin Isotypes
Spondylitis, Ankylosing
Flow Cytometry
Thyroid Gland
Histones
Antibodies, Monoclonal, Murine-Derived
Retrospective Studies
Glycoproteins
Vaccination
Chronic Disease
Hepatitis B Antibodies
Binding, Competitive
Histocytochemistry
Peptide Fragments
Immunity, Maternally-Acquired
Microscopy, Fluorescence
Neutrophils
Case-Control Studies
Reproducibility of Results
Centromere
Recombinant Fusion Proteins
Precipitin Tests
DNA, Single-Stranded
Species Specificity
Antigens, Protozoan
Peptides
Penicillamine
Antibody-Dependent Cell Cytotoxicity
Skin
Prospective Studies
Single-Domain Antibodies
Chromatography, Affinity
Iodine Radioisotopes
Follow-Up Studies
Prevalence
Immunosuppressive Agents
Liver
Bacterial Vaccines
Cloning, Molecular
Protein Binding
Immunochemistry
Viral Envelope Proteins
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.
Antinuclear antibody
Libby, Montana
Anti-p62 antibodies
Primary biliary cholangitis
Autoimmune disease
List of autoimmune diseases
Cell nucleus
PLAID syndrome
Levamisole induced necrosis syndrome
Ross Petty (pediatrician)
Systemic scleroderma
Dermatomyositis
Anti-dsDNA antibodies
Haploinsufficiency of A20
Rheumatoid factor
Anti-Jo1
Childhood arthritis
Canine discoid lupus erythematosus
Cold sensitive antibodies
Lupus
Nuclear bodies
STING-associated vasculopathy with onset in infancy
Pierre Grabar
Scleromyositis
Autoantibody
Anti-Hu associated encephalitis
Immunoglobulin E
Dihydrolipoyl transacetylase
Anti-cardiolipin antibodies
HLA A1-B8-DR3-DQ2
Anti-Scl-70 antibodies
Per- and polyfluoroalkyl substances
Uveitis
Centromere
Spondyloenchondrodysplasia
ANF
IPEX syndrome
Stiff-person syndrome
List of MeSH codes (D12.776)
1984 in the United Kingdom
Arthritis
Ernst H. Beutner
Adult-onset Still's disease
Dapsone
HLA A1-B8 haplotype
List of MeSH codes (D12.776.124)
Systemic vasculitis
Antibody
Primary sclerosing cholangitis
Anti-nRNP
Robert Ira Lewy
Juvenile idiopathic arthritis
Antinuclear antibody panel: MedlinePlus Medical Encyclopedia
Antinuclear Antibodies (ANA)
Increasing Prevalence of Antinuclear Antibodies in the United States
Antinuclear Antibody: Reference Range, Interpretation, Collection and Panels
What Is a Healthy Range of Antinuclear Antibodies (ANAs)?
Comparison of the complement-fixing activity of antinuclear antibodies in lupus nephritis, mixed connective tissue disease, and...
Hidden anti-nuclear antibodies in rheumatic diseases - PubMed
Hidden anti-nuclear antibodies in rheumatic diseases - PubMed
Response to: 'Antinuclear antibodies: mitotic patterns and their clinical associations' by Betancur and Gómez-Puerta | Annals...
Antinuclear Antibodies Immunofluorescence Biopsy Tissue - Preparation, Procedure, Cost, Normal Range | Practo
Antinuclear antibody profiling in uveitis<...
Antibodies against High Mobility Group Box protein-1 (HMGB1) versus other anti-nuclear antibody fine-specificities and disease...
Anti Nuclear Antibody, EIA in New Delhi from Tata 1mg Labs ( Tata 1mg Technologies Private Limited): view price,...
Ophthalmologic Manifestations of Ankylosing Spondylitis: Overview, Etiology, Prognosis
Antinuclear antibody Titer and Pattern | drcelaya.com
Bahrain Medical Laboratory | Antinuclear Antibodies (ANA), Serum
Antinuclear Antibodies (ANA) Level Costs | NH Health Cost
ABH1 / Anti-Nuclear cap-binding protein subunit 1 Antibody
The significance of dense fine speckled pattern in antinuclear antibody-associated rheumatic disease and coexisting...
Range of antinuclear antibodies in 'healthy' individuals<...
Presumptive Abortive Human Rabies --- Texas, 2009
Glomerulonephritis: MedlinePlus Medical Encyclopedia
Optic Atrophy Workup: Imaging Studies, Other Tests
Table - Current Guidelines, Common Clinical Pitfalls, and Future Directions for Laboratory Diagnosis of Lyme Disease, United...
The use of laboratory tests in the diagnosis of SLE | Journal of Clinical Pathology
Autoimmune Lymphoproliferative Syndrome (ALPS) Symptoms & Diagnosis | NIH: National Institute of Allergy and Infectious Diseases
Anti-Nuclear Antibody (ANA IFA) Test In Gurgaon : Anti-Nuclear Antibody (ANA IFA) Test At Home @ Best Prices
Identify & Evaluate Patients with Chronic Kidney Disease - NIDDK
Positivity1
- The authors conclude that no relationship could be established between chemical exposures and antinuclear antibody positivity. (cdc.gov)
ANAs3
- 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)
Serum7
- 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)
Autoantibodies7
- 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 an8
- 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)
Systemic9
- 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)
Titer3
- 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)
Immunofluorescence4
- 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)
ELISA7
- 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)
Antiphospholipid antibodies8
- 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)
Prevalence4
- 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)
Connective tissue d1
- Sera of positive cases were analyzed for additional classes of antinuclear antibodies associated with specific connective tissue diseases. (cdc.gov)
Proteins2
- 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)
Tissues6
- 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)
Test17
- 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)
Titers1
- 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)
Clinical5
- 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)
Antigens1
- 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)
Scleroderma2
Body's1
- White blood cells in the body's immune system make antibodies to spot and attack foreign agents that cause infections or disease. (rheumatology.org)
Lupus1
- Monoclonal HMGB1-targeting antibodies can ameliorate murine polyarthritis and lupus-like disease. (biomedcentral.com)
Pattern2
- 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)
Bloodstream1
- Many women with unexplained infertility actually have antibodies in their bloodstream which are working against conception. (sharedjourney.com)
Immunoassay2
- 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)
Immune system3
- 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)
Patterns2
- 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)
Exposure1
- Mercury Exposure and Antinuclear Antibodies among Females of Reproductive Age in the United States: NHANES. (nih.gov)
Nucleus2
- 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)
Tests1
- 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)
Blood5
- 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)
Presence1
- The presence of these antibodies is considered to be very harmful as they increase the chances of getting targeted by autoimmune diseases. (flebo.in)
Positive2
- 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)
Common1
- We confirm that anti-HMGB1 antibodies are common in SLE and correlate with disease activity variables. (biomedcentral.com)
Chemicals1
- In the general population, women, older adults, and individuals exposed to certain drugs and chemicals are more likely to have the antibodies. (nih.gov)
Infections1
- Antibodies are special cells that are supposed to help our bodies attack foreign invaders, like bacteria from colds and infections. (sharedjourney.com)
Complications1
- There are a number of complications associated with high levels of antiphospholipid antibody. (sharedjourney.com)
Cells1
- Rabbit anti-HMGB1 antibodies gave rise to cytoplasmic, but not nuclear, staining of HEp-2 cells. (biomedcentral.com)