Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis C virus (HCV) infection has been associated with multiple autoimmune manifestations. The immune response to HCV infection encompasses the development of autoantibodies, immune complex formation and deposition, and cryoglobulinemia complicated by vasculitis, glomerulonephritis, or neuropathy. HCV infection has been associated with antiphospholipid antibody syndrome, RA, SLE, PM/DM, and thyroid disease. HCV-infected patients also have a high incidence of sicca symptoms with sialoadenitis, and reports of low-grade lymphoproliferative malignancies have emerged. Optimal treatment for HCV-related autoimmune disease remains to be determined, but patients seem to respond to immunosuppression with classic agents or interferon.
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PMID:Hepatitis C-associated autoimmune disorders. 960 63

The antiphospholipid antibody syndrome (APS) is defined broadly by the presence of antiphospholipid antibodies, venous and arterial thrombosis, thrombocytopenia and fetal wastage. APS can be primary or secondary, in which APS occurs in the context of another defined disease such as autoimmune disease, malignancy, drug-induced disease, etc. APS is primary in one-half of patients and secondary in the rest, mainly to systemic lupus erythematosus. Several cardiac manifestations of APS have been reported. These include valvular heart disease, coronary artery disease, intracardiac thrombosis and cardiomyopathy. The literature has shown a prevalence of approximately 35% of valvular abnormalities detected by echocardiography in patients with APS. A patient with primary APS who developed aortic stenosis with vegetations on a bioprosthetic porcine valve is presented.
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PMID:Antiphospholipid antibody syndrome with involvement of a bioprosthetic heart valve. 970 81

Immunoablation followed by allogeneic stem cell (SC) transplantation has been shown to be capable of curing a large spectrum of experimental autoimmune disorders, hereditary and/or induced. Superimposable results, albeit with some exceptions, have been obtained in human patients affected by coincidental autoimmune and blood diseases. However, both because of encouragine experimental results and of the procedure's greater safety, autologous SC are being increasingly utilized worldwide. Case reports are being collected in the registry of the European Group for Blood and Marrow Transplantation (EBMT)/European League against Rheumatism (EULAR) Autoimmune Disease Stem Cell Project. Among the severe autoimmune diseases (SADs), which are the target of autologous transplantation, severe refractory systemic lupus erythematosus (SLE) is a condition which may benefit from this procedure. We report here the case of a 19 year old female patient with a six year history of SLE with secondary antiphospholipid syndrome (APS), who later developed refractory Evans syndrome. She was transplanted with autologous mobilized CD34+ SC and progenitor cells after conditioning with cyclosphosphamide, anti-T lymphocyte globulin and prednisone. Eight months after transplant, the patient is alive and well, with normal blood counts and persistent low-titre direct antiglobulin (DAT, Coombs) and anti-nuclear antibody (ANA) tests. Anti-double stranded DNA antibody (Anti-dsDNA), lupus anticoagulant tests and anti-cardiolipin antibody (ACA) test are negative.
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PMID:Autologous peripheral blood stem and progenitor (CD34+) cell transplantation for systemic lupus erythematosus complicated by Evans syndrome. 979 53

The aim of the present study was to evaluate the urea resistance and binding characteristics of anti-beta 2-glycoprotein I (anti-beta 2GPI) antibodies using standard anticardiolipin (aCL) and anti-beta 2GPI enzyme immunosorbent assays (ELISAs). Sera from patients with antiphospholipid syndrome (APS) (n = 22) and non-APS (n = 24), positive in a standard aCL ELISA, were tested in an anti-beta 2GPI ELISA performed in polystyrene-irradiated ELISA plates. Urea resistance aCL and anti-beta 2GPI ELISAs were performed by measuring the ability of antibodies to recognize antigen in the presence of 2 M urea. The serum dilution after urea treatment (D) expressed as a percentage of the serum dilution without urea treatment (D(o)) corresponding to the same optical density was defined as residual activity (RA = 100 D/D(o)). The higher the RA, the higher the resistance of the antibodies to urea. APS compared to non-APS sera had higher aCL binding (absorbance values ranging between 0.180 and 1.400; median, 0.717 vs 0.120-1.273; median, 0.250, respectively; P < 0.004). Six APS patients' sera had low aCL levels but they expressed RA > or = 30%. Anti-beta 2GPI antibodies were detected in 15 of 22 APS vs 3 of 24 non-APS patients (P < 0.03); RA > or = 30% was detected in 15 of 22 APS vs 1 of 23 non-APS patients (P < 0.004). Using a CL affinity column, antibodies were purified from three APS anti-beta 2GPI negative and three non-APS anti-beta 2GPI-positive patients and tested in a aCL ELISA, using highly purified bovine serum albumin (BSA) as a blocking agent (modified ELISA); reactivity was not detected in two APS and one non-APS sera. On the contrary, the reactivity of the purified antibodies was high when beta 2GPI was incubated with CL in the ELISA plates; thus some anti-beta 2GPI negative sera from APS patients recognized the CL/beta 2GPI complex, rather than CL or beta 2GPI alone. In conclusion, anti-beta 2GPI antibodies are common in the APS patients, but a number of such patients recognize the CL/beta 2GPI complex and not CL or beta 2GPI. Antibodies to either beta 2GPI or the CL/beta 2GPI complex derived from APS sera present a high resistance to urea. Anti-beta 2GPI antibodies of low urea resistance exist in a minority of non-APS patients with autoimmune disease.
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PMID:Antibodies to beta 2-glycoprotein-I: urea resistance, binding specificity, and association with thrombosis. 985 82

Lupus anticoagulant antibodies have never been reported to disappear after either allogeneic or autologous bone marrow transplantation in humans. We report the first case of disappearance of lupus anticoagulant antibodies in a patient without systemic lupus erythematosus or clinical evidence of other autoimmune disorders, who received an allogeneic bone marrow transplant as treatment for chronic myeloid leukemia. Although marrow transplantation is not a recognized therapy for antiphospholipid syndrome, our observation should be considered another example of the capability of intensive chemo-radiotherapy followed by stem cell transplantation to ablate a pathologic marrow clone resulting in an autoimmune disorder and improve, or even cure, some severe autoimmune diseases.
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PMID:Disappearance of lupus anticoagulant after allogeneic bone marrow transplantation. 1003 55

Systemic lupus erythematosus (SLE) remains a challenging autoimmune disease in term of its etiology, pathogenesis, and management. Much progress has been made in the past year in searching for the SLE susceptibility genes, particularly by several genome-wide screening groups. Cumulative evidence about the association of infections and hormones with SLE has been gathered. Researchers believe that childhood SLE involves more severe organ involvement than adult SLE. Central nervous system complicated lupus continues to be problematic because functional imaging can be abnormal in otherwise asymptomatic lupus individuals. Whether these abnormalities result from subclinical central nervous system involvement or from false positives remains to be determined. With the wide use of corticosteroids as a cornerstone therapy for major organ involvement in childhood SLE, potential complications, especially those involving the growing bone or osteoporosis, are a cause of concern. Evidence suggests that regular exercise, as well as calcium and vitamin D supplementation, may help alleviate bone complications. Researchers have also updated information about pediatric antiphospholipid antibody syndrome. Follow-up studies on neonatal lupus and its pathogenesis have progressed, leading to a better understanding of its natural history and, in turn, to proper counseling of mothers of infants with neonatal lupus and of women with positive anti-Ro or anti-La antibodies. Drug-induced lupus in children is not uncommon. Minocycline and zafirlukast have been increasingly used, and were reported to induce lupus in children.
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PMID:Systemic lupus erythematosus and related disorders of childhood. 1050 59

In an attempt to evaluate the frequency of autoimmune markers in autoimmune thrombocytopenic purpura (AITP) and to determine if autoimmune markers in patients with isolated AITP were associated with particular disease manifestations, we analyzed records of 122 consecutive adults with AITP. Twenty-nine patients (24%) had significant titers of one or several autoimmune markers at AITP onset. Among them, 16 (13%) had antinuclear antibodies. The presence of autoimmune markers did not correlate with presenting feature, response to treatment or long-term outcome of AITP. Six patients (5%) developed seven autoimmune diseases during follow-up, comprising systemic lupus erythematosus, an antiphospholipid syndrome, autoimmune haemolytic anemia (n = 2), Grave's disease, Hashimoto's disease and primary biliary cirrhosis. At AITP onset, three of these patients had isolated biological markers of the autoimmune disease they later developed. The annual average incidence rate of autoimmune diseases was 1% per patient-year in the entire group and 0.4% in the group of patients with no autoimmune markers at AITP onset. This low rate is probably due to careful assessment at diagnosis for concomitant overt autoimmune disease. We recommend extensive screening for autoimmune markers at AITP onset, and careful follow-up of patients with autoimmune markers. Routine screening for autoimmune markers during AITP follow-up is not necessary for patients with no autoimmune markers at AITP onset. Systemic lupus erythematosus (SLE) and other autoimmune disorders can complicate autoimmune thrombocytopenic purpura (AITP) or be diagnosed concomitantly with otherwise unremarkable AITP (1, 2). However, the frequency and prognostic value of isolated autoimmune markers (i.e. not associated with an autoimmune disorder), particularly antinuclear antibodies (ANA) at AITP onset or during follow-up is controversial (3-8). For example, the committee organized by George et al. (9) to write guideline on the diagnosis and treatment of AITP stated that the search for ANA and lupus anticoagulant were of "uncertain appropriateness at diagnosis and during follow-up". In an attempt to help practicians to make decisions, we analyzed the frequency of autoimmune markers and autoimmune disorders at onset and during the follow-up in 122 adults with AITP and no overt autoimmune disease at diagnosis. These consecutive patients were followed by the same physician for a mean period of 6 years, and had routine screening tests for autoimmune markers and disorders at onset, before steroid therapy, and regularly during follow-up.
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PMID:Screening for autoimmune markers is unnecessary during follow-up of adults with autoimmune thrombocytopenic purpura and no autoimmune markers at onset. 1066 52

Antiphospholipid syndrome (APS) is an autoimmune disease that accompanies anti-phospholipid antibodies measured as either anti-cardiolipin antibodies (aCL) or lupus anticoagulant. beta(2)-glycoprotein I (beta(2)GPI) is the most common and apparently the best-characterized antigenic target for aCL. To investigate T-cell responses to beta(2)GPI, we stimulated PBMC of 18 APS or systemic lupus erythematosus (SLE) patients carrying anti-beta(2)GPI and 10 healthy controls, using a peptide library covering the beta(2)GPI sequence. We established seven CD4(+) T cell lines reactive with beta(2)GPI peptide. Three of four epitopes for patient-derived T cell lines were p244-264, whereas one T cell line from a control subject also recognized p244-264. Furthermore, there was no tendency for particular HLA class II molecules to present beta(2)GPI peptides. However, cytokine producing patterns were significantly different between T cell lines from patients and those from healthy individuals (p =.028); patients' T cells tend to exhibit higher IL-4 and lower IFN-gamma responses. These T cell lines did not react to beta(2)GPI purified from human plasma. These results indicate that beta(2)GPI-reactive CD4(+) T cells of APS/SLE patients mainly recognize cryptic p244-264 in the context of various HLA class II molecules, and exhibit Th0-Th2-type responses. Our findings may provide a clue to the pathogenesis of APS.
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PMID:Analysis of T cell responses to the beta 2-glycoprotein I-derived peptide library in patients with anti-beta 2-glycoprotein I antibody-associated autoimmunity. 1071 14

The pathogenesis of autoimmune disease is still an enigma. Whereas the diverse clinical manifestations of many autoimmune diseases cannot be explained by the existence of autoantibodies, idiotypic dysregulation may provide an alternative explanation. Experimental models, serum level changes of pathogenic idiotypes during exacerbation and remission, and the increased expression of pathogenic idiotypes following common infections all support this notion. In this article we review experimental models of autoimmune disease induction (systemic lupus erythematosus, antiphospholipid syndrome, Goodpasture's syndrome, autoimmune thyroiditis, and vasculitis) by manipulation of the idiotypic network, and discuss the utilization of idiotypes for the immunotherapy of autoimmune diseases and other conditions that involve the immune system (e.g., atherosclerosis).
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PMID:Idiotypic network dysregulation: a common etiopathogenesis of diverse autoimmune diseases. 1082 56

The clinical manifestations of the antiphospholipid syndrome(APS) include arterial and venous thrombosis and a fetal loss, but the pathogenic mechanisms remain unclear. To clarify the mechanism of thrombogenic state in APS, we investigated the markers for thrombosis including thrombin-antithrombin complex(TAT) in patients with antiphospholipid antibodies(aPL). Prothrombin fragment 1 + 2(F1 + 2) in patients with APS and in autoimmune disease patients with aPL increased significantly compared with those obtained in autoimmune disease patients without aPL or in control subjects. However, there was not a significant difference in the TAT level of each group, suggesting that the formation of TAT was impeded in APS. To investigate which aPL is responsible for the disturbance of the TAT formation, the ratio of F1 + 2/TAT was calculated. The ratio increased in patients with lupus anticoagulant, especially with prolonged kaolin clotting time, and furthermore the ratio strongly increased in patients with IgG type-anticardiolipin antibodies(aCL). Our results suggest that IgG-aCL is associated with thrombogenic state in APS because free thrombin is present in patients' blood by impeding the formation of TAT by mainly IgG-aCL.
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PMID:[Evaluation of F1 + 2/TAT ratios in Japanese patients with antiphospholipid syndrome]. 1089 73


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