Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02749 (beta2-glycoprotein I)
 836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured serum antiphospholipid antibodies (aPL) in patients with multiple sclerosis (MS) using enzyme linked immunosorbent assay (ELISA) and examined the correlations between these antibodies and MS. This study included thirty-two patients with clinically definite MS, thirteen patients with other autoimmune neurological diseases excluding collagen diseases (disease control A), eight patients with collagen vascular diseases (disease control B) and twenty-six healthy persons (normal control). In MS group IgG antibody against cardiolipin (CL) was detected in 3 (9%); among them, cofactor (beta 2-glycoprotein I) dependency was shown in 2 but one was cofactor independent. IgM antibody was elevated in 14 of 32 patients (44%) with MS, but cofactor dependency was not determined. However, this was significantly higher in frequency than that of the disease control A (p < 0.01) and normal control (p < 0.01). Results of antibodies against phosphatidylserine were found similar to CL, but antibodies against phosphatidylcholine were in most cases negative. Each of anti-CL IgG antibody purified from four patients with diverse immunological disorders (primary antiphospholipid antibody syndrome, MS, polyarteritis nodosa and systemic lupus erythematosus) had different reactivities against DNA. In addition, the aPL positive group in MS possessed the autoantibodies such as antinuclear antibody at higher rate than the negative group. However, clinically two groups of MS were indistinguishable. The higher incidence of aPL may imply that a broad spectrum of autoantibodies might be produced in MS; some antibodies presumably related directly to MS pathogenesis are yet to be identified.
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PMID:Characterization of serum anti-phospholipid antibodies in patients with multiple sclerosis. 872 2

A 29-year-old woman was referred for abdominal pain. Results of tests for lupus anticoagulant and antibodies to phosphatidylserine and to beta2-glycoprotein I were positive, but the patient had no features of systemic lupus erythematosus (SLE). Abdominal ultrasonography showed a thickening of the gallbladder wall without cholelithiasis. A surgical procedure revealed necrotic areas of the gallbladder wall, and a cholecystectomy was performed. Histologic examination of the gallbladder showed multiple thrombi and no vasculitis. Despite full-dose heparin, the patient developed a catastrophic antiphospholipid syndrome (APS) and subsequently died. Among connective tissue disorders, acute acalculous cholecystitis has been reported in patients with polyarteritis nodosa and/or SLE. APS should be considered as a possible cause of acalculous cholecystitis.
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PMID:Acalculous ischemic gallbladder necrosis in the catastrophic antiphospholipid syndrome. 966 91