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)

Antiphospholipid antibodies (aPL) have been detected in various liver diseases, particularly cirrhosis. The role of alcoholic consumption per se has been suggested. The aim of our study was to assess the prevalence of aPL in patients with alcoholic liver disease at various states and to correlate the presence of aPL with both liver injury and alcoholic consumption. Three groups were prospectively included. Group A: 74 controls (age- and sex-matched); group B: 46 patients with alcoholic steatosis; group C: 28 patients with alcoholic cirrhosis. For each patient, lupus anticoagulant, anticardiolipin antibodies and anti-beta2-glycoprotein I antibodies were tested. The prevalence of aPL (presence of at least one positive test) was 5% in group A, 20% in group B and 50% in group C (P < 0.04). No correlation appeared between aPL and Child Pugh score in group C. No correlation was found between the presence of aPL and alcohol intake in patients with either steatosis or cirrhosis. Our study confirms that aPL positivity is more frequently encountered in patients with alcoholic liver disease than in controls. Their prevalence increases with the degree of histological damage but not with the level of alcoholic intake.
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PMID:Antiphospholipid antibodies in alcoholic liver disease are influenced by histological damage but not by alcohol consumption. 1098 50

There are few case reports on the association between autoimmune hepatitis (AIH) and anticardiolipin antibodies (anti-CLAbs) and/or antiphospholipid syndrome (APLS). We studied the anti-CLAbs prevalence in AIH and other hepatic diseases. We also investigated whether anti-CLAbs are co-factor dependent and which is their avidity since co-factor dependency or increased resistance is associated with APLS. Fifty-nine AIH patients, 228 HCV, 50 HBV, 123 with other non-viral and non-autoimmune liver disorders (nV-nALD) and 267 healthy people were investigated for anti-CLAbs and antibodies against beta-2-glycoprotein I (anti-beta2-GPI). Resistance of IgG anti-CLAbs was evaluated using 2 M urea. IgG anti-CLAbs detected in 39% of AIH, 19.7% of HCV (p=0.006), 14% of HBV (p=0.01), 8.1% of nV-nALD (p=0.000) and 1.1% of healthy (p=0.000). IgG anti-CLAbs were associated with the presence of cirrhosis and active AIH while their resistance to urea was high. Anti-beta2-GPI was detected in two AIH patients. We demonstrated a significantly higher prevalence of anti-CLAbs in patients with AIH compared to other diseases and healthy people. Anti-CLAbs were associated with AIH stage but no association was found with APLS clinical manifestations (thrombosis, pregnancy morbidity, thrombocytopenia). However, their avidity was comparable with that of APLS indicating the need for prospective studies in order to address whether anti-CLAbs in AIH may contribute to the progression of liver disease or APLS development.
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PMID:Prevalence and clinical significance of anticardiolipin antibodies in patients with type 1 autoimmune hepatitis. 1584 48

Apolipoprotein E (ApoE) and H (ApoH) genotypes are known to affect plasma lipoprotein concentrations. By modulating transport and entry of the hepatitis B virus into hepatocytes, apolipoproteins may influence the course of infection. To verify this hypothesis, 105 patients with chronic HBV infection were examined. Sixty-two of the patients were followed-up for a median time of 21 years. One hundred two controls were included. ApoE and ApoH genotypes were determined by the restriction fragment length polymorphism method. A trend was found for progressive overrepresentation of ApoE3/E3 among patients with advanced liver disease: 13/27 (48%) of inactive HBV carriers, 36/61 (59%) of chronic hepatitis B patients and 16/17 (94%) of patients who received liver transplants (P < 0.005). Being an E3/* carrier was associated with a lower probability of loss of HBsAg: 9/56 (16%) versus 3/6 (50%) (P < 0.05); it was also associated with a longer time before HBsAg loss (P < 0.05). No influence of ApoH genotypes on clinical outcomes was found. The probability of disease progression was higher, and that of loss of HBsAg was lower, among patients with the ApoE3 allelic variant. Downregulation and/or reduced binding of the LDL receptor may explain the more benign course of hepatitis B among carriers of ApoE2-E4.
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PMID:Genetic polymorphism at the apolipoprotein E locus affects the outcome of chronic hepatitis B. 2002 1