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 have been demonstrated in chronic hepatitis C, but their clinical and pathogenetic significance remains elusive. We prospectively studied 115 patients (85 men, mean age 36.9 years) with chronic hepatitis C without cirrhosis and treated by alpha-interferon (alpha-IFN). Antiphospholipid determinations comprised anticardiolipin (ACA), anti-beta2-glycoprotein I and anti-prothrombin antibodies of the IgG and IgM classes. At entry, 24 patients (21%) were found to possess low to moderate ACA levels (18 IgG, two IgM and four both isotypes) compared with only 4/115 age- and sex-matched control subjects (3.5% P=0.001). ACA positivity rate increased to 31% (P=0.01) after a 6-month course of alpha-IFN treatment. In contrast, the prevalence of anti-beta2-glycoprotein I and anti-prothrombin antibodies was not significantly different from controls at either time point. The presence of ACA correlated with that of antinuclear antibodies (P=0.0002), but was not associated with parameters such as histological activity, viral burden and response to alpha-IFN, nor with a history of thrombosis or pregnancy loss. However, a non-significant trend of higher incidence of mild thrombocytopenia among ACA-positive patients was observed. We conclude that low-titre ACA positivity is a common finding in patients with chronic hepatitis C, especially following alpha-IFN treatment, but does not select a category with different clinical features. These data are in keeping with the absence of associated anti-beta2GPI and anti-prothrombin antibodies, and do not support a role for HCV infection in the pathogenesis of the antiphospholipid syndrome.
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PMID:Prevalence and significance of anticardiolipin, anti-beta2 glycoprotein I and anti-prothrombin antibodies in chronic hepatitis C. 963 88

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