Open AccessClinical Relevance of Antibodies to Cardiolipin in Patients with Chronic Hepatitis C
Author(s) -
Himoto Takashi,
Yoneyama Hirohito,
Kurokohchi Kazutaka,
Mori Hirohito,
Inukai Michio,
Masugata Hisashi,
Goda Fuminori,
Haba Reiji,
Watanabe Seishiro,
Senda Shoich,
Masaki Tsutomu
Publication year - 2012
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.21529
Subject(s) - cardiolipin , antibody , clinical significance , chronic hepatitis , immunology , relevance (law) , medicine , virology , hepatitis , chemistry , political science , biochemistry , virus , phospholipid , membrane , law
The significance of antibodies to cardiolipin (anti‐CL) remains uncertain in patients with chronic hepatitis C (CH‐C). The main purpose of this study was to elucidate the clinical characteristics of patients with CH‐C seropositive for anti‐CL. The prevalence of anti‐CL and clinical parameters associated with anti‐CL in those patients were examined. Six of the 45 (13%) patients with CH‐C had anti‐CL. However, none of these six CH‐C patients fulfilled the criteria for antiphospholipid syndrome. Serum triglyceride and apolipoprotein B (ApoB) levels in CH‐C patients with anti‐CL were significantly higher than those in CH‐C patients without anti‐CL. Serum triglyceride levels positively correlated with serum ApoB levels. CH‐C patients with anti‐CL had significantly more progressive hepatic fibrosis than those without anti‐CL. The degree of 8‐hydroxy 2′‐deoxyguanosine (8‐OHdG) expression in the liver tissue was more severe in CH‐C patients with anti‐CL than in those without it. However, the emergence of anti‐CL in CH‐C patients was independent of insulin resistance, hepatic steatosis, and iron overload. These findings suggest that the emergence of anti‐CL is associated with oxidative stress and that CH‐C patients seropositive for anti‐CL have clinical characteristics of hypertriglyceridemia, which derives from the facilitation of ApoB synthesis, and progressive hepatic fibrosis. J. Clin. Lab. Anal. 26:342‐348, 2012. © 2012 Wiley Periodicals, Inc.