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Mannose binding lectin gene mutations are associated with progression of liver disease in chronic hepatitis B infection
Author(s) -
Yuen ManFung,
Lau ChakSing,
Lau YuLung,
Wong WaiMan,
Cheng ChiChung,
Lai ChingLung
Publication year - 1999
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510290417
Subject(s) - cirrhosis , hepatocellular carcinoma , hepatitis b , mannan binding lectin , medicine , hepatitis , liver disease , immunology , mutation , virology , gastroenterology , biology , gene , lectin , genetics
Mannose‐binding lectin (MBL) plays an important role in immune defense. We examined the MBL gene mutations and MBL levels in Chinese hepatitis B and hepatitis C patients with and without symptomatic cirrhosis. We recruited 190 hepatitis B and C patients, and 117 normal Chinese as controls. Serum MBL levels were measured by enzyme‐linked immunosorbent assay. MBL gene mutation at codons 52, 54, and 57 was detected by polymerase chain reaction (PCR) assay. In asymptomatic hepatitis B and C patients, there was no increase in codons 52, 54, and 57 mutation, but the MBL levels were significantly lower than those in the controls. Codon 54 mutation rate was increased to 44.4% ( P = .007) in symptomatic hepatitis B cirrhosis and 64.3% ( P = .0026) in patients with spontaneous bacterial peritonitis (SBP). There was no increase in codon 54 mutation rate in hepatitis B–related hepatocellular carcinoma (HCC). In chronic hepatitis B infection, the odds ratio for an individual with codon 54 mutation to develop cirrhosis was 1.84 (95% CI: 1.21‐2.81) and to develop SBP was 4.58 (95% CI: 1.73‐12.16). Chronic hepatitis B and hepatitis C infection lowered the MBL levels, probably by suppressing MBL production. Codon 54 mutation of MBL was associated with progression of disease in chronic hepatitis B infection