Smoking and alanine aminotransferase levels in hepatitis C virus infection: implications for prevention of hepatitis C virus progression.
BACKGROUND
Alcohol consumption is a well-known risk factor for elevated ALT levels, but the role of cigarette smoking is unclear.


METHODS
We collected a cross-sectional sample of 6095 inhabitants 35 years or older in a community with hyperendemic hepatitis B and C virus infections. We assayed levels of serum alanine aminotransferase (ALT), hepatitis B surface antigen (HBsAg), and anti-hepatitis C virus antibody (anti-HCV). Multivariate logistic regression was performed to determine the factors for elevated ALT levels (> or =40 U/L) among people with different hepatitis infection statuses.


RESULTS
Prevalence of elevated ALT levels in individuals who were seronegative for both infections or seropositive for HBsAg or anti-HCV was 3.9%, 11.1%, and 30.8%, respectively. Subjects with elevated ALT levels were more likely to be seropositive for anti-HCV, male, and seropositive for HBsAg; to drink alcohol; to smoke; and to have undergone blood transfusion (P<.05). An association was found between elevated ALT levels and the consumption of cigarettes and alcohol among anti-HCV-seropositive subjects. In multivariate logistic analyses, alcohol consumption (odds ratio [OR], 2.2; 95% confidence interval [CI], 1.2-4.1) and smoking (OR, 1.8; 95% CI, 1.1-2.7) were significantly associated with elevated ALT levels among anti-HCV-seropositive subjects, but no such association was found among HBsAg-seropositive subjects. The odds of elevated ALT levels were 7 times higher (95% CI, 2.7-18.8) for the anti-HCV-seropositive patients who smoked 1 or more packs of cigarettes per day and frequently drank alcohol than for those who did not.


CONCLUSIONS
Smoking and alcohol consumption are independently associated with elevated ALT levels among anti-HCV-seropositive individuals but not among HBsAg-seropositive individuals. Patients who are seropositive for anti-HCV are strongly advised not to smoke and drink alcohol to reduce the possible risk for aggravating the liver dysfunction.
Wang
Chong-Shan
CS
National Yang-Ming University, Institute of Public Health, Shih-Pai, Taipei 112, Taiwan, Republic of China. wangcsh@mail.ncku.edu.tw
Wang
Shan-Tair
ST
Chang
Ting-Tsung
TT
Yao
Wei-Jen
WJ
Chou
Pesus
P
D000328:Adult; D000410:Alanine Transaminase / Q000097:blood*; D000428:Alcohol Drinking / Q000009:adverse effects / Q000097:blood; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D006509:Hepatitis B / Q000201:enzymology / Q000453:epidemiology; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006526:Hepatitis C / Q000201:enzymology* / Q000453:epidemiology; D018937:Hepatitis C Antibodies / Q000097:blood*; D006801:Humans; D008107:Liver Diseases / Q000453:epidemiology / Q000517:prevention & control; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D012907:Smoking / Q000009:adverse effects* / Q000097:blood; D013624:Taiwan / Q000453:epidemiology
D015415:Biomarkers; D006514:Hepatitis B Surface Antigens; D018937:Hepatitis C Antibodies; D000410:Alanine Transaminase