For reasons not yet determined, chronic liver disease (CLD) has been a lead
ing cause of excess morbidity and mortality in central Harlem. We conducted
a case series and case-control analysis of demographic, clinical, epidemio
logical, and alcohol-intake-related information from patients with CLD and
age- and sex-matched hospitalized control patients. Patients' sera were tes
ted for markers of viral hepatitis. The presumed etiology of CLD among case
-patients was as follows: both alcohol abuse and hepatitis C virus (HCV) in
fection, 24 persons (46% of case-patients); alcohol abuse alone, 15 (29%);
HCV infection alone, 6 (12%); both alcohol abuse and chronic hepatitis B vi
rus (HBV) infection, 3 (6%); and 1 each (2%) from: 1) schistosomiasis, 2) s
arcoidosis, 3) unknown causes, and 4) alcohol abuse, chronic HBV, and HCV c
ombined. In the case-control analysis, patients who had both alcoholism and
either HBV (odds ratio [OR]: 6.3; 95% CI: 0.5-334) or HCV (OR: 2.9; 95% CI
: 1.3-6.2) were at increased risk for CLD, whereas patients who had only on
e of these three factors were not at increased risk for CLD. Patients who t
ested positive for the hepatitis G virus (HGV) did not have a significantly
increased risk of CLD, and neither severity of CLD nor mortality was great
er among these patients. Most patients in central Harlem who had CLD had li
ver damage from a combination of alcohol abuse and chronic viral hepatitis.
Alcohol and hepatitis viruses appear to be synergistically hepatotoxic; th
is synergy appears to explain both the high rate of CLD in central Harlem a
nd the recent reductions in this rate. Persons at risk for chronic HBV and
HCV infection should be counseled about their increased risk of CLD if they
consume excessive alcohol. Morbidity and mortality from liver disease coul
d be decreased further by a reduction in alcohol consumption among persons
who have chronic HBV and HCV infection, avoidance of needle sharing, and he
patitis B vaccination.