As part of a multicenter V.A. Cooperative Study, 437 male veterans with varying stages of alcoholic liver injury were followed over a 4.5 year period. Their ethnic distribution consisted of 256 Caucasians, 109 black Afro-Americans, 63 Puerto Rican Hispanics, and 9 Native American Indians. Survival analyses revealed significant differences between groups (P = 0.0002): 66% of Afro-Americans were still living at 42 months; Caucasians were intermediate with 40% survival; and only 28% of Hispanics were alive. The number of Native American Indians enrolled was too small to draw conclusions but none of those enrolled survived beyond 24 months. Survival regression analysis of 30 clinical, laboratory, histologic and nutritional parameters, revealed the following significant risk factors: clinical severity (P less than 0.0001), histologic severity (P less than 0.0001), race (P = 0.001), age (P = 0.002), BUN (P = 0.01) and ALT (P = 0.02). These analyses indicated that ethnicity, independent of other variables, is significantly associated with outcome from the disease.
We studied the relationship between the ratio of serum aspartate aminotransferase
(ASAT) to alanine aminotransferase (ALAT) and histologic changes in human and
experimental alcoholic liver disease. The patient population included 52 hospitalized
patients enrolled in a Veterans Administration Cooperative study. The experimental animal
group consisted of male Wistar rats fed an ethanol-liquid diet. Of the 52 patients with
alcoholic hepatitis, 33 had evidence of cirrhosis. The mean ± SD for the ASAT/ALAT ratio
in the group with alcoholic hepatitis and no cirrhosis was 1.47 ± 0.84, the mean ± SD in the
group with hepatitis and cirrhosis was significantly higher (2.68 ± 1.32, p < 0.01). There
was no difference in the ratio between the rats with and without liver fibrosis. The cause for
the increased AS AT/ALAT ratio in serum in the presence of cirrhosis is unknown and may
reflect more severe liver damage.
From 8 Department of Veterans Affairs Medical Centers, 296 patients with varying degrees of alcoholic liver disease were tested for hepatitis C (HCV) infection using an EIA and RIBA 2. A high frequency of positive response was observed with 13.9% reactive to both and an additional 4.4% positive only to RIBA 2 (total 18.3%). An evaluation of known risk factors (injection drug use and prior blood transfusions) failed to account for the mode of transmission in 42.6% of the HCV+ patients. The clinical severity of the liver disease and degree of liver pathology were nearly identical in HCV+ vs. HCV- patients. However, the process was accelerated in the HCV+ patients occurring at a 12.8% younger age (p < 0.0001) with a 43% increase in ALT (p = 0.05). The most striking differences were observed in immune parameters. In peripheral blood, total lymphocyte counts were increased 20% (p = 0.01) accompanied by a 56% increase in B cells (p = 0.01) and a 35% elevation of IgG levels (p = 0.0001) in HCV+ patients. T cell changes consisted of a 50% increase in CD8 cells (p = 0.047). However, lymphocyte infiltration into liver was not significantly different (HCV+ vs. HCV-) for any of the subsets studied (CD4, CD8, B cells, NK cells). The combined presence of HCV and alcohol injury did not significantly increase mortality but did significantly increase the number of hospitalizations from 2.4 to 4.0 per year (p = 0.0005).
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