Interrelationships among histologic features of alcoholic liver disease were studied in 24 chronic alcoholics who took part in a double‐blind, controlled trial of prednisolone vs. placebo therapy. Each patient underwent liver biopsy at the start and upon completion of the 1‐month study. Although all patients had a clinical diagnosis of alcoholic hepatitis and had at least mild alcoholic hepatitis with alcoholic hyalin in their initial liver biopsy specimens, each of the histologic features studied (fat accumulation, bile stasis, alcoholic hyalin, acute inflammation, active intralobular fibrosis, chronic inflammation, bile duct proliferation, established fibrosis, and parenchymal nodularity) covered a wide spectrum of severity. Relationships of the severities of the individual histologic features were studied within the initial biopsy specimens and between the pre‐ and posttreatment biopsies. Four major histopathologic categories were evident in the correlation patterns: fat accumulation; cholestasis; alcoholic hepatitis, and cirrhosis. While having common pathogenetic ties and thus often occurring together, the severities of these categories in a given patient at a given time were little related and they are best considered as separate features of alcoholic liver disease. The amount of alcoholic hyalin appeared to be the best single indicator of the severity of alcoholic hepatitis in these patients and was the best predictor in the pretreatment biopsies of the amounts of hepatocellular injury, active fibrosis, acute inflammation, and total inflammation in the posttreatment biopsy specimens. Active fibrosis and hepatocellular injury in turn appeared to be the most immediate precursors of established fibrosis and parenchymal nodularity. Bile duct proliferation was, in part, a reflection of cholestatic disease and, in part, a more nonspecific reflection of chronic alcoholic liver injury, correlating with the amount of established fibrosis. The relationship of chronic inflammation to other histologic features was complex, but probably included an intralobular component related to the severity and stage of alcoholic hepatitis and another, more nonspecific, component related to the amount of established fibrosis or bile duct proliferation. One month of prednisolone therapy (40 mg per day) significantly decreased the amount of inflammation, but did not have a comparable effect on hepatic fibrosis. The statistical methods used in this study to investigate the multiple interrelationships among histologic features are useful in evaluating potential pathogenetic relationships and are quite helpful in assessing the effects of treatment.
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