Studies were undertaken to determine if
cholestasis in alcoholic or viral
hepatitis is related to immunologic hyperreactivity as suggested for
cholestasis due to type-II
drug-induced hepatitis, and evaluate possible mechanisms involved in lymphokine-induced
cholestasis. Results indicate that a
cholestatic factor exists in alcoholic and acute viral
hepatitis. Supernatants of lymphocytes from patients with
alcoholic hepatitis stimulated by an extract of alcoholic hyalin evoked a 28% +/- 7.3 SEM reduction in rat bile flow (P less than 0.03). Supernatants of lymphocytes from patients with acute viral
hepatitis activated by liver-specific
protein caused a reduction in rat bile flow of 24% +/- 5.9 SEM (P less than 0.03). A decrease in bile flow also occurred following
injections of sera from patients with alcoholic or acute viral
hepatitis. In contrast, injection of supernatants of non-stimulated lymphocytes or those from
chronic active hepatitis or healthy subjects did not produce a significant change in bile flow. Supernatants of stimulated lymphocytes from
tuberculin-sensitized guinea pigs caused a similar decrease in rat bile flow and reduced excretion of human
secretory immunoglobulin A (
IgA). Despite reductions in rat bile flow there were no alterations in liver morphology, liver plasma membrane Na-K-
ATPase activity, microsomal cholesterol-7 alpha-
hydroxylase activity or low-dose
indocyanine green clearance during the period of observation.