Continuing hepatic injury despite cessation of ethanol intake has suggested a potential role for altered humoral and cellular immunity in the pathogenesis of alcoholic liver disease. Variation of cell-mediated response has been observed most commonly in patients with alcoholic hepatitis. These alterations include decreased mitogen response in vitro, reduction of circulating T-cell numbers with a corresponding increase of intrahepatic T-cells, lymphokine production in vitro in response to isolated alcoholic hyalin (Mallory bodies), and in vitro evidence of increased spontaneous cell-mediated cytotoxicity. Fewer immunologic alterations are detected in patients with alcoholic fatty liver or cirrhosis. At present, these observations have not established a definite causal relationship between ethanol-induced liver injury and immunologic mechanisms. Studies utilizing in vitro correlates of cellular immunity in alcoholics are carried out after development of hepatic injury. To establish the role of humoral and cellular immune events in the pathogenesis of alcoholic liver injury will require development of a suitable animal model.

The value of cimetidine in treatment of duodenal ulcer and the Zollinger-Ellison syndrome appears to be well established. The drug has been enthusiastically embraced and widely used by practicing physicians. As with virtually all drugs used in the practice of medicine, cimetidine is not without its adverse effects. In some instances these effects may result from actions of cimetidine on H2-receptors on many widely distributed and diverse cells other than parietal cells, to which its potent acid-inhibiting properties are directed. Other adverse effects of cimetidine may be idiosyncratic, and, therefore, not predictable on a pharmacologic basis. In some instances the mechanisms responsible for cimetidine's adverse effects hav e yet to be defined. An assortment of abnormalities reported in patients receiving cimetidine have been suggested, but not proven, to represent adverse effects of the drug. Considering its extremely wide use, serious toxicity with cimetidine is rare. However, no potent drug, including cimetidine, used in the practice of medicine is without its adverse effects. Recognizing the present and projected extensive and probably long-term use of cimetidine, physicians and surgeons treating patients with cimetidine must maintain continued surveillance in order to detect and clarify potential undesired consequences of cimetidine administration.

We critically reviewed the English language literature pertaining to drug-induced pancreatitis and attempted to determine whether the reported association between each drug and pancreatitis was valid. The following drugs seem to cause pancreatitis: azathioprine, thiazides, sulfonamides, furosemide, estrogens, and tetracycline. Less convincing, but suggestive evidence exists for: 1-asparaginase, iatrogenic hypercalcemia, chlorthalidine, corticosteroids, ethacrynic acid, phenformin, and procainamide. Evidence implicating other drugs is either inadequate or contradictory. Little is known about the pathogenesis of drug-induced pancreatitis. Ethanol was not considered in this review.