Arteriovenous shunting and cholestasis in hepatic hemangiomatosis associated with metoclopramide.

Diffuse hemangiomatosis of the liver became apparent in a 22-year-old woman while she was receiving medication with metoclopramide and experiencing the well-known adverse effect of the drug, hyperprolactinemia with secondary amenorrhea and galactorrhea. The hemangiomatosis was demonstrated by ultrasonography, computerized tomography, arteriography, and laparotomy with biopsy. When arteriovenous shunting became life-threatening and severe abdominal pain and cholestasis developed, the patient's name was placed on the waiting list for liver transplantation. However, after stopping the medication with metoclopramide, abdominal pain disappeared, cholestasis decreased, and the arteriovenous shunts in the liver closed completely. This course of disease represents either a spontaneous or a drug-induced activation and regression of hepatic hemangiomatosis. However, the long-term metoclopramide medication indicates a potential role of this drug in the promotion of hepatic angiogenesis. Hepatic angiomatosis in the adult seems to be neither a static nor a steadily progressive disorder but a process with active and regressive phases probably induced by a transient imbalance of angiogenic and angiostatic factors. Such a course should be kept in mind when major surgery or liver transplantation for hepatic hemangiomatosis is planned. It seems prudent to obtain a thorough drug history of all patients with hepatic hemangiomatosis. Whether hepatic hemangiomatosis can be drug induced or not, further investigation of the factors involved in hepatic angiogenesis is warranted.