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Fatty metamorphosis in patients with jejunoileal bypass.

Two-thirds of all preoperative patients had some degree of fatty metamorphosis of the liver; at least 8 to 10 per cent had marked steatosis prior to performance of the jejunoileal shunt. In preoperative patients, marked fatty metamorphosis was seen most prevalently in the heaviest patients, while the incidence of moderate to minimal fatty infiltration was highest in those not as massively obese. Nevertheless, marked degrees of fatty metamorphosis were seen in patients just meeting the minimal weight criterion for operation, and minimal steatosis or normal livers were seen in more massive candidates. Subsequent to the bypass operation 95 per cent of patients had a moderate to severe degree of fatty metamorphosis apparent within the first 300 days. Subsequently, the incidence of fatty infiltration rapidly decreased so that by 1,500 to 2,000 days the incidence of severe steatosis had returned to that seen preoperatively. In fact, only those patients having associated problems late in the course showed a severe degree of fatty metamorphosis after 1,000 days. A screen of liver function studies was not found helpful in detecting minimal to moderate degrees of fatty metamorphosis and showed only inconsistent changes in those patients with severe steatosis. These tests were not helpful in detecting a quiescent cirrhosis of the liver. Cirrhosis of the liver was seen in two patients. In one, it occurred late in the course after the liver had completely cleared of fat. The cause was thought to be acute alcoholism, and steatosis cleared when drinking ceased. A second patient had a degree of cirrhosis at the time of the bypass operation. There has been slight progress in the ensuing seven or eight years that may be unrelated to the presence of the shortened intestine. Liver function studies do not indicate activity. Because the severe degrees of fatty infiltration seen in patients having previously normal or minimally infiltrated livers occurred during the time of rapid weight loss, it is presumed that the extensive mobilization of depot stores of fat to fulfill caloric requirements of the patient results in accumulation of triglyceride in the liver. Steatosis may be further aggravated by the fact that protein absorption is reduced and, therefore, the formation of low density lipoproteins by the liver is curtailed. In this series, no patients have died as a result of fatty infiltration and liver failure alone.