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Liver. 1987 Oct;7(5):271-6.

Pattern of progression in liver injury following jejunoileal bypass for morbid obesity.

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Institute of Pathology, Herlev Hospital, University of Copenhagen, Denmark.


Liver biopsies from 34 patients with morbid obesity, performed before and 5-9 months after jejunoileal bypass, were studied. The patients were divided into four groups according to preoperative findings: A: no or slight steatosis (15 patients), B: moderate-severe steatosis (6), C: steatohepatitis (steatosis + lobular lymphocytic inflammation) (8), D: steatofibrosis (steatosis + pericellular fibrosis) (5). In Group A, 12 patients showed postoperative progression to either moderate/severe steatosis, steatohepatitis, or steatofibrosis. In Group B, all patients progressed to steatohepatitis or steatofibrosis, and one developed septate fibrosis. All patients in Group C progressed to steatofibrosis, and 5 developed septate fibrosis or cirrhosis. In Group D, 3 developed bridging fibrosis. Mallory bodies appeared postoperatively in 11 patients (32%), all of whom preoperatively had either severe steatosis, steatohepatitis, or steatofibrosis. Only patients with postoperative pericellular fibrosis and Mallory bodies developed deranged architecture: 6 septate/bridging fibrosis, and 3 cirrhosis. Five patients, all with deranged architecture, developed reversible liver insufficiency. Progressive liver injury after jejunoileal bypass appears to reflect aggravation of a pre-existing liver lesion. The sequence of events: increasing steatosis, lobular lymphocytic inflammation, pericellular fibrosis, Mallory bodies, and deranged architecture is similar to that of the alcoholic liver lesion, indicating common pathogenetic mechanisms.

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