Pattern of progression in liver injury following jejunoileal bypass for morbid obesity.
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.
Institute of Pathology, Herlev Hospital, University of Copenhagen, Denmark.
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M
Vyberg
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V
Ravn
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B
Andersen
D001706:Biopsy; D005500:Follow-Up Studies; D006801:Humans; D007581:Jejunoileal Bypass / Q000009:adverse effects; D008099:Liver / Q000473:pathology*; D011183:Postoperative Complications