Effects of surgical treatment of the metabolic syndrome on liver fibrosis and cirrhosis

Background. Both weight loss and gastrointestinal surgery for obesity can cause liver disease, making their role in the treatment of obesity-related liver disease controversial. Methods. Six hundred eighty-nine severely obese women (n = 551) and men (n = 138), BMI = 47 ± 9 kg·m^-2 (mean ± SD), without known liver disease, underwent biliopancreatic diversion (BPD) with liver biopsy. Fourteen patients (2%) had cryptogenic cirrhosis, 11 of whom underwent multiple repeat biopsies. After 38 ± 18 kg weight loss, 104 of the 689 patients underwent routine second biopsies during reoperations 41 ± 25 months after BPD. All biopsy specimens were graded for steatosis, fibrosis, and inflammation by a blinded hepatopathologist. Results. All 689 patients lost weight accompanied by improvements in the metabolic syndrome. Among the 104 patients who underwent reoperation, severe flbrosis (grade 3-5) decreased in 28 whereas mild fibrosis (grade 1-2) appeared in 42. Increased fibrosis was related to low-normal serum albumin, uncontrolled diarrhea, low intake of alcohol, and menopausal status. Fibrosis and inflammation decreased over time (P < .01). The 11 patients with cirrhosis exhibited decreased fibrosis from a mean grade 5 to grade 3, as well as reduced inflammation, Mallory bodies, and glycogenated nuclei. Seven patients had disappearance and 2 regression of nodules and fibrous bridging. Conclusions. The metabolic syndrome of obesity is a determinant of liver fibrosis and cirrhosis, treatable by substantial weight loss after malabsorptive surgery.