BACKGROUND: The most common cause of hepatic iron overload is a genetic mutation (C282Y) that causes an increase in serum transferrin saturation and ferritin levels. Abnormalities in iron metabolism as well as nonalcoholic steatosis are known conditions associated with obesity. The purpose of this study was to analyze the hepatic DNA of morbidly obese patients undergoing Roux-en-Y gastric bypass (RYGB) for genetic mutations. Additional goals were to measure serum ferritin and iron levels in these patients and correlate genetic mutations leading to hepatic iron overload with surgical outcomes after RYGB.
METHODS: Prospective data was collected from 760 patients undergoing Roux-en-Y gastric bypass and wedge liver biopsies. These were analyzed for hepatic iron overload. Patients were stratifed into hepatic iron overload (HFE)and non-overload groups (Normal) . DNA from patients in both groups was analyzed using polymerase chain reactions (PCR) for the C282Y and the H63D gene mutations. 136 patients were found to have hepatic iron overload (HFE) and 624 patients were found to have normal hepatic iron levels (Normal). The groups were compared for gender, age, BMI and liver histology. 127 of the HFE patients had specimens with analyzable DNA as did 583 patients in the normal group. Serum iron, TIBC and Ferritin were measured. The perioperative mortality, LOS, and complications including leak rate and wound infection were calculated to evaluate differences in outcomes.
RESULTS: There was no significant difference in age, gender or liver histology between the HFE and normal groups. The body mass index in the HFE group was 48.50 versus 47.79 (p=0.37) in the normal iron group . The C282Y mutation was not significantly different between the groups. However, the H63D mutation was significantly more comon in the HFE group (TABLE). TIBC and serum iron were not different between groups but serum ferritin levels were significantly higher in the HFE group (169 v 49;p
Session: Podium Presentation
Program Number: S047
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