Abstract

Patients developing the short bowel syndrome (SBS) are at risk for hepatobiliary disease, as are morbidly obese individuals. We hypothesized that morbidly obese SBS individuals would be at increased risk for developing hepatobiliary complications. We reviewed 79 patients with SBS, 53 patients with initial body mass index (BMI) < 35 were controls. Twenty-six patients with initial BMI > 35 were the obese group. Obese patients were more likely to be weaned off parenteral nutrition (PN) (58% vs. 21%). Pre-resection BMI was significantly lower in controls (26 vs. 41). BMI at 1, 2, and 5 years was decreased in controls but persistently increased in obese patients. Obese patients were more likely to undergo cholecystectomy prior to SBS (42% vs. 32%) and after SBS (80% vs. 39%, p < 0.05). Fatty liver was more frequent in the obese group prior to SBS (23% vs. 0%, p < 0.05) but was similar to controls after SBS (23% vs. 15%). Fibrosis (8% vs. 13%) and cirrhosis/portal hypertension (19% vs. 21%) were similar in obese and control groups. Overall, end stage liver disease (ESLD) was similar in obese and control groups (19% vs. 11%) but was significantly higher in obese patients receiving PN (45% vs. 14%, p < 0.05). Obese patients developing SBS are at increased risk of developing hepatobiliary complications. ESLD was similar in the two groups overall but occurs more frequently in obese patients maintained on chronic PN.

Highlights

  • Patients developing the short bowel syndrome (SBS) are at risk for hepatobiliary complications, especially if receiving parenteral nutrition (PN) [1]

  • Cholestasis and portal inflammation are present in two thirds of intestinal failure patients on PN; extensive portal fibrosis and cirrhosis develop later in 40% of such patients [3]

  • Radiographic evidence of fatty liver prior to developing SBS was more frequent in the obese group

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Summary

Introduction

Patients developing the short bowel syndrome (SBS) are at risk for hepatobiliary complications, especially if receiving parenteral nutrition (PN) [1]. One third of SBS patients will develop cholelithiasis [2]. Cholestasis and portal inflammation are present in two thirds of intestinal failure patients on PN; extensive portal fibrosis and cirrhosis develop later in 40% of such patients [3]. These complications have generally been attributed to several therapy related factors, including excess calories or lipid infusion, deficiencies of essential fatty acids or other nutrients, lack of enteral intake, toxicity of components of PN and sepsis [3]. The risk of liver disease, such as non-alcoholic fatty liver disease,

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