P459 Obesity in patients with an ileoanal pouch due to ulcerative colitis is not associated with an increased risk for pouchitis

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Background: Obesity is characterized by low grade inflammation in the visceral fat tissue (VFT) which may be a major causative factor in the development of insulin resistance (IR). A surrogate marker for IR is the ratio between triglycerides (TG) and high density lipoprotein (HDL). VFT wrapping the small bowel characterizes Crohn's disease (CD) and has been shown to produce proinflammatory cytokines. Patients with ulcerative colitis (UC) undergoing proctocolectomy with ileal pouch-anal anastomosis (IPAA) commonly develop pouchitis-de novo inflammation in a previously normal small bowel. We hypothesize that pouchitis may represent the small intestinal inflammation characterizing CD. We aimed to assess whether obesity affected intestinal inflammation in obese UC-pouch patients.

Methods: Retrospective case control series in UC pouch patients recruited at a tertiary referral center. Clinical and biochemical indices were compared between obese (BMI≥30 kg/m2) and normal BMI (nBMI, 18.5–24.9 kg/m2) pouch patients, matched for age and gender. Nutritional trends were obtained from food frequency questionnaires (FFQs).

Results: Thirty one patients (8.6% of pouch patients in our cohort, 20 females) were obese with a mean BMI of 33.9±4.5 kg/m2, pouch patients with nBMI - 22.9±2.6 kg/m2. Groups were comparable for smoking, disease duration, indication for surgery and pouch age. However, significantly lower rates of pouchitis were detected in the obese compared to nBMI group, 41% vs 79% (p=0.028) respectively. Obese patients had significant metabolic abnormalities: Glucose 103.5±39.9 vs. 83.8±10.7 mg/dl (p=0.028); HDL 47.9±14.2 vs 63.9±17.08 mg/dl (p=0.003); TG 190.33±124.8 vs 118.7±58.76 mg/dl (p=0.015), respectively. TG/HDL ratio was higher in the obese group 4.4±3.4 vs 2.1±1.4 (p=0.006 vs. nBMI). Sugared beverages consumption was significantly higher in the obese group (p<0.01 vs. nBMI).

Conclusions: Pouchitis rates were surprisingly lower in obese UC-pouch compared to nBMI UC pouch patients. This may be due to dietary intake restriction in patients with pouchitis, potentially contributing to lower weight so obesity may prevail mainly in patients with a normal pouch, eating freely. An alternative explanation may be that in pouchitis metabolic expenditure is increased contributing to lower BMI. Obese UC-pouch patients are prone to metabolic abnormalities and IR. A high consumption of simple carbohydrates may impact TG levels and weight gain in these patients. Dietary treatment for IBD patients should target all nutritional aspects including metabolic abnormalities to improve health status and quality of life.

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