Background:Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the United States. Binge eating disorder (BED) is the most common form of eating disorder. NAFLD and BED have similar risk factors, including obesity, insulin resistance, and metabolic syndrome. The aim of our study was to examine prevalence of BED in NAFLD patients.Methods:We administered the Binge Eating Scale (BES), a questionnaire validated to screen for BED, to NAFLD patients at our Fatty Liver Center. Demographics were retrieved retrospectively from our electronic medical record.Results:Of the total 95 NAFLD patients screened, 22 (23.1%) had binge eating tendencies; 6 of the 22 (6.3%) scored 27 or more points, suggestive of severe binge eating. Patient demographics included 59 females and 36 males (14 females and 8 males positive for BED). Liver disease severity and of metabolic syndrome presence were similar in both groups: 45 patients had steatosis, 25 steatohepatitis, and 24 cirrhosis, of which 10 steatosis, 5 steatohepatitis, and 7 cirrhosis patients screened positive for BED. Of the NAFLD patients with BED, 50.0% had insulin resistance, 68.2% hypertension, and 50.0% hyperlipidemia, whereas among non-BED NAFLD patients 58.9% had insulin resistance, 63.0% hypertension, and 67.1% hyperlipidemia.Conclusions:This pilot study suggests that BED may have a higher prevalence among NAFLD patients than in the general population. Based on these preliminary results, further study into the prevalence of BED is recommended. More data is need to identify effects of BED on the progression of NAFLD and role of BED treatment.

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INTRODUCTION: Post-colonoscopy diverticulitis is a rare but potentially significant complication. We report a case of colonoscopy-induced diverticulitis in a patient with no prior history of diverticulitis. CASE DESCRIPTION/METHODS: A 59-year-old female with a past medical history of hypertension, hypothyroidism and gastroesophageal reflux disease presented for a screening colonoscopy. Colonoscopy findings included a few small and large-mouthed diverticula in the sigmoid colon, a 4mm sessile polyp in the sigmoid colon removed with cold biopsy forceps, and non-bleeding grade I internal hemorrhoids. Pathology of the polyp returned as tubular adenoma. Two days post-procedure, she reported worsening lower abdominal pain as well as nausea and was recommended to go to the emergency room. On arrival, she was afebrile and hemodynamically stable. She was noted to have tenderness to palpation along her lower abdomen, greatest in the left lower quadrant. She denied fevers, chills or rectal bleeding. Labs were significant for a white blood cell count of 11.63 × 103/μL (reference range 4.5-11 × 103/μL). CT abdomen/pelvis with IV contrast showed inflamed diverticulum within the sigmoid colon with surrounding inflammatory changes, consistent with uncomplicated sigmoid diverticulitis. She was discharged home with a 10 day course of ciprofloxacin and metronidazole, and was doing well at her follow up visit. DISCUSSION: Although colonoscopy-induced diverticulitis is a rare finding, it is important to consider it as a complication in patients with symptoms after colonoscopy. Potential causes of post-colonoscopy diverticulitis include barotrauma, multiple attempts for intubation, and direct pressure of the scope. Another possible cause is reactivation of silent diverticulitis, with air insufflation unsealing micro-perforations in diverticula. Prior history of diverticulitis is associated with incomplete colonoscopy and can be a risk factor for developing diverticulitis; this is likely due to deformed colonic architecture from prior severe inflammation. Our patient had no prior history of diverticulitis, and presented with diverticulitis two days after her first colonoscopy. More research needs to be done on the risk of post-colonoscopy diverticulitis in those without a prior history of diverticulitis, as the prevalence of this complication is likely higher than reported.

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