INTRODUCTION: Colonic varices are a rare finding during endoscopy, especially in an individual without known liver disease. Based on limited case reports, the estimated incidence of colonic varices is 0.07%, irrespective of the etiology[1]. Common causes of colonic varices include portal hypertension from underlying liver disease, non-cirrhotic portal hypertension, most commonly from pre-sinusoidal disease in the form of splenic vein thrombosis, arteriovenous malformation, and idiopathic colonic varices[1, 2]. We present a case of colonic varices in a non-cirrhotic patient leading to an unexpected diagnosis. CASE DESCRIPTION/METHODS: A 23 year-old male was referred for iron deficiency anemia noted on a routine health visit. Initial labs demonstrated a hemoglobin of 12.4 g/dL and a ferritin level below 15 ng/mL. He was referred to the gastroenterology clinic where he reported a prior diagnosis of iron deficiency anemia 10 years ago without endoscopic investigation and treated with iron supplements, but otherwise was in his usual state of health. He denied change in his bowel movements, but endorsed scant, intermittent blood in his stools with wiping. He underwent EGD which was normal and a colonoscopy which was notable for large submucosal varices at the splenic flexure and in the proximal descending colon, multiple erythematous polyps ranging in size from 5-15 mm from the descending colon to the rectum, and erythematous, ulcerated, and friable mucosa from the descending colon to the rectum. CT angiography was performed which showed marked pelvic and lower abdominal lipomatosis with mass effect on the small bowel and abdominal vasculature. The patient was diagnosed with severe left sided ulcerative colitis with mesenteric adipose tissue hypertrophy resulting in colonic varices. He was lost to follow-up prior to initiation of biologic therapy. DISCUSSION: Mesenteric adipose tissue hypertrophy is a known complication of severe Crohn’s disease[3, 4]. Mechanistically, transmural inflammation in Crohn’s disease allows bacterial translocation into the mesenteric adipose tissue, which elaborates a cascade of adipocytokines resulting in inflammatory cell recruitment and adipose tissue hypertrophy, which serves as an additional barrier to systemic bacterial infection[3-5]. This case is unique in that it demonstrates mesenteric adipose tissue hypertrophy in long-standing, untreated UC that created a mass effect, resulting in colonic varices.Figure 1.: Coronal view - mesenteric adipose tissue hypertrophy resulting in visceral organ displacement and colonic varices.Figure 2.: Coronoal view - mesenteric adipose tissue hypertrophy resulting in visceral organ displacement.Figure 3.: Cross-sectional view - colonic varices in the transverse colon.