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Associated Ulcerative Colitis, Sclerosing Cholangitis, and Insulin*Dependent Diabetes Mellitus

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Associated Ulcerative Colitis, Sclerosing Cholangitis, and Insulin*Dependent Diabetes Mellitus CASE REPORT Associated ulcerative colitis, sclerosing cholangitis, and insulin*dependent diabetes mellitus MARSHA KAY, MD; ROBERT WYLLIE, MD; WILLIAM MICHENER, MD; MAUREEN CAULFIELD, MD; RITA STEFFEN, MD LINICALLY symptomatic We report two young men with clinical and laboratory evidence ulcerative colitis, sclero- of macroscopic ulcerative colitis, sclerosing cholangitis, and insu- sing cholangitis, and in- lin-dependent diabetes mellitus. The first patient presented at age Csulin-dependent diabe- 15 with vomiting, abdominal pain, weight loss, and abnormal tes mellitus have not previously liver function test results. Liver biopsy and endoscopic retrograde been reported in the same patient. cholangiopancreatography (ERCP) demonstrated sclerosing cho- Although each may be associated langitis. Colonoscopy with biopsy revealed ulcerative colitis with the other, their occurrence in which responded to sulfasalazine. Diabetes occurred at age 18 and the same individual implies a com- insulin therapy was begun. mon susceptibility, perhaps involv- The second patient was 19 at presentation with diarrhea, hema- ing the immune system. We have tochezia, and weight loss. Proctosigmoidoscopy revealed identified two patients with each ulcerative colitis, and sulfasalazine led to clinical remission. Three of these disorders. These two months later he developed diabetes requiring insulin therapy. At young men were followed up at age 28, he developed elevated alkaline phosphatase, and ERCP re- The Cleveland Clinic Foundation vealed sclerosing cholangitis. At age 37 he expired from adenocar- between 1970 and 1992. cinoma that metastasized to the liver. Literature review revealed only one possible case report of this PATIENT I; CASE HISTORY association with microscopic asymptomatic ulcerative colitis in that patient. Statistical analysis suggests that this association is Patient 1 presented at age 15 real rather than a chance occurrence. An autoimmune process years with a chief complaint of ab- may be involved and a specific histocompatibility locus antigen dominal pain and vomiting for 4 (HLA) type may exert a regulatory influence. months. He denied diarrhea, con- stipation, hematemesis, hemato- • INDEX TERMS: COLITIS, ULCERATIVE; CHOLANGITIS, SCLEROSING; DIABETES MEL- chezia, melena, fever, and joint, LITUS, INSULIN-DEPENDENT • CLEVE CLIN J MED 1993; 60:473-478 mouth, or skin problems. His medi- cal history was unremarkable. From the Section of Pediatric Gastroenterology and Nutrition, Family history revealed a maternal The Cleveland Clinic Foundation. Address reprint requests to R.W., Head, Section of Pediatric Gas- great uncle and a paternal aunt troenterology and Nutrition, Department of Pediatrics, A120, The with diabetes mellitus. Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, His local physician performed an OH 44195. upper gastrointestinal study with a small-bowel follow-through, which revealed thickening of the duode- nal sweep but was otherwise unre- NOVEMBER » DECEMBER 1993 CLEVELAND CLINIC JOURNAL OF MEDICINE 473 Downloaded from www.ccjm.org on October 1, 2021. For personal use only. All other uses require permission. ULCERATIVE COLITIS • KAY AND ASSOCIATES markable. He was treated with dicyclomine hydro- denoscopy revealed linear erosions in the gastric chloride and hydroxyzine hydrochloride without fundus. Colonoscopy demonstrated diffusely granu- symptomatic relief and was admitted to his local lar mucosa with punctate areas of hemorrhage from hospital. A blood workup revealed the following val- the rectum to the cecum consistent with ulcerative ues, with normal ranges in parentheses: an amylase colitis. Biopsy revealed diffuse chronic inflamma- level of 310 U/L (23 to 85 U/L), lipase 50IU/L (4 to tion with crypt abscess formation, and no granu- 24 IU/L), erythrocyte sedimentation rate 101 lomas. Endoscopic retrograde cholangiopancrea- mm/hour (0 to 15 mm/hour), platelet count 515 000 tography (ERCP) showed several areas of irregular (130 to 400 x 103), alkaline phosphatase 496 IU/mL filling in the common bile duct, common hepatic (50 to 136 IU/mL), alanine aminotransferase (ALT) duct, and intrahepatic ducts consistent with primary 96 IU (10 to 35 IU), aspartate aminotransferase 102 sclerosing cholangitis. The pancreatic duct was nor- IU (7 to 50 IU), total protein 10 g/dL (6 to 8 g/dL), mal. Repeat liver biopsy demonstrated expansion of and globulin 5.5 g/dL (2.3 to 3.5 g/dL). Ceruloplas- the portal tracts with a mixed acute and chronic min levels were normal. Hepatitis B surface antigen inflammatory infiltrate, fibrosis with focal areas of (HBsAg) and hepatitis B core antibody (anti-HBc) pseudo-bile-duct proliferation, hyalinization of con- were negative. Tests for antimitochondrial, antinu- nective tissues around preexisting bile ducts, slight clear factor, toxoplasmosis, and cytomegalovirus an- ballooning within the liver parenchyma, and bridg- tibodies were negative. Anti-smooth-muscle anti- ing between the portal tracts, consistent with body was positive, with a titer of 1:40 (reference: sclerosing cholangitis. negative). A liver scan and abdominal ultrasound The patient's condition was stabilized, and he was suggested a mass in the head of the pancreas. Com- discharged on sulfasalazine, 1 g bid. He did well, puterized tomography of the abdomen was normal. with a 30-kg weight gain, decreased stool frequency Exploratory laparotomy revealed intra-abdominal and abdominal pain, resolution of hematochezia, lymphadenopathy and a normal pancreas. Liver bi- and normalization of liver function tests. opsy performed during surgery showed widened por- He presented 3 years later with an 8-kg involun- tal tracts, portal edema and fibrosis, focal ductal pro- tary weight loss over 6 weeks, diminished energy, liferation, and neutrophilic infiltration of the bile polydipsia, and nocturia. He was admitted to the ducts. Several bile ducts were surrounded by lympho- hospital. Laboratory examination revealed urinaly- cytic and histiocytic infiltrates and dense fibrotic sis with 30 mg/dL glucose and trace ketones, blood tissue, consistent with primary sclerosing cholangitis. glucose values between 200 and 300 mg/dL (normal Patient 1 was subsequently referred to The range 65 to 110 mg/dL), elevated glycosylated he- Cleveland Clinic Foundation for further evaluation. moglobin 14.4% (3.5% to 6.5%), and a diminished Physical examination revealed a height at the 80th insulin level 2.5 |i.U/mL (4 to 24 fxU/mL); serum percentile and a weight at the 30th percentile. His electrolytes, complete blood count, and thyroid liver span was 7 cm with no lymphadenopathy. Rec- function tests were normal. tal exam was positive for occult blood. The physical His condition was stabilized on a regimen of regu- examination was otherwise unremarkable. Labora- lar and intermediate-acting insulin, and he was dis- tory studies demonstrated elevation of amylase to charged. Since discharge, he has regained his lost 533 IU (83% salivary origin) (normal range 10 to weight and his liver function tests have remained 135 U/L), and a Westergren sedimentation rate of normal. Histocompatibility locus antigen (HLA) 62 mm/hour (normal range 0 to 20 mm/hour); the testing was positive for the B8 and DR3 loci. ERCP alanine aminotransferase level and platelet count repeated 2 years later demonstrated irregularity of were mildly elevated. Aspartate aminotransferase the common bile duct with a short segmental irregu- and alkaline phosphatase values were normal. larity and stenosis of multiple intrahepatic ducts. Hepatitis A (anti-HAV), hepatitis B (HBsAg, anti- The cystic duct was normal. HBs), and antimitochondrial antibody studies were negative. Smooth muscle antibody studies were PATIENT 2: CASE HISTORY positive, with a titer of 1:10. Ultrasound of the gallbladder and pancreas re- The second patient was 19 when he presented to vealed a distended gallbladder without biliary duct our institution in 1970 with a complaint of loose dilation and a normal pancreas. Esophagogastroduo- bowel movements for 3 years. He had a 9-kg invol- 474 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 60 • NUMBER 6 Downloaded from www.ccjm.org on October 1, 2021. For personal use only. All other uses require permission. ULCERATIVE COLITIS • KAY AND ASSOCIATES untary weight loss over 3 preceding months. A re- spite chemotherapy, he died 7 months later at age view of systems and his medical history were other- 37. HLA typing was not done. wise unremarkable. A family history revealed a cousin with diabetes mellitus. DISCUSSION Physical exam and vital signs were unremarkable. Proctosigmoidoscopy revealed patchy friability and The association of ulcerative colitis and sclerosing edema of the colonic mucosa; a barium enema study cholangitis has been well documented, but not in showed loss of haustral markings and mucosal pat- combination with insulin-dependent diabetes melli- tern. A regimen of sulfasalazine was started for the tus. We have been unable to find any reports linking ulcerative colitis. He gained weight, stool frequency these three disorders, either in the same patient or in diminished, and the proctosigmoidoscopic appear- first-degree relatives, and this was one of our reasons ance improved. for investigating the apparent association. Three months later he presented with polydipsia, Neither patient demonstrated convincing evi- polyuria, and involuntary weight loss. He was diag- dence of pancreatitis as the etiology of insulin-de- nosed as having diabetes mellitus, and a regimen of pendent
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