Hindawi Publishing Corporation Case Reports in Medicine Volume 2010, Article ID 536207, 4 pages doi:10.1155/2010/536207 Case Report A Gentleman with Anemia and Cholestasis Siu-Tong Law,1 Wai-Ki Lee,2 Michael Kin-Kong Li,1 and Ka-Ho Lok1 1 Division of Gastroenterology and Hepatology, Department of Medicine and Geriatrics, Tuen Mun Hospital, Tuen Mun, Hong Kong 2 Department of Pathology, Tuen Mun Hospital, Hong Kong Correspondence should be addressed to Siu-Tong Law, stl168@hotmail.com Received 11 September 2010; Accepted 4 November 2010 Academic Editor: Yolanda T. Becker Copyright © 2010 Siu-Tong Law et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Primary sclerosing cholangitis is a rare cause of cholestasis caused by progressive inﬂammation and ﬁbrosis of both intrahepatic and extrahepatic bile ducts leading to multifocal ductal strictures. Herein, we report a case of primary sclerosing cholangitis and inﬂammatory bowel disease. The concomitant diagnosis of these two diseases is not typical. The management includes the treatment of inﬂammatory bowel disease and potential complications of primary sclerosing cholangitis, including dominant strictures of bile duct, portal hypertension, gallbladder diseases, cholangiocarcinoma, and colonoscopic surveillance. 1. Introduction Primary sclerosing cholangitis is a rare cause of chronic cholestasis in adult with prevalence of about 1–5/100,000 in Caucasian inhabitants. There is a close association with inﬂammatory bowel disease. The clinical course is, yet vari- able and unpredictable, slowly progressive and develops into biliary cirrhosis and corresponding complications. Thera- peutic measures aim in improving bile ﬂow to prevent the progression of biliary obstruction and liver transplantation is the treatment of choice in advanced stage of the disease. 2. Case Report A 31-year-old man was admitted to the hospital because of hypochromic microcytic anemia He had chronic nonspeciﬁc epigastric pain for the past six months which had bloating sensation without radiation and any relationship to meal. He consulted a private practitioner. The complete blood picture showed that the hemoglobin was only 6 g/dl, and so he was referred to our unit for further management. His appetite reduced with subjective weight loss in the past three months’time. His bowel opening increased up to two times per day more loose in nature. All being along there was no per rectal bleeding. His past health was well except for taking herbal medicine for acne for the past seven months. On examination he was pale with the absence of stigmata of chronic liver disease. The abdominal examination showed hepatomegaly. Laboratory data were as follows: hemoglobin, 4.3 g/dL (normal: 13.4–17.2); mean cell volume, 49.6 ﬂ (normal: 83–98); white blood cell count, 9/mm3 (normal: 3.9–10.7); platelet count, 508/mm3 (normal: 152–358); total bilirubin, 17 umol/L (normal: 5–20); alkaline phos- phatase, 1541 IU/L (normal: 46–127); γ-glutamyl transpep- tidase, 366 IU/L (normal: 12–57); alanine aminotransferase, 102 IU/L (normal: 10–57); albumin, 34 g/l (normal: 35–50); globulin, 40 g/l (no reference); iron saturation, 1% (normal: 20–55); hemoglobin A2, 4.8% (normal: 1.6–3.5). The preliminary investigations revealed that he had severe iron deﬁciency anemia coexisting with β thalassaemia trait and cholestatic liver derangement. The esophagogas- troduodenoscopy (OGD) showed no abnormality down to the third part of duodenum. Early colonoscopy performed one week later showed that the colonic mucosa was ery- thematous with loss of vascular pattern and multiple small superﬁcial ulcerations in which the proximal parts including ascending and transverse colon were more severely aﬀected. The mucosa of terminal ileum, sigmoid, and rectum was endoscopically normal looking. The histology revealed that there was inﬂammatory cell inﬁltration at lamina propria of terminal ileum, and colon, the latter also having dis- torted cryptal architecture. The abdominal ultrasonography showed that the liver was enlarged with 16.7 cm of span