Abdominal Tuberculosis Leading to Prehepatic Portal Hypertension: A Case ReportXuelian Dan, Li Feng, Wanqin Wang and Li Yang*
Division of Digestive Diseases, West China Hospital, Sichuan University, Chengdu 610041, PR China
- *Corresponding Author:
- Li Yang
Division of Digestive Diseases
West China Hospital, Sichuan University
Chengdu 610041, PR China
Received Date: August 02, 2014; Accepted Date: September 09, 2014; Published Date: September 09, 2014
Citation: Dan X, Feng L, Wang W, Yang L (2014) Abdominal Tuberculosis Leading to Prehepatic Portal Hypertension: A Case Report. J Cytol Histol 5:278. doi: 10.4172/2157-7099.1000278
Copyright: © Dan X, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Tuberculosis can affect any organ or tissue in the abdomen such as gastrointestinal tract, peritoneum, lymphatic system and solid organs. Lymphadenopathy is the most common manifestation of abdominal tuberculosis which can be the only sign of the disease, especially in the periportal region or combined with peritoneal or solid organ involvement. There are a number of causes for prehepatic noncirrhotic portal hypertension, but there were a few reports of prehepatic portal hypertension associated with tuberculosis. Here we report a rare case of intra-abdominal tuberculosis as a cause for portal hypertension and recurrent gastrointestinal bleeding. Enlarged lymph nodes at hepatic hilum compressed the portal vein which caused portal hypertension and portal hypertensive gastropathy and enteropathy. The patient was managed by anti-tuberculosis therapy followed by splenectomy, surgical portaazygous devascularization and splenorenal shunt. In the 2-year followup after operation, the patient was free of symptoms and had cavernous portal vein transformation on CT, and disappearance of varices and portal hypertensive gastroenteropathy on EGDs.