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| Relations of Budd-Chiari syndrome to prothrombin gene mutation |
| Guo-Ling Lin, Pei-Qin Xu, Hua Qi, Jian-Hua Lian, Hong Zheng and Xiao-Wei Dang |
Zhengzhou, China
Author Affiliations: Department of General Surgery, First Affiliated Hospital of Zhengzhou University (Lin GL, Xu PQ and Dang XW); the Faculty of Cytobiology and Medical Genetics, Medical School, Zhengzhou University (Qi H, Lian JH and Zheng H), Zhengzhou 450052, China
Corresponding Author: Pei-Qin Xu, MD, Department of General Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China (Tel: 86-371-6964308; Email: vl_institute@163.com) |
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Abstract hypertension and/or hypertension of the inferior vena cava (IVC) due to the obstruction of the hepatic veins (HV) and/or intrahepatic IVC outlet. Being etiologically complicated and obscure, BCS can be acquired or idiopathic and several gene mutations may be contributable. This study was to explore whether prothrombin gene mutation (FⅡ G20210A) takes part in the pathogenesis of BCS and to investigate their correlativity.
METHODS: In 38 proven BCS patients and 70 controls, polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to find FⅡ G20210A mutation. To detect whether there are any mutations, four steps were taken: purification of genome DNA from whole blood, amplification of special fragment by polymerase chain reaction, digestion of the fragment via restriction endonuclease, and analysis of results by polyacrylamide gel electrophoresis.
RESULTS: FⅡ G20210A mutation was not detected in all patients and controls.
CONCLUSIONS: No FⅡ G20210A mutation exists in Chinese patients with BCS, nor correlativity between the occurrence of BCS and FⅡ G20210A mutation. The etiology of BCS in the Chinese needs further investigation.
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2004, Vol. 3 
