ORIGINAL ARTICLESAntithrombin Cambridge II(A384S) mutation frequency and antithrombin activity levels in 120 of deep venous thrombosis and 150 of cerebral infarction patients in a single center in Southern ChinaZhang, Guang-sena; Tang, Yang-minga; Tang, Mei-qinga; Qing, Zi-Jub; Shu, Changc; Tang, Xiang-qid; Deng, Ming-yanga; Tan, Li-mingdAuthor Information aDepartment of Hematology, P.R of China bClinical Laboratory, P.R of China cDepartment of Vascular Surgery, P.R of China dDepartment of Neurology; The Second Xiang-Ya Hospital, Central South University, Changsha, Hunan, 410011, P.R of China Received 23 October, 2009 Revised 21 June, 2010 Accepted 26 June, 2010 Correspondence to Guang-sen Zhang, Department of Hematology, The Second Xiang-Ya Hospital, Central South University, Changsha, Hunan, 410011, P.R of China Tel: +86 73185292166; e-mail: firstname.lastname@example.org Blood Coagulation & Fibrinolysis: September 2010 - Volume 21 - Issue 6 - p 588-591 doi: 10.1097/MBC.0b013e32833dbe68 Buy Metrics Abstract Antithrombin Cambridge II(A384S) mutation shows a relatively high frequency in western population. Some studies suggest that the mutation is an independent genetic risk factor both for deep vein thrombosis (DVT) and for arterial thrombosis, but whether the mutation has racial difference or has a general significance for thrombophilia remains unclear. In this study we performed an analysis of the prevalence of the mutation in Chinese southern population; Also, the antithrombin activity levels were evaluated in each investigated individual. The studies included 120 patients with DVT, 150 patients with cerebral infarction, and 110 controls. The mutation was detected using polymerase chain reaction/PvuII restrictive fragment length polymorphism procedures. Antithrombin activity assay was done using chromogenic substrate method. The results showed that no antithrombin Cambridge II mutation was detected in all three groups (DVT, cerebral infarction and controls), the incidence was 0/380. Plasma antithrombin activity was 91.37% ± 16.15% in the DVT patients and 102.68% ± 13.10% in the controls; the antithrombin activity was significantly reduced in the DVT group (P < 0.0001). In DVT patients, eight cases were identified as primary antithrombin deficiency, accounting for an incidence of 6.7%. No significant difference was found for antithrombin activity between cerebral infarction group and controls. These results suggest that antithrombin Cambridge II mutation has a racial difference, and may not be a valuable risk factor of thrombophilia in Asian population, and antithrombin deficiency remains a major genetic risk factor for DVT patients in China. © 2010 Lippincott Williams & Wilkins, Inc.