High prevalence of antithrombin III, protein C and protein S deficiency, but no factor V Leiden mutation in venous thrombophilic Chinese patients in Taiwan

被引:146
作者
Shen, MC [1 ]
Lin, JS [1 ]
Tsay, W [1 ]
机构
[1] NATL TAIWAN UNIV HOSP,DEPT LAB MED,TAIPEI,TAIWAN
关键词
venous thrombophilia; inhibitor protein deficiencies; factor V mutation;
D O I
10.1016/S0049-3848(97)00141-2
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
We studied the prevalence of antithrombin III (AT III), protein C (PC) and protein S (PS) deficiencies and factor V Leiden mutation in thrombophilia in Taiwan. Eighty-five consecutive and unrelated patients with otherwise unexplained venous thrombophilia were studied. Both antigen and activity of inhibitors were determined using commercial kits (Stage), activated PC sensitivity ratio (APC SR) by Coatest (Chromogenix), and factor V mutation by polymerase chain reaction with sequence specific primer. Of 85 patients, 41 were male, 44 female, and mean age 49.4 years (17-82 years). None had factor V mutation, or APC SR of less than 2; 50 (58.8%) showed a deficiency of inhibitor proteins; 34 (68.0%) were hereditary, 16 (32.0%) non-hereditary; 3 had an AT III deficiency, 16 a PC deficiency, 28 a PS deficiency, and 3 a combined deficiency. Thirty-five were non-deficient without a known cause. The average age at the first thrombotic episode was 48.5 years (13-81 years). Thrombosis occurred spontaneously in 39 (78.0%) of 50 deficient patients. In conclusion, a relatively higher prevalence of AT III, PC and PS deficiency (59%), but no factor V Leiden mutation, was found in venous thrombophilic Chinese patients in Taiwan compared to that in western countries. Screening for inhibitor protein deficiency in Chinese thrombophilic patients is highly recommended. (C) 1997 Elsevier Science Ltd.
引用
收藏
页码:377 / 385
页数:9
相关论文
共 28 条
[1]
BENTAL O, 1989, THROMB HAEMOSTASIS, V61, P50
[2]
MUTATION IN BLOOD-COAGULATION FACTOR-V ASSOCIATED WITH RESISTANCE TO ACTIVATED PROTEIN-C [J].
BERTINA, RM ;
KOELEMAN, BPC ;
KOSTER, T ;
ROSENDAAL, FR ;
DIRVEN, RJ ;
DERONDE, H ;
VANDERVELDEN, PA ;
REITSMA, PH .
NATURE, 1994, 369 (6475) :64-67
[3]
BRANSON HE, 1983, LANCET, V2, P1165
[4]
BRIET E, 1987, THROMB HAEMOSTASIS, V58, P39
[5]
Collett D., 1994, Modelling Survival Data in Medical Research
[6]
RECURRENT VENOUS THROMBOEMBOLISM IN PATIENTS WITH A PARTIAL DEFICIENCY OF PROTEIN-S [J].
COMP, PC ;
ESMON, CT .
NEW ENGLAND JOURNAL OF MEDICINE, 1984, 311 (24) :1525-1528
[7]
FAMILIAL THROMBOPHILIA DUE TO A PREVIOUSLY UNRECOGNIZED MECHANISM CHARACTERIZED BY POOR ANTICOAGULANT RESPONSE TO ACTIVATED PROTEIN-C - PREDICTION OF A COFACTOR TO ACTIVATED PROTEIN-C [J].
DAHLBACK, B ;
CARLSSON, M ;
SVENSSON, PJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (03) :1004-1008
[8]
INHERITED ANTITHROMBIN DEFICIENCY CAUSING THROMBOPHILIA [J].
EGEBERG, O .
THROMBOSIS ET DIATHESIS HAEMORRHAGICA, 1965, 13 (3-4) :516-&
[9]
FUJIMURA H, 1995, THROMB HAEMOSTASIS, V74, P1379
[10]
GLADSON CL, 1988, THROMB HAEMOSTASIS, V59, P18