In a whole year from July 1997 to June 1998, a total of 50 patients with so
nogram-proved venous thrombosis who called on our hematology clinic consecu
tively entered into the study. Their mean age was 59.1 +/- 17.5 years, rang
e 18-83 years, and 29 were male. A series of examinations were performed in
order to find out the cause of venous thrombosis. These examinations inclu
ded antithrombin, protein C, protein S, plasminogen, heparin cofactor ii, a
ctivated protein C ratio, factor V Leiden mutation, fibrinogen, factors VII
I and XII, euglobulin lysis time, 677 C-->T mutation of methylenetetrahydro
folate reductase (MTHFR), prothrombin 20210 (PT 20210) A allele mutation, l
upus anticoagulant, anticardiolipin antibody, and complete blood count. Fiv
e patients (10%) were found to have malignancy; an inferior vena cava throm
bosis in one patient was due to venous compression by hydronephrosis; two p
atients had lupus anticoagulant; two had varicose veins of legs; two had pr
otein C deficiency; four had protein S deficiency; two had plasminogen defi
ciency; two had antithrombin deficiency. No activated protein C resistance,
elevated factor VIII level, factor V Leiden, PT 20210 A allele or heparin
cofactor II deficiency was found in the present study. Homozygous MTHFR 677
C-->T gene mutation was found in 7 patients (14%); one of them also had a
plasminogen deficiency. No possible risk factor of venous thrombosis could
be found in 24 patients (48%), In conclusion, malignancy and protein S defi
ciency were the most frequent acquired and congenital causes of venous thro
mbosis in the Chinese, respectively. Am. J, Hematol, 63:74-78, 2000, (C) 20
00 Wiley-Liss, Inc.