Deep venous thrombosis of the upper extremity (DVTUE) is a rare thrombotic disorder that may occur spontaneously but is most often related to predisposing factors, such as an indwelling central venous catheter, malignancy, or exercise. The role of coagulation disorders, i.e., a hypercoagulable state in the pathogenesis of DVTUE is not well known. We have evaluated both genetic and acquired thrombophilia parameters in consecutive patients with DVTUE. A hypercoagulable state was found in 32% of the patients. The most frequent coagulation abnormality was the presence of lupus anticoagulant or anticardiolipin antibodies (27%). Factor V Leiden mutation was detected in two patients, antithrombin deficiency in one, and none of the patients had the prothrombin G20210A gene variant or protein C or S deficiency. The prevalence of coagulation abnormalities was not significantly different in a subgroup of patients with spontaneous DVTUE as compared to those with an obvious predisposing factor, such as an indwelling central venous catheter. We conclude that antiphospholipid antibodies are frequently found in patients with DVTUE. Factor V Leiden mutation, prothrombin 20210A gene variant, protein C deficiency, and protein S deficiency do not seem to play a major pathogenetic role in DVTUE. Am. J. Hematol. 67:15-19, 2001.
Background: To determine whether 2148 C/T fibrinogen gene promoter polymorphism increases stroke risk by modifying the fibrinogen level. Design: A case-control study of patients with first ever ischaemic stroke, confirmed by computed tomography. Methods: Venous blood samples were collected for fibrinogen and routine coagulation tests one week after the stroke, and after three months in about half the patients. Population controls were age and sex matched. 2148 C/T fibrinogen polymorphism was determined by polymerase chain reaction followed by digestion with restriction enzymes HindIII/AluI. Results: There were 124 patients and 125 controls, mean age 56 years (range 18 to 75); 34 patients (27%) and 41 controls (33%) were heterozygous for 2148 C/T fibrinogen polymorphism; six patients (5%) and five controls (4%) had the T/T genotype. The odds ratio of ischaemic stroke associated with CC homozygotes v T carriers was 0.8 (95% confidence interval, 0.5 to 1.4). Relative risk for ischaemic stroke associated with fibrinogen levels in the highest quartile was 3.9 (1.9 to 8.4) at one week, decreasing to 1.4 (0.6 to 3.3) at three months. Conclusions: 2148 C/T fibrinogen gene polymorphism was not a strong risk factor for ischaemic stroke. High fibrinogen levels early after acute stroke probably represent an acute phase response.
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