Abdominal venous thrombosis with prothrombin gene mutation

Ergul, Sitki; Lima, Caio S. Rocha; Farber, Joshua M.

doi:10.1002/(sici)1096-8652(200002)63:2<106::aid-ajh15>3.0.co;2-8

Cited by 2 publications

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“…More recently, the C 677 →T mutation of the methylenetetrahydrofolate reductase enzyme (MTHFR), *Correspondence to: Paul Ames, M.D., 75 Canterbury House, Royal Street, London SE1 7EH, United Kingdom. E-mail: paxmes@aol.com factor V A 506 →G (Leiden), and prothrombin mutation G 20210 }A were associated with splanchnic vein occlusion (SVT) in some series [15][16][17][18][19][20][21][22][23]. The occurrence of thrombophilic genotypes in thrombotic patients with MPD has been documented only in case reports [24,25].…”

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confidence: 99%

Thrombophilic genotypes, natural anticoagulants, and plasma homocysteine in myeloproliferative disorders: Relationship with splanchnic vein thrombosis and arterial disease

et al. 2003

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The contribution of pro-thrombotic factors towards the development of arterial disease (AD) and splanchnic vein thrombosis (SVT) was retrospectively evaluated in 79 patients (39M, 40F, mean age 55 ± 16 years) with myeloproliferative disorders (MPD) (essential thrombocythemia [n = 26], primary proliferative polycythemia [n = 27], and idiopathic myelofibrosis [n = 26]). Of these, 18 had AD and 17 SVT, the remaining 44 were nonthrombotic (NT). Plasma concentrations of natural anticoagulants, plasma homocysteine (HC), IgG anticardiolipin antibodies (aCL), and thrombophilic genotypes (methylenetetrahydrofolate reductase C 677 T, factor V Leiden, prothrombin G 20210 →A) were determined. Isolated protein C deficiency was found in 23% of patients from the SVT group, in 5% from the AD group, in 6.8% from the NT group, and in 1% of historical controls (P = 0.0001). The prevalence of thrombophilic genotypes and that of the other natural anticoagulants did not differ across the groups. The proportion of patients with elevated plasma HC was 66% in the AD group, 27% in the non-thrombotic group, 12% in the SVT group and 4.5% in the control group (P < 0.0001). Patients with AD had higher plasma HC (24.4 ± 23 µmol/L) than NT patients (12.3 ± 7.7 µmol/L), SVT patients (9 ± 4.9 µmol/L), and healthy controls (7.9 ± 3 µmol/L) (P < 0.0001). In a logistic regression model lower protein C was independently associated with SVT, whereas elevated plasma HC was independently associated with AD. Measurement of plasma HC and protein C in MPD may identify patients more likely to suffer arterial disease and splanchnic vein thrombosis and who may require plasma HC lowering in the former case. Am. J. Hematol. 72:75-81, 2003.

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