{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,23]],"date-time":"2025-09-23T13:12:17Z","timestamp":1758633137800},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2003,1,28]],"date-time":"2003-01-28T00:00:00Z","timestamp":1043712000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2003,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The contribution of pro\u2010thrombotic factors towards the development of arterial disease (AD) and splanchnic vein thrombosis (SVT) was retrospectively evaluated in 79 patients (39M, 40F, mean age 55 \u00b1 16 years) with myeloproliferative disorders (MPD) (essential thrombocythemia [<jats:italic>n<\/jats:italic> = 26], primary proliferative polycythemia [<jats:italic>n<\/jats:italic> = 27], and idiopathic myelofibrosis [<jats:italic>n<\/jats:italic> = 26]). Of these, 18 had AD and 17 SVT, the remaining 44 were non\u2010thrombotic (NT). Plasma concentrations of natural anticoagulants, plasma homocysteine (HC), IgG anticardiolipin antibodies (aCL), and thrombophilic genotypes (methylenetetrahydrofolate reductase C<jats:sup>677<\/jats:sup>T, factor V Leiden, prothrombin G<jats:sup>20210<\/jats:sup>\u2192A) 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 (<jats:italic>P<\/jats:italic> = 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\u2010thrombotic group, 12% in the SVT group and 4.5% in the control group (<jats:italic>P<\/jats:italic> &lt; 0.0001). Patients with AD had higher plasma HC (24.4 \u00b1 23 \u03bcmol\/L) than NT patients (12.3 \u00b1 7.7 \u03bcmol\/L), SVT patients (9 \u00b1 4.9 \u03bcmol\/L), and healthy controls (7.9 \u00b1 3 \u03bcmol\/L) (<jats:italic>P<\/jats:italic> &lt; 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\u201381, 2003. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajh.10254","type":"journal-article","created":{"date-parts":[[2003,1,29]],"date-time":"2003-01-29T15:36:05Z","timestamp":1043854565000},"page":"75-81","source":"Crossref","is-referenced-by-count":30,"title":["Thrombophilic genotypes, natural anticoagulants, and plasma homocysteine in myeloproliferative disorders: Relationship with splanchnic vein thrombosis and arterial 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