{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T08:14:33Z","timestamp":1766391273480},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,7,11]],"date-time":"2006-07-11T00:00:00Z","timestamp":1152576000000},"content-version":"vor","delay-in-days":7162,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[1986,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Although large vessel thrombi are occasionally reported in patients with homozygous sickle cell disease, the role of intravascular coagulation in typical pain crises is controversial. Therefore, we studied 24 sickle cell patients during and between episodes of pain crisis, using several sensitive tests of hemostasis. Fibrinogen was measured by a clotting assay, \u03b23\u2010thromboglobulin (\u03b2\u2010TG) and fibrinopeptide A (FPA) were quantitated by radioimmunoassay, and protein C was determined by absorbing the zymogen from test plasma, activating it with thrombin\u2010thrombomodulin complex, and measuring activity with a selective synthetic substrate. Fibrinogen was elevated in asymptomatic patients (355 \u00b1 145 mg\/dl) but was no different from the value in these same patients during crisis (333 \u00b1 180 mg\/dl, p &gt; 0.1). Similarly, \u03b2\u2010TG 136 \u00b1 52 ng\/ml vs 118 \u00b1 56; FPA 3.7 \u00b1 4.8 ng\/ml vs 5.2 \u00b1 4.5, and protein C 71 \u00b1 20% vs 66 \u00b1 19 showed no important changes during crisis. However, all these values were significantly different from those in age\u2010 and sex\u2010matched healthy controls. (\u03b2\u2010TG, fibrinogen, and FPA were elevated (p &lt; 0.001, 0.005, and 0.05, respectively), and protein C was decreased (p &lt; 0.003). We conclude that while chronic intravascular coagulation is common in patients with sickle cell disease, there is no evidence that the pain crisis per se is a thrombotic event.<\/jats:p>","DOI":"10.1002\/ajh.2830230403","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T10:38:51Z","timestamp":1172054331000},"page":"317-321","source":"Crossref","is-referenced-by-count":49,"title":["Is sickle cell crisis a thrombotic event?"],"prefix":"10.1002","volume":"23","author":[{"given":"David","family":"Green","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John 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