{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T12:12:29Z","timestamp":1790338349952,"version":"4.1.0"},"reference-count":52,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,9,7]],"date-time":"2015-09-07T00:00:00Z","timestamp":1441584000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000862","name":"Doris Duke Charitable Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000862","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    Recent epidemiologic data suggest that sickle cell trait (Hb\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    ;\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    ) is a risk factor for venous thromboembolism. We conducted an exploratory study of healthy subjects with\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    under baseline conditions to determine whether a chronic basal hyperactivation of coagulation exists, and if so, what mechanism(s) contribute to this state. Eighteen healthy\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    individuals were compared to 22 African\u2010American controls with a normal haemoglobin profile (Hb\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    ;\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    ) and 17 patients with sickle cell disease (Hb\n                    <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>\n                    ;\n                    <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>\n                    ). Plasma thrombin\u2010antithrombin complexes and D\u2010dimer levels were elevated in\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    relative to\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    patients (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00\u00b70385 and\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00\u00b7017, respectively), and as expected, were much higher in\n                    <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>\n                    <jats:italic>versus<\/jats:italic>\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0&lt;\u00a00\u00b70001 for both). Thrombin generation in platelet poor plasma was indistinguishable between\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    subjects, whereas a paradoxical decrease in endogenous thrombin potential was observed in\n                    <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>\n                    (\n                    <jats:italic>P\u00a0<\/jats:italic>\n                    \u2264\u00a00\u00b70001). Whole blood tissue factor was elevated in\n                    <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>\n                    compared to\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00\u00b7005), but did not differ between\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    . Plasma microparticle tissue factor activity was non\u2010significantly elevated in\n                    <jats:styled-content style=\"fixed-case\">AS<\/jats:styled-content>\n                    (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00\u00b7051), but was clearly elevated in\n                    <jats:styled-content style=\"fixed-case\">SS<\/jats:styled-content>\n                    patients (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00\u00b7004) when compared to\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    controls. Further studies in larger cohorts of subjects with sickle cell trait are needed to confirm the results of this preliminary investigation.\n                  <\/jats:p>","DOI":"10.1111\/bjh.13641","type":"journal-article","created":{"date-parts":[[2015,9,7]],"date-time":"2015-09-07T03:36:53Z","timestamp":1441597013000},"page":"638-646","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Coagulation activation in sickle cell trait: an exploratory study"],"prefix":"10.1111","volume":"171","author":[{"given":"Chirag","family":"Amin","sequence":"first","affiliation":[{"name":"Department of Medicine University of North Carolina School of Medicine Chapel Hill NC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soheir","family":"Adam","sequence":"additional","affiliation":[{"name":"Department of Medicine University of North Carolina School of Medicine Chapel Hill NC 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