{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T01:46:28Z","timestamp":1769046388307,"version":"3.49.0"},"reference-count":33,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2016,6,28]],"date-time":"2016-06-28T00:00:00Z","timestamp":1467072000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2016,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Patients with mild hypomegakaryocytic thrombocytopenia (<jats:styled-content style=\"fixed-case\">HMT<\/jats:styled-content>) that does not meet the diagnostic criteria for a definite disease entity may potentially progress to aplastic anaemia (<jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>) that is refractory to therapy. To clarify the clinical picture of <jats:styled-content style=\"fixed-case\">HMT<\/jats:styled-content>, we prospectively followed 25 <jats:styled-content style=\"fixed-case\">HMT<\/jats:styled-content> patients with white blood cell count &gt;3\u00b70\u00a0\u00d7\u00a010<jats:sup>9<\/jats:sup>\/l, haemoglobin level &gt;100\u00a0g\/l and platelet count of &lt;100\u00b70\u00a0\u00d7\u00a010<jats:sup>9<\/jats:sup>\/l in the absence of morphological and karyotypic abnormalities in the bone marrow. Glycosylphosphatidylinositol\u2010anchored protein\u2010deficient blood cells [paroxysmal nocturnal haemoglobinuria (<jats:styled-content style=\"fixed-case\">PNH<\/jats:styled-content>)\u2010type cells] were detected in 7 of the 25 (28%) patients and elevated plasma thrombopoietin (<jats:styled-content style=\"fixed-case\">TPO<\/jats:styled-content>, also termed <jats:styled-content style=\"fixed-case\">THPO<\/jats:styled-content>) levels (&gt;320\u00a0pg\/ml) were observed in 11 (44%) patients. Five (four <jats:styled-content style=\"fixed-case\">PNH<\/jats:styled-content>+ and one <jats:styled-content style=\"fixed-case\">PNH<\/jats:styled-content>\u2212) of six <jats:styled-content style=\"fixed-case\">TPO<\/jats:styled-content><jats:sup>high<\/jats:sup> patients who were treated with ciclosporin (<jats:styled-content style=\"fixed-case\">CsA<\/jats:styled-content>) showed improvement. Among the 21 patients who were followed without treatment, thrombocytopenia progressed in four of ten <jats:styled-content style=\"fixed-case\">TPO<\/jats:styled-content><jats:sup>low<\/jats:sup> patients and four of 11 <jats:styled-content style=\"fixed-case\">TPO<\/jats:styled-content><jats:sup>high<\/jats:sup> patients. The 3\u2010year failure\u2010free survival rate of the <jats:styled-content style=\"fixed-case\">CsA<\/jats:styled-content>\u2010treated <jats:styled-content style=\"fixed-case\">TPO<\/jats:styled-content><jats:sup>high<\/jats:sup> patients (100%) was significantly higher than that of the untreated <jats:styled-content style=\"fixed-case\">TPO<\/jats:styled-content><jats:sup>high<\/jats:sup> patients (20%). These results suggest that a significant population of <jats:styled-content style=\"fixed-case\">HMT<\/jats:styled-content> patients has an immune pathophysiology that is similar to <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and may be improved by early therapeutic intervention with <jats:styled-content style=\"fixed-case\">CsA<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/bjh.14210","type":"journal-article","created":{"date-parts":[[2016,6,29]],"date-time":"2016-06-29T10:18:44Z","timestamp":1467195524000},"page":"246-251","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Hypomegakaryocytic thrombocytopenia (HMT): an immune\u2010mediated bone marrow failure characterized by an increased number of PNH\u2010phenotype cells and high plasma thrombopoietin 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