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Cyclic thrombocytopenia in a patient treated with cyclosporine for refractory idiopathic thrombocytopenic purpura
Author(s) -
Shirota Tsunemichi,
Yamamoto Hirobumi,
Fujimoto Hiroaki,
Harada Yoshimi,
Okada Kiyoshi,
Uchida Hiroyuki,
Roppongi Hisashi,
Hayashi Toru
Publication year - 1997
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/(sici)1096-8652(199712)56:4<272::aid-ajh13>3.0.co;2-b
Subject(s) - platelet , thrombocytopenic purpura , refractory (planetary science) , medicine , immunology , pathogenesis , bone marrow , megakaryocyte , mean platelet volume , haematopoiesis , biology , stem cell , genetics , astrobiology
Cyclic thrombocytopenia (CT) is a rare disorder with cyclic changes of the platelet counts. Though the pathogenesis of this disorder has not been clarified, recent reports suggest that periodic destruction and/or ineffective production of platelets may be important causes of the disease. We report a case of a patient with refractory idiopathic thrombocytopenic purpura (ITP) in whom CT developed after cyclosporine A (CyA) therapy. There was an inverse relation between platelet counts and the serum levels of platelet‐associated immunoglobulin G (PAIgG). The ploidy of bone marrow megakaryocytes also had an inverse relation with platelet counts. When the platelet count was low, the ploidy of megakaryocytes increased ( P < 0.01). The number and area of bone marrow megakaryocytes were unrelated to platelet counts. These results indicate the possibility of platelet destruction caused by immunological mechanisms in CT. Cyclosporine A could have certain but fluctuating regulatory effects against antibody production for circulating platelets, which could lead to cyclic changes of the platelet counts. This case also suggests that CyA can be effective in severe refractory ITP. Regulatory mechanisms of platelet production and destruction and appropriate doses of CyA should be further studied in autoimmune‐mediated thrombocytopenias. Am. J. Hematol. 56:272–276, 1997. © 1997 Wiley‐Liss, Inc.