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Comparative Study of IgG Binding to Megakaryocytes in Immune and Myelodysplastic Thrombocytopenic Patients

Overview
Journal Ann Hematol
Specialty Hematology
Date 2021 May 13
PMID 33982136
Citations 3
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Abstract

Immune thrombocytopenia (ITP) is a disorder in which autoantibodies are responsible for destruction and decreased production of platelets. In the meantime, thrombocytopenia is frequent in patients with myelodysplastic syndromes (MDS) and immune clearance of megakaryocytes could be a reason. The aim of the present study is to evaluate and compare IgG binding to megakaryocytes in bone marrow of ITP and MDS patients to determine megakaryocytes targeting by autoantibodies in vivo as a mechanism of platelet underproduction in these disorders. The study was carried out on 20 ITP (group I) patients, 20 thrombocytopenic patients with (MDS) (group II), and 20 non-ITP patients as a control (group III) who were admitted to Minia University Hospital. Serial histological sections from bone marrow biopsies were stained for IgG. All patients in group I and 50% of group II patients showed bleeding tendency and the difference was significant (p < 0.001). No patient experienced fatigue in group I while 35% of patients in group II complained of easy fatigability, and the difference was significant (p < 0.008). High IgG antibody binding was found in ITP and MDS compared to the control group but no significant difference between ITP and MDS patients (14/20 (70%) vs. 13/20 (65%)) (p value = 0.736). Antibody binding to megakaryocytes in a proportion of MDS patients suggests that immune-mediated mechanism underlies platelet underproduction in those patients.

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References
1.
Rodeghiero F, Stasi R, Gernsheimer T, Michel M, Provan D, Arnold D . Standardization of terminology, definitions and outcome criteria in immune thrombocytopenic purpura of adults and children: report from an international working group. Blood. 2008; 113(11):2386-93. DOI: 10.1182/blood-2008-07-162503. View

2.
Ballem P, Segal G, Stratton J, Gernsheimer T, Adamson J, Slichter S . Mechanisms of thrombocytopenia in chronic autoimmune thrombocytopenic purpura. Evidence of both impaired platelet production and increased platelet clearance. J Clin Invest. 1987; 80(1):33-40. PMC: 442198. DOI: 10.1172/JCI113060. View

3.
McMillan R . The pathogenesis of chronic immune (idiopathic) thrombocytopenic purpura. Semin Hematol. 2000; 37(1 Suppl 1):5-9. DOI: 10.1016/s0037-1963(00)90111-2. View

4.
Kashiwagi H, Tomiyama Y . Pathophysiology and management of primary immune thrombocytopenia. Int J Hematol. 2013; 98(1):24-33. DOI: 10.1007/s12185-013-1370-4. View

5.
Olsson B, Andersson P, Jernas M, Jacobsson S, Carlsson B, Carlsson L . T-cell-mediated cytotoxicity toward platelets in chronic idiopathic thrombocytopenic purpura. Nat Med. 2003; 9(9):1123-4. DOI: 10.1038/nm921. View