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Hemostatic and thrombotic markers in patients with hemoglobin E/β‐thalassemia disease
Author(s) -
Angchaisuksiri Pantep,
Atichartakarn Vichai,
Aryurachai Katcharin,
Archararit Napaporn,
Chuncharunee Suporn,
Tiraganjana Arjit,
Rattanasiri Sasivimol
Publication year - 2007
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/ajh.20945
Subject(s) - medicine , fibrinogen , fibrinolysis , protein c , plasminogen activator , antithrombin , thalassemia , endocrinology , thrombosis , hemoglobin e , gastroenterology , coagulation , immunology , heparin
Increased frequency of thrombosis has been observed in patients with hemoglobin E/β‐thalassemia (Hb E/β‐thal) disease, particularly those who have previously been splenectomized. We compared various hemostatic and thrombotic markers in blood from 15 Hb E/β‐thal patients who were not splenectomized (NS), 15 who had been splenectomized (S), and 15 normal controls (NC). Levels of plasma thrombin‐antithrombin, β2 thromboglobulin, C‐reactive protein, tissue plasminogen activator antigen were significantly higher in the S group than in either the NS or the NC groups, and levels of prothrombin fragment 1.2 were significantly higher in the S than in the NC group. Levels of plasminogen activator inhibitor‐1 antigen were significantly higher in the S than in the NS group. Levels of protein C, protein S, antithrombin, and fibrinogen were significantly lower in the S and NS groups than in the NC group. Plasma lipoprotein(a) levels in the S and NS groups were not statistically different from NC. Our findings indicated that there is evidence of chronic low‐grade coagulation and platelet activation, chronic low‐grade inflammation, endothelial cell injury, impaired fibrinolysis, and decreased naturally occurring anticoagulants in splenectomized Hb E/β‐thal patients. These changes may account for the increased risk of thrombosis in these patients. Am. J. Hematol., 2007. © 2007 Wiley‐Liss, Inc.