Effects of high-dose methylprednisolone therapy on coagulation factors in patients with acute immune thrombocytopenic purpura


Oner A., Bay A., Kuru M., Uner A., Arslan S., Caksen H.

CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS, cilt.11, ss.489-492, 2005 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 11 Konu: 4
  • Basım Tarihi: 2005
  • Doi Numarası: 10.1177/107602960501100418
  • Dergi Adı: CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS
  • Sayfa Sayıları: ss.489-492

Özet

Autoimmune thrombocytopenic purpura (ITP) is a disease that presents with skin and mucous membrane bleeding due to thrombocytopenia. In the literature, there are a few studies about the effect of high-dose steroid therapy on coagulation tests in different diseases, but their results are still controversial. In this study, coagulation parameters were investigated that might have a role in hemostatic compensation in childhood acute ITP before and after highdose methylprednisolone (HDMP) treatment. The study includes 21 children age 1.5 to 14 years with acute ITP and 21 healthy age-matched control subjects. All patients with acute ITP received HDMP for 7 days. Before and after HDMP treatment (0 and 8 days) prothrombin time, partial thromboplastin time, fibrinogen, Protein C, Protein S, antithrombin 111, and the levels of factor II (FII), FV, FVII, FVIII, FIX, FX, FXI, and FXII were studied in all subjects. The results were compared with those of the control group. Pre-treatment Protein C and Protein S levels in the patient group were significantly lower than those in the control groups (p < 0.05). Protein S and Protein C levels were significantly improved after HDMP treatment in patient group. There were lower FV, FVII, FX values in the patient group compared to the control groups on admission. There was no difference in AT III and fibrinogen levels before and after treatment. As a result, some changes in the coagulation system associated with thrombocytopenia were observed in patients with acute ITP. These changes may be accepted as compensatory mechanisms to maintain hemostasis.