Chronic immune thrombocytopenia. Egyptian experience

被引:0
|
作者
El Husseiny N.M. [1 ]
El Sobky A. [2 ]
Khalaf A.M. [3 ]
Fateen M. [2 ]
El Demerdash D.M. [1 ]
Youssef H. [1 ]
Salah M. [1 ]
El Ghany S.E.S.A. [1 ]
El Husseiny S. [4 ]
Gamil M. [1 ]
机构
[1] Clinical Haematology Unit, Internal Medicine Department, Cairo University, Cairo
[2] Clinical Pathology Department, Cairo University, Cairo
[3] Internal Medicine Department, Bani Sweif University, Beni Suef
[4] Clinical Pathology Department, Bani Sweif University, Beni Suef
关键词
Chronic ITP; IL-12; IL-23; IL-35; TGF-β;
D O I
10.1007/s00580-018-2659-8
中图分类号
学科分类号
摘要
Pathogenesis of thrombocytopenia is heterogeneous and resistance to treatment is a great challenge. In this study, we reviewed the demographic features of thrombocytopenic Egyptian patients. We also analyzed the role of T cell in chronic immune cases. IL-12, IL-35, IL-17, and TGF-β were measured by ELISA. The median age at the time of diagnosis was 30 years and its range was 14–70. The median platelet count at the time of diagnosis was 15 × 109/L. Regarding treatment and follow-up, there was an indication for treatment in 96% of patients. Of the 150 ITP patients who were given first-line therapy (corticosteroid 1 mg/kg/day PO), there was a complete response (CR) in 40.3% while 59.7% patients were nonresponsive to therapy. Forty-five chronic cases fulfilled the criteria for cytokine assay. Comparison between the case group and the control group revealed statistically significant lower platelet count in cases, while the four measured cytokines were statistically significant higher in cases rather than the control. Correlation between the platelet count and the level of cytokines was statistically insignificant. The remission rate in ITP on steroid as first-line therapy is less than 50%. The higher expression of IL-12 and IL-35in chronic ITP is due to the persistently higher Th1 activity which explains the continuity of the disease, while the higher expression of Treg cytokines (IL-17 and TGF-β) may be explained by effect of immunosuppression or upregulation of the receptors on Treg cells. © 2018, Springer-Verlag London Ltd., part of Springer Nature.
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页码:735 / 739
页数:4
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