Chronic immune thrombocytopenia. Egyptian experience

• Published in: Comparative clinical pathology 2018-05, Vol.27 (3), p.735-739
• Main Authors: El Husseiny, Noha M., El Sobky, Amira, Khalaf, Ahmed M., Fateen, Mohamed, El Demerdash, Doaa M., Youssef, Heba, Salah, Marwa, El Ghany, Sara El Sayed Abd, El Husseiny, Sherin, Gamil, Mona
• Format: Article
• Language: English
• Subjects: Corticosteroids; Cytokines; Diagnosis; Enzyme-linked immunosorbent assay; Hematology; Idiopathic thrombocytopenic purpura; Immunosuppression; Interleukin 12; Interleukin 17; Lymphocytes T; Medicine; Medicine & Public Health; Oncology; Original Article; Pathology; Platelets; Remission; Statistical analysis; Thrombocytopenia
• ISSN: 1618-5641; 1618-565X
• DOI: 10.1007/s00580-018-2659-8

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 × 10 9 /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.