부산대학교 도서관

Objectives: Based on the concept of immune dysregulation in immune thrombocytopenic purpura (ITP) and that Interleukin-18 (IL-18) is an inflammatory cytokine that plays an important role in autoimmune disease by inducing interferon-γ secretion; this study aimed to assess a possible association between the IL-18 promoter polymorphisms (−607 C/A site) and genetic susceptibility to ITP and the impact of the immunoglobulins (Igs) concentrations level on disease severity and response to therapy. Methods: A cross-section study was done on 105 patients’ age range from 10 to 28 years, with newly diagnosed ITP at the Oncology Center Mansoura University over the past 2 years and 100 healthy subjects as a control group. For all patients and controls, the IL-18 promoter polymorphism (−607 C/A site) as well as serum Ig (IgG, IgM, IgA) concentration was determined. Results: The IL-18 promoter polymorphism (−607 C/A site) was not significantly different between ITP patients and normal controls. The number of patients respond to standard line of therapy was significantly higher in those with low IgA levels as compared to those with high IgA levels (P = 0.02). On the other hand, the number of patients respond to standard therapy was significantly higher in those patients with high IgM levels as compared to those with low IgM levels (54.7 vs. 36.5%) (P < 0.05). The number of patients with bleeding manifestation was significantly higher among those with high IgA as compared to those with low IgA (43 of 79, 54.4%; vs. 36 of 79, 45.6%;P = 0.04). A change in IgG levels was not associated with response to treatment, bleeding tendency, or platelet counts. Conclusion: There is no association between IL-18 promoter polymorphisms (−607 C/A site) and genetic susceptibility to ITP. High IgA and low IgM levels are a bad index for treatment response to standard therapy. [ABSTRACT FROM AUTHOR]