The role of nuclear factor kappa beta in pathogenesis of immun thrombocytopenic purpura

Aim: Immüne thrombocytopenic purpura (ITP) is an acquired immüne-mediated disease characterized by increased risk of bleeding depending on the degree of thrombocytopenia, which migt be temporary or permanent. Nuclear factor kappa beta (NFκB) controls the expression of many genes involved in cell growth, differentiation, cytokine production, apoptosis and immünity. In this study we aimed to determine the relationship between the NFκB and an autoimmüne disease ITP. Materials and Methods: Eighty-six ITP patients and 30 lymphoma patients with no bone marrow involvement as a control group; over the age of 18 were included in the study. Biochemical, hematological data, anti-nuclear antibody, anti-mitochondrial antibody, anti-smooth muscle antibody positivity, hepatitis and human immünodeficiency virus positivity, stool Helicobacter pylori antigen positivity at diagnosis and hematological parameters on follow-up of the ITP patients were recorded. Demographic data of the patient and control groups were recorded. NFκB (p65) was evaluated by using avidine and biotin immünohistochemistry on 3 micron thick sections from the bone marrow biopsy samples of 40 ITP and 30 lymphoma patients. Results were evaluated as negative and positive semi-quantitatively. Results: We determined that ITP patients had significant NFκB positivity compared to the control group (p<0,001). Conclusion: NFκB activation is increased in patients with ITP. Further studies with larger patient populations may be necessary to determine the contribution of NFκB signaling pathway on ITP pathophysiology and may lead to new treatment modalities. Key Words: Immüne thrombocytopenic purpura, Nuclear factor kappa beta