الفهرس 
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Abstract
Summary
Immune thrombocytopenia (ITP) is a heterogeneous disorder, which is characterized by anti-platelet autoantibody-mediated autoimmune response targeting megakaryocyte or platelet leading to impairment of platelet production or acceleration of platelet destruction, resulting in lower platelet count which may have a propensity to bleeding. Runx1 has been reported to affect Th 17 differentiation and IL17 transcreption through interaction with Th17 master regulator retinoic-acid- receptor-related orphan receptor γ-t (RORγT). Th17 and associated cytokine (IL17) are identified to be implicated in the pathogenesis of ITP.
Given the critical role in the regulation of the differentiation of Th17 cells, whether RUNX1 was involved in ITP remains poorly understood, the current study was designed with an aim to study the expression level of (Runx1) in immune thrombocytopenic patients as compared with healthy controls.
The current study was a case-control study that conducted on the pediatrics hematology outpatient clinic in Beni-Suef University hospital, during the period from November 2020 (after the approval of the ethical committee) to November 2021. It included 49 patients having ITP (subdivided into three groups: active= 20 patients, remission= 11 patients, and chronic= 18 patients) and 20 healthy subjects as controls.
from the analysis of our data we found that :
- RUNX-1 expression levels were significantly higher in ITP patients compared to controls.
- Active ITP patients showed significantly higher levels of expression compared to remission and control groups.
- There were no significant differences between the remission subgroup and healthy controls.
- Chronic ITP patients had significantly higher RUNX1 expressions compared to remission and controls groups.
- There was no significant difference between active and chronic ITP groups regarding the RUNX-1 expression levels.
- There was a significant linear negative correlation between direct platelets count and RUNX1 expression levels.
- Other studied variables showed non-statistically significant correlation with RUNX1 expression levels among ITP patients
In conclusion, our study demonstrated a significantly higher expression of RUNX1 in active ITP patients, which was restored into normal value in remission patients. Meanwhile, a negatively correlation of RUNX1 with platelets count was found in ITP patients. Our results indicated that RUNX1 might be involved in the pathogenesis of ITP possibly through regulation of Th17 cell differentiation and targeting it may be a new therapeutic approach in the treatment of ITP. Future studies are required to further characterize these findings.