الفهرس 
Immune ThrombocytopeniaOnly 14 pages are availabe for public view
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Abstract
Immune thrombocytopenia (ITP) is an immunologically mediated bleeding disorder in which autoantibodies against platelet antigens cause premature platelet destruction that leads to thrombocytopenia.
The incidence of ITP varies according to age, gender and geographical areas. The incidence in childhood is approximately 4‒5/100,000 person/year in Europe and 8/100,000 in North America, with a peak incidence at the age of 1‒5 years (median 4 years) with a male dominated pattern. In adults, the overall incidence of ITP is about 2.9/100,000 in European countries and about 10‒12/100,000 person-year in North America. Its incidence is higher in woman than men in patients below age 64, and vice versa in patients of age 65 and older.
All the mechanisms underlying platelet destruction and decreased platelet production in ITP are not completely understood. ITP classically has been explained by the presence of IgG autoantibodies produced by B cells. The autoantibodies most commonly target glycoprotein IIb/IIIa and glycoprotein Ia/IX, but autoantibodies against multiple platelet antigens are also commonly seen in ITP.
Additional potential mechanisms include; autoreactive cytotoxic T cells, humoral and cellular autoimmunity against megakaryocytes and complement- mediated destruction and increased mononuclear phagocytic activation.
Human interleukin (IL)-37 is a member of IL-1 family and is primarily known as an anti-inflammatory cytokine that acts both in an extracellular and intracellular mode. Extracellularly, IL-37 activates an anti-inflammatory signaling cascade by forming a complex with IL-18 receptor α (IL-18Rα) and IL-1R8.
IL-37 is expressed in circulating monocytes as well as tissue macrophages, dendritic cells, tonsillar B cells, and plasma cells. IL-37 induced anti-inflammatory M2-like macrophages and inhibited the pro-inflammatory M1 macrophages. IL-37 can be activated by pro-inflammatory stimuli and participates in the process of several inflammatory diseases.
Patients with systemic lupus erythematosus, rheumatoid arthritis, and primary Sjögren’s syndrome had higher plasma/serum IL-37 which was positively correlated with disease severity, while the baseline expression level in healthy controls is very low. Interleukin-37 (IL-37) is a fundamental natural suppressor of innate immunity and inflammatory responses in several autoimmune diseases.
This case control study was conducted on 80 children; 40 newly diagnosed ITP patients and 40 age- and sex-matched aberrantly healthy controls. All enrolled subjects underwent full history taking, thorough clinical examination and laboratory investigations including; complete blood count, serum level of IL-37 by ELISA and relative expression of IL-37 gene by RT-PCR.
The results of this study showed that cases demonstrated significantly lower platelets compared to controls. In contrast, they had significantly higher IL-37 serum and expression levels. No significant difference was observed regarding hemoglobin and WBCs.
Also, IL-37 serum and expression levels revealed a significant negative correlation with platelets count and a significant positive correlation with disease severity. No significant correlations were reported with age, disease duration, hemoglobin and WBCs.
ROC analysis was done for IL-37 serum and expression levels in diagnosing thrombocytopenia which was found to be highly sensitive and specific for discrimination between ITP patients and healthy controls.
Also, multivariate logistic regression analysis was done to predict thrombocytopenia which revealed that serum IL-37 was a significant predictor for ITP.
Conclusion
IL-37 may have a pivotal role as a diagnostic marker for ITP and a potential predictor for severe disease.