Pathogenesis of Chronic Urticaria and The Role of Platelets in Disease Severity

سال انتشار: 1397
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 413

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شناسه ملی سند علمی:

ICMHS01_029

تاریخ نمایه سازی: 20 خرداد 1398

چکیده مقاله:

Chronic Urticaria (CU) is one of the most common skin diseases with prevalence ranging between 15 and 25%. This disease takes more than 6 weeks and is often associated with angioedema.The pathogenesis of chronic urticaria is not well delineated and the treatment is palliative as it is not tied to the pathomechanism. Autoimmune origin of chronic urticaria, albeit controversial, is well documented. Numerical and behavioral alterations in basophils accompanied by changes in signaling molecule expression and function as well as aberrant activation of extrinsic pathway of coagulation are other alternative hypotheses. An increasing recognition of chronic urticaria as an immune mediated inflammatory disorder related to altered cytokine chemokine network consequent to immune dysregulation resulting from disturbed innate immunity is emerging as yet another pathogenic explanation. Platelets are implicated in many pathophysiological processes, including inflammation and immunity. Ever growing evidence suggests the active involvement of platelets in the pathogenesis of various inflammatory disorders, including cutaneous inflammatory diseases. A limited number of studies have investigated the role of platelets in chronic urticaria (CU). In this review, we summarize the cur rent knowledge regarding the role of platelets in chronic spontaneous and inducible urticarias. A literature search was performed using PubMed and Google Scholar, and the references of relevant literature were reviewed. Overall, in CU patients, conflicting results have been obtained from the assessment of platelet indices, such as mean platelet volume, platelet count and distribution width, as well as markers of platelet aggregation and activation. Nevertheless, a few studies showed significant changes of such parameters in CU patients compared to controls, in apparent correlation with clinical severity, autoreactivity and or inflammatory status. In the absence of definitive conclusions, the pathogenic role of platelets in CU needs to be further explored. Platelets might represent a link between inflammation, coagulation and histamine release in the pathophysiological network of CU.

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نویسندگان

Maryam Taburak

Student Kermanshah University of Medical Sciences, Kermanshah, Iran