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Chronic spontaneous urticaria (CSU) is occurrence of recurrent transient raised pruritic lesions (wheals) arising spontaneously on most days of the week for more than six weeks which resolve without disruption of the epidermis and last for between one hour and several days, The term “spontaneous” is used to distinguish CSU from the inducible (physical) urticarias (Katelaris H et al., 2019)
CSU is a common condition in adults, with a life time prevalence of about 1.8% of the general population (Zuberbier et al, 2010) and a point prevalence rate in adults of 0.1-0.8%. It affects females more often than males (females 68-80% of cases) (Broder MS et al., 2015).
Intradermal injection of autologous serum was found to induce a wheal and flare reaction in some patients with CSU, denoting the presence of serum histamine-releasing factors (HRF) (Katelaris H et al., 2019).
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by recurrent eczematous lesions, intense pruritus, a relapsing disease course, as well as associated atopic diseases in the personal or family history. It affects approximately 20% of all children at age 6 years and 5% of adults in Western countries (Simona D et al., 2019)
Inflammasome is an inflammatory proteins complex that can identify pathogens in the development of innate immune response. Recent evidence has shown that inflammasomes have a great effect on skin inflammation. Previous studies have shown that the NLRP3 inflammasome components or the downstream activated signal cytokines play vital roles in allergic dermatitis and that targeting the NLRP3 inflammasome with small molecule inhibitors may provide help in treating allergic dermatitis. However, to confirm NLRP3 as a new promising target for the treatment of allergic diseases, more studies investigating the effects of specific NLRP3 inhibitors or gene therapy should be carried out. Furthermore, clinical studies investigating targeted NLRP3 treatment for allergic diseases should be considered in the future (Xiao Y et al., 2018)
This study was carried out in order to detect the polymorphism in inflmmasome gene in patients with chronic spontaneous urticaria and atopic dermatitis, find the relation between the level of serum total IgE with symptom severity and polymorphism in inflmmasome gene in atopic dermatitis patients, and find the relation between positive autologous skin test result, total IgE level, symptom severity and inflammasome gene polymorphism in chronic spontaneous urticaria patients.
This is a case control study which was conducted on patients recruited from the outpatient clinic of Allergy and Clinical Immunology at of Ain Shams University and Zagazig university hospitals from October 2018 to March 2019. A total 93 adult subjects (both male and females) of aged ≥ 18, years were included in this study.
Subjects were divided into three groups (each group had 31 subjects) as follows: CSU group included 31 patients, AD group included 31 patients and Control group of 31 healthy volunteers
All participants were subjected to the following: Thorough history taking & examination, Serum total IgE level measurement by enzyme linked immunosorbent assay (ELISA), Autologous serum skin testing for CSU patients and Inflammasome gene(NLRP3) polymorphism detection using polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) technique.
The following results were observed:
o About one fourth of the studied patients had mild UAS score. The largest percentage of them had negative ASST and about 39% of the studied patients had severe SCORAD score
o Also, there was non-significant difference between total IgE and disease severity among patients with CSU and patients with AD
o There was statistically significant difference between the studied groups regarding polymorphism or alleles where presence of CC gene non-significantly increased risk of CSU by 3.01 folds and presence of C allele significantly increased risk of CSU by 2.22 folds.
o Also, presence of GG gene non-significantly increased risk of AD by 3.07 folds and presence of G allele significantly increased risk of AD by 2.33 folds
o There was statistically non-significant difference between polymorphism and UAS score. CC was higher among patients with severe CSU. CC polymophism increased risk of severe lesion by 1.22 folds and C allele was higher among patients with severe CSU. C allele increased risk of severe lesion by 2.38 folds
o Also, there was statistically significant difference between polymorphism and ASST. CC was higher among patients with positive ASST. CC polymophism increased risk of positive ASST by 56.66 folds and C allele was higher among patients with positive ASST where C allele increases risk of positive ASST by 21 folds.
o Regarding SCORAD score, there was statistically significant difference between polymorphism and SCORAD score. GG was higher among patients with severe AD and GG polymophism increases risk of severe lesion by 10.83 folds. Also, G allele was higher among patients with severe AD. G allele increased risk of severe lesion by 7.17 folds