RESUMEN
BACKGROUND: The pathogenesis of chronic spontaneous urticaria involves interplay between the genetic and environmental factors, most of which is still poorly understood. It is well-recognized that 30-40% of chronic spontaneous urticaria is autoimmune in nature. Chronic autoimmune urticaria is caused by anti-Fc¿R1β and less frequently, by anti-IgE auto antibodies that lead to mast cell and basophil activation, thereby giving rise to the release of histamine and other proinflammatory mediators. We investigated the association between SNP loci in Fc¿R1β and chronic spontaneous urticaria and to see its relation with serum IgE levels in Kashmiri population. METHODS: The autologous serum skin test was used as a screening test for chronic autoimmune urticaria. PCR-RFLP was used to detect the genotype of the SNP loci. Serum IgE levels were assessed by ELISA kit. RESULTS: No significant difference was found between the study population and control group in genotype distribution (wild and variant) among Fc¿R1β loci (P value = 0.06, odds ratio = 0.29). The frequency of c¿R1β (C109T) in autologous serum skin test positive chronic autoimmune urticaria patients with the CT genotype was found to be statistically non-significant when compared with the wild genotype (P = 0.35). Carriers of Fc¿R1β (T allele) had a more significant risk of developing CAU than those with C allele (P = 0.01). In our population serum total IgE levels did not find any statistical significance with regard to ASST positive & ASST negative patients (P = 0.26). CONCLUSIONS: There is statistically no significant association between Fc¿R1β gene polymorphism and CSU in Kashmiri population; however, there is a probability of developing CSU in patients carrying Fc¿R1β T allele. Furthermore, serum total IgE levels had no significant association with the development of CAU
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