IgE FcεR1β polymorphism and risk of developing chronic spontaneous urticaria: A study in an ethnic Kashmiri population

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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Relationship between Serum Soluble Interleukin-2 Receptor and Renal Allograft Rejection: A Hospital-Based Study in KashmirValley.

BACKGROUND: Even after adequate immunosuppression therapy, acute rejection continues to be the single most important cause of graft dysfunction after renal transplantation. Renal allograft biopsy continues to be the reference standard, though certain clinical and biochemical parameters are helpful in assessment of these patients. Renal allograft rejection is mediated by T lymphocytes, expressing cell surface interleukin-2 receptors (IL-2R) which has been suggested as a marker of acute rejection episodes after organ transplantation. OBJECTIVE: To determine the pre- and post-transplantation serum soluble IL-2R levels in live related kidney transplant patients to predict acute rejection episodes. METHODS: Serial serum samples from 75 recipients and 41 healthy controls were assessed for soluble IL-2R levels by ELISA. The outcome of the graft was also determined for each recipient. RESULTS: The mean±SD serum soluble IL-2R levels in renal allograft recipients with rejection were significantly (p<0.001) higher than those without rejection (329.85±59.22 vs 18.12±11.22 pg/mL). The elevation of serum soluble IL-2R was evident in acute rejection episodes and found before elevation of serum creatinine. The higher values of serum soluble IL-2R in the rejection group were significantly reduced after recovery of allograft function by adequate anti-rejection therapy. 36.4% of patients in the rejection group had proven positive biopsies for the rejection and higher creatinine values, which was found to be statistically significant (p<0.001). A cohort of 41 healthy controls showed significantly (p<0.05) lower serum soluble IL-2R concentrations (15.27±7.79 pg/mL) when compared with the rejection group. CONCLUSION: Serum soluble IL-2R concentrations showed significant correlation with the acute rejection episodes in the renal allograft recipients. Prediction of soluble IL-2R levels might help the early detection of rejection episodes, which may pave way for the management of immunosuppression regimes and better graft functioning.

IgE FcɛR1ß polymorphism and risk of developing chronic spontaneous urticaria: A study in an ethnic Kashmiri population.

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-FcɛR1ß 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 FcɛR1ß 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 FcɛR1ß loci (P value=0.06, odds ratio=0.29). The frequency of FcɛR1ß (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 FcɛR1ß (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 FcɛR1ß gene polymorphism and CSU in Kashmiri population; however, there is a probability of developing CSU in patients carrying FcɛR1ß T allele. Furthermore, serum total IgE levels had no significant association with the development of CAU.