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Introduction: Chronic urticaria requires well-defined treatment strategies in order to achieve a maximum treatment response and maintain the quality of life. Since 2014, omalizumab has been used in chronic urticaria. However, many studies showed that some patients are resistant to omalizumab. Aim: To determine the effects of single nucleotide changes in the FCER1A and FCER1B genes, which are thought to be related to resistance mechanisms, in our population of patients who have not responded to omalizumab treatment. Material and methods: We included 100 patients with chronic urticaria who were treated with omalizumab and 50 healthy individuals. Frequently observed gene polymorphisms, FCER1A (rs2251746) and FCER1B (rs569108), were examined in peripheral blood samples. The regions of rs2251746 and rs569108 gene polymorphisms were amplified using fluorescently labelled probes through real-time polymerase chain reaction (PCR). The analysis was performed bioinformatically via the SNP genotype profiling program. Results: There was no statistically significant relationship between FCER1A (rs2251746) and FCER1B (rs569108) gene polymorphisms in patients and their clinical, demographic characteristics, and the resistance to treatment (p > 0.05). In our study, the mean patient age was found to be higher in the CT group (44.71 ±12.5 years) compared to the TT group (37.34 ±11.5 years) only in the rs2251746 polymorphism (p < 0.05). Conclusions: In our study, there was no significant relationship between FCER1A and FCER1B gene polymorphisms and resistance to omalizumab therapy. Further, multicentre, large-scale studies are needed to support our results.
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INTRODUCTION: IL-17A and IL-17F cytokines have important roles in the pathogenesis of psoriasis. AIM: To examine the associations of IL-17A rs2275913 and IL-17F rs763780 variants with the development of psoriasis and whether these polymorphisms affect the responsiveness of biological agents. MATERIAL AND METHODS: In our case-controlled study, which included 83 psoriatic patients who were treated with different biological agents and 69 healthy controls, we genotyped IL-17A rs2275913 and IL-17F rs763780 variants using TaqMan probes. RESULTS: We did not observe statistically significant changes in genotype frequencies of IL-17A rs2275913 (p = 0.922) and IL-17F rs763780 (p = 0.621) variants between patient and control groups. Although we did not find any association between these polymorphisms and the development of psoriasis, statistical analyses showed that individuals with the IL-17A AA genotype had shorter disease duration (9.09 ±6.82, p = 0.020) and AA genotype frequency was higher in patients who used single conventional treatment (34.6%; p = 0.025). IL17A/rs2275913 variant in terms of disease duration, it was observed that individuals with AA genotype had a shorter disease duration (less than 10 years) (p = 0.009). For patients with PASI90 and PASI100 response, the IL-17A AA genotype was significantly higher (p = 0.015). On the other hand, we did not detect any statistically significant correlation between variants and response to biological agents. CONCLUSIONS: According to our results, we may suggest that rs2275913 variant seems to be associated with disease duration, use of single conventional treatment and responsiveness of PASI90 and PASI100 however both variants have no effect on the susceptibility to psoriasis in the population of Eastern Turkey.