Abstract

Samir Sorour Sorour, Nasser Nagieb Mohammed, Marian Asaad Gerges, Boles Samir Sabr

The expression level of glucocorticoid receptor (GR) isoforms α and β might interfere with the response to exogenous glucocorticoids (GC) in different allergic disorders. No much data concerning allergic rhinitis (AR) currently exists. The aim of this study was to detect the change in the expression level of GRα in the nasal mucosa of AR patients, compared to healthy subjects, following 4 weeks of intranasal GC application, and whether this change was correlated to the clinical response of those patients.Twenty AR patients (mean age 31.3 ± 8.7) and 10 healthy volunteers (mean age 32.5 ± 17.7) were enrolled in this clinical trial. Intranasal mometasone furoate was applied for all participants for 4 weeks. The level of GRα expression, before and after treatment, was compared by quantitative real time PCR. Total nasal symptom score (TNSS) was used to assess the clinical response of AR patients. This study revealed that GRα was down-regulated in 85% of AR patients compared to 100% of healthy volunteers. Mann Whitney-U test (MW) revealed insignificant difference in the mean fold change (FC) of GRα expression between AR patients and healthy subjects (0.8±1.1 compared to 0.4±0.2) (P0.1). Chi squared test revealed decreased GRα expression among higher ratio (92.3%) of patients with residual symptoms after treatment than those with total improvement (71.4%), which was insignificant statistically (P0.2). MW revealed more decrease in GRα expression in patients with residual symptoms (mean FC 0.8 ± 1.3), compared to patients that were totally improved (mean FC 0.9 ± 0.6), that was statistically insignificant (P0.2). The test also revealed a significant (P 0.0) decrease of TNSS of AR patients after treatment, though weakly correlatedto the change in GRα expression with Spearman correlation coefficient of -0.2 (P0.3). Therefore, GRα expression in AR patients, following 4 weeks of intranasal GC, is variable and might not be a contributing factor determining the response of AR patients to exogenous GC.