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Abstract
Objectives: Deregulation of glucocorticoid (GC) secretion could be associated with rheumatoid arthritis (RA). The GC receptor (GR) has two isoforms. In the present study, we explored the role of GR‐α polymorphisms rs33388, rs33389, and Bcl I, and the GR‐β variant rs6198 in RA susceptibility.
Methods: One hundred and thirty‐six RA patients and 148 ethnic matching controls were studied. Polymorphisms rs33388 and Bcl I were genotyped by polymerase chain reaction restriction fragment length polymorphism (PCR‐RFLP), and variants rs33389 and rs6198 by polymerase chain reaction single‐strand conformation polymorphism (PCR‐SSCP) coupled with sequencing. Arlequin and SPSS softwares were used in the statistical analysis.
Results: The polymorphisms studied were in Hardy–Weinberg equilibrium in both groups. A marginally statistical significant difference was observed in the distribution of rs33388 genotypes between RA patients and controls (p = 0.053). When the A and T alleles were compared, the statistical significance was p = 0.025. Specific complex genotypes were also differentially distributed: the GR‐α complex genotypes (a) [homozygote (homo) wild‐type (wt) rs33388–homo wt rs33389] (11% RA vs. 21% controls; p = 0.023), (b) [homo wt rs33388–homo wt rs33389–homo non‐wt Bcl I] (0.7% RA vs. 4.7% controls; p = 0.042), and (c) the GR‐β complex genotype [homo wt rs33388–homo wt rs33389–homo non‐wt Bcl I–homo wt rs6198] (0.7% RA vs. 4.7% controls; p = 0.042).
Conclusions: GR‐α and GR‐β polymorphisms are potentially associated with RA susceptibility. However, additional studies in larger and other ethnic groups of patients are needed to confirm the results of the present study.