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The occurrence of glucocorticoid dependent or refractory disease courses is a major clinical problem not only in inflammatory bowel disease (IBD) but also in other chronic inflammatory conditions such as asthma and rheumatoid arthritis.1 It would be of great value if the responsiveness of patients to glucocorticoids could be evaluated before their administration to avoid ineffective treatment.
The response to steroids is mediated by the glucocorticoid receptor (hGR) of which two isoforms exist, hGRα and hGRβ. Both are products of alternative splicing of the primary transcript of GR messenger RNA (mRNA).2 The hGR isoforms differ in their carboxyl termini: whereas hGRα is ligand activated, modulating the expression of glucocorticoid responsive genes by binding to specific glucocorticoid response elements (GREs), hGRβ does not bind glucocorticoids and is transcriptionally inactive. Therefore it has been suggested that hGRβ might be an endogenous inhibitor of glucocorticoid action and a negative regulator determining glucocorticoid sensitivity in the target tissues.3
In 2000 Honda and coworkers published a study indicating that hGRβ mRNA was detectable in peripheral blood …
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