SummaryUp to 20% of Crohn's disease (CD) patients respond poorly to glucocorticoids (GC). A product of an alternative splicing of the glucocorticoid receptor (GR) premRNA, GR b , may play a role as a dominant inhibitor of the glucocorticoid response. Increasing evidence suggests that inflammatory cytokines such as interleukin (IL)-18 alternate the splicing of the primary transcript between the two isoforms GR b and GR a in hGR gene of CD patients. The aim of this study is to assess the expression of GR a and GR b in patients with CD and to look for a possible correlation between these receptors and the response to glucocorticoid treatment. Forty-two CD patients and 17 healthy volunteers were studied. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was performed using real-time PCR techniques. Serum IL-18 protein levels were measured by enzyme-linked immunosorbent assay (ELISA). The amount of hGR a -mRNA in patients in remission was significantly lower than in controls ( P < 0·05). The amount of hGR b -mRNA was significantly higher in GC-resistant patients in the active stage of disease compared with all other groups ( P < 0·05). Patients in the active stage of the disease had higher levels of IL-18 than patients in remission and both had higher levels than controls ( P < 0·05). The amounts of IL-18 were directly correlated with the amount of hGR b mRNA in GC-resistant patients with an active disease. High levels of hGR b might be connected to GC resistance. IL-18 might participate in the alternative splicing of the hGR preliminary mRNA of CD patients. The results support the theory that augmented hGR b mRNA expression level in PBMC is connected with GC-resistance of CD patients.
SummaryA case of lymphocytic lymphoma in a patient with coincidental sarcoidosis is described, and the possible relationship of the two conditions is discussed. A revised set of diagnostic criteria is proposed to overcome previous difficulties encountered in validating such dual pathology.
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