Grzanka Alicja, Rogala Barbara
Clinical Department of Internal Diseases, Allergology and Clinical Immunology Medical University of Silesia, Katowice, Poland.
Arch Immunol Ther Exp (Warsz). 2003;51(5):327-34.
Glucocorticoid (GCs) hormones are widely used in the treatment of bronchial asthma. However, not all aspects of their pharmacological effects are well understood as yet. It is know that the effects of GCs are mediated through GC receptors (GCRs). We sought to evaluate the effect of short-term and chronic GC therapy on GCR number in peripheral blood lymphocytes, the relationship between GCR number and cortisol concentrations in asthma patients treated with GCs as well as the response to GC therapy in various pictures of this disease. Sixty-nine patients with bronchial asthma were investigated. Thirty-five of them had received steroid therapy: 18 patients for 1 to 15 years and 17 patients for 13 days after a prior 3-month discontinuation of steroid treatment. The control group consisted of 28 healthy, age-matched volunteers. GCR numbers were determined using tritriated dexamethasone as a ligand. The scatchard method was applied to calculate the maximal specific binding and the dissociation constant. The number of receptor sites per lymphocyte was calculated. Cortisol was measured by radioimmunoassay. Lymphocyte GCR numbers in patients with bronchial asthma who were not treated with steroids, did not differ from age-matched healthy persons (means 8115+/-812 and 7905+/-832). A significant decrease in receptor number was seen in patients receiving steroid therapy (mean 4331+/-1041). There was also a significant difference in receptor number between the groups with short-course (mean 3741+/-549) and chronic steroid therapy (mean 4885+/-1095). The number of GCRs did not correlate with age, sex, clinical state or serum cortisol concentration in either group.
