Elevated glucocorticoid receptor concentrations before and after glucocorticoid therapy in peripheral mononuclear leukocytes of patients with atopic dermatitis
| Autor: | Otto P. Hornstein, Norbert Wodarz, Peter Riederer, Johannes Kornhuber, H. U. Koch, Rainer Rupprecht, M. Rupprecht |
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| Rok vydání: | 1991 |
| Předmět: |
Adult
Contraceptives Oral/pharmacology Male medicine.medical_specialty Hydrocortisone Adolescent medicine.drug_class 610 Medizin Dermatology Leukocytes Mononuclear/chemistry 3' 5'-Cyclic-AMP Phosphodiesterases/physiology Hydrocortisone/blood Methylprednisolone Peripheral blood mononuclear cell Dexamethasone Dermatitis Atopic Receptors Glucocorticoid Glucocorticoid receptor Internal medicine Cyclic AMP medicine Humans Methylprednisolone/therapeutic use Receptor ddc:610 business.industry Cyclic AMP/physiology Dexamethasone/therapeutic use Endocrinology Dermatitis Atopic/immunology 3' 5'-Cyclic-AMP Phosphodiesterases Leukocytes Mononuclear Corticosteroid Female business Glucocorticoid Receptors Glucocorticoid/analysis Contraceptives Oral medicine.drug |
| DOI: | 10.5283/epub.16341 |
| Popis: | The number and affinity of glucocorticoid binding sites in peripheral mononuclear leukocytes of patients with atopic dermatitis (AD) and healthy controls were determined under baseline conditions and after a defined oral glucocorticoid treatment. Patients with AD (n = 15) exhibited significantly more glucocorticoid receptors (GR) per cell than the control group (n = 22), while the GR affinity did not differ. Methylprednisolone treatment resulted in a significant reduction of the GR sites per cell in the steroid-treated control group (n = 10) in contrast to the patients. The dissociation constant was not affected by methylprednisolone treatment in either group. In view of the therapeutic efficiency of glucocorticoids in AD and findings of abnormal cAMP and cAMP-phosphodiesterase activity, the elevated GR concentrations in AD lend support to the hypothesis of a compensatory GR upregulation due to an insufficient action of endogenous cortisol or to altered cAMP-induced GR expression. |
| Databáze: | OpenAIRE |
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