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Both generalised and tissue-specific glucocorticoid resistance is increasingly being recognised. In one study, 1–2% of patients evaluated for adrenal disorders were glucocorticoid-resistant (Werner et al. 1992). At the molecular level, resistance to glucocorticoids is usually defined using specific markers. Some cells, such as lymphocytes, exhibit a very clear phenotypic change in response to glucocorticoids, enabling this to be used as a marker of glucocorticoid action (Kaspers et al. 1994). In most cells, however, changes in target gene expression are used. Either endogenous or transfected genes can be used; however, endogenous genes are often subject to tissuespecific regulation, and measurement of the steady-state mRNA level is an insensitive measure of glucocorticoid action. Transfection of short, carefully defined sequences of glucocorticoid-regulated DNA linked to a suitable reporter gene (Fig. 1) enables small differences in the EC₅₀ and V_max values of glucocorticoid action to be confidently measured (Ray et al. 1994b). Typically, positively

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				J. A. Ellison, L. Patel, D. W. Ray, and P. E. Clayton Hypothalamic-Pituitary-Adrenal Function and Glucocorticoid Sensitivity in Atopic Dermatitis Pediatrics, April 1, 2000; 105(4): 794 - 799. [Abstract] [Full Text]