Clinical Perspective: What Do Addison and Cushing Tell Us About Glucocorticoid Action?

Abstract

This chapter is distinct from the others in its clinical subject matter. I will attempt to outline the major points of interest in glucocorticoids clinically. To aid the illustration in the evaluation of a patient with Cushing disease I have created a case study.

The effects of chronic glucorticoid stimulation on erythropoiesis in Cushing syndrome

“…These include species-specific differences in how murine and human proerythroblasts respond to GCs (5) and the nearubiquitous use of dexamethasone (Dex) and SCF in expanding proerythroblasts in vitro, giving rise to confounding effects (4). Endocrine disorders offer opportunities to study GC effects on in vivo erythropoiesis under conditions of constitutively active (Cushing's syndrome) or altogether absent (Addison's disease) GC/GRα activation (6). Hence it is surprising that only one publication has previou reported erythrocytosis (an increase in red blood cell mass) in one Cushing's patient with ACTH-secreting pituitary adenoma (7).…”

“… 4 Endocrine disorders offer opportunities to study the effects of glucocorticoids on in vivo erythropoiesis under conditions of constitutively active (Cushing syndrome) or altogether absent (Addison disease) glucocorticoid/GRα activation. 6 Hence it is surprising that only one publication has previously reported erythrocytosis (an increase in red blood cell mass) in one Cushing patient with an adrenocorticotropic hormone-secreting pituitary adenoma. 7 This is redressed in the study by Varricchio et al , who recruited a relatively large (n=13) cohort of Cushing syndrome patients with active hypercortisolemia (active-phase patients) and an equal number of eucortisolemic patients in remission following surgical removal of the pituitary adenoma (remission-phase patients).…”