Electron Microscopic investigation of crooke’s change in the pituitaries of patients with hypercorticism

Human pituitary corticotropins have unique morphologic markers: bundles of type-1 filaments, measuring approximately 70 A in width and representing cytokeratin. The extreme ring-like accumulation of type-1 filaments, known as Crooke's hyalinization, signals functional suppression of the corticotropins and occurs in endogenous and exogenous glucocorticoid excess, caused by ACTH-secreting pituitary adenoma, glucocorticoid secreting adrenocortical tumor, ectopic ACTH-syndrome and administration of pharmacologic doses of glucocorticoids. Cells of autonomous corticotroph adenomas usually do not show Crooke's hyalin change. A minority of these tumors, however, retains sensitivity to the negative feed-back effect of elevated blood glucocorticoid levels and display typical Crooke’s change.In the present study pituitary corticotropins in various phases of Crooke's hyalinization were investigated in patients with glucocorticoid excess of various origin, applying histology, immunocytochemistry, count of argyrophilic nucleolar organizer regions (AgNOR), and transmission electron microscopy.

Adrenals in Ectopic ACTH Syndrome

In Dr. Gilbert S. Omenn's1 otherwise excellent review of ectopic hormone syndromes associated with tumors in childhood we find the following sentence: "Completely characterized cases of ectopic ACTH syndrome have bilateral adrenal hyperplasia, normal pituitary basophils, positive assay for ACTH in the tumor, and failure of suppression of elevated plasma ACTH by dexamethasone." I have no personal experience with the ectopic ACTH syndrome in childhood, but in three cases seen in adults the basophils (more accurately, the ACTH-MSH cells among them), far from being normal, showed the expected profound Crooke's hyalinization characteristic of severe hypercortisolism.2