In four patients with Cushing's disease given the adrenocorticolytic agent o,p′DDD, the therapeutic objective of reducing cortisol secretion without producing aldosterone deficiency was achieved after several months of treatment. To avoid gastrointestinal intolerance, low doses (about 3 gm per day) were used. Patients with subnormal plasma 17-hydroxycorticosteroids were given dexamethasone, 0.5 mg daily, as a safeguard against glucocorticoid deficiency. Aldosterone secretion rates were normal or slightly elevated, and the patients adapted to sodium deprivation with virtually complete renal conservation of sodium. Electron microscopy revealed degenerative changes in the mitochondria of the zona fasciculata, with sparing of the zona glomerulosa. Plasma ACTH concentrations were originally elevated and remained so. Adrenal responsiveness to the infusion of ACTH was greatly reduced.
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Temple et al. (1969) studied this question.
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