Abstract
This chapter discusses the influence of steroid production on serum albumin in Cushing's syndrome In Cushing's syndrome, the impaired ability to compensate for increased catabolism in less active tissues would produce the protein-wasting seen in osteoporosis, muscle atrophy, thin skin, and diminished fibrous tissue repair. In all cases, the diagnosis was made on the basis of clinical observations and laboratory findings using the double-isotope method for plasma cortisol determination, dexamethasone suppression test, and cortisol secretion rates. Excess glucocorticoids were presumed to have produced accelerated albumin catabolism, partly compensated for by increased synthesis. Only the case with operated adenoma shows normal results. Chemical treatment, either by the inhibition of adrenocorticotropic hormone ( ACTH )-production or by the influence on steroid synthesis, does not have sufficient inhibiting influence on albumin catabolism, as shown by biological half-life and by the absolute turnover rate of 131 I human serum albumin.
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