ACTH RESISTANCE IN ACROMEGALY

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Abstract
Eosinopenic response has been criticized clinically and experimentally since its widespread adoption as a criterion for evaluation of adrenocortical function (1–4). Investigating the eosinopenic response in neuroendocrine disorders, we found either resistance or a paradoxical reaction to subcutaneous insulin, epinephrine, and intramuscular ACTH in acromegalic patients (5). These findings could not be solely explained by the concept of diminished adrenocortical reserve, in view of the generally accepted consideration that there is hyperplasia of the adrenal cortex in acromegaly (6). We then attempted to test the same subjects by intravenous infusion of ACTH and found that the circulating eosinophils responded normally in almost all cases. Therefore, the phenomenon observed following intramuscular injection may be due to local inactivation of ACTH and designated properly as “resistance.” This termoriginated with Forsham et al. (7, 8), who found that repeated intramuscular administration caused increasing unresponsiveness to the hormone; nevertheless, ACTH-resistant subjects were found to respond normally to intravenous administration of the same material.