Dhp. Streeten et al., THE POTENTIAL FOR SERIOUS CONSEQUENCES FROM MISINTERPRETING NORMAL RESPONSES TO THE RAPID ADRENOCORTICOTROPIN TEST, The Journal of clinical endocrinology and metabolism, 81(1), 1996, pp. 285-290
Despite unequivocal published evidence that patients with subnormal hy
pothalamic-pituitary-adrenal (HPA) function may respond normally to AC
TH, such normal results are still considered reliable indications of u
nimpaired HPA function. This view was tested in four patients with cli
nical features suggesting corticotropin deficiency, in whom cosyntropi
n (0.25 mg, iv) raised serum cortisol above 560 nmol/L (20 mu g/dL) at
1 h. All four patients had subnormal responses to metyrapone and exce
llent persistent improvement during subsequent glucocorticoid therapy.
Serum cortisol concentrations 1 h after cosyntropin treatment in thes
e patients closely resembled cortisol concentrations 1 h after uncompl
icated cholecystectomy in six other patients. However, the rapid ACTH
test in the patients with hypopituitarism failed to indicate whether m
ore prolonged stimulation by ACTH or their endogenous stress would sti
mulate the normal continuing rise in serum cortisol, which reached 135
8 +/- 170 nmol/L (+/- SE) 5 h alter the incision in the cholecystectom
ized patients. As the three hypocorticotropic patients who were recogn
izably stressed had unstressed serum cortisol levels despite persisten
t adrenocortical reserve (shown by their ACTH responses) and recovered
during glucocorticoid therapy, the ACTH test, if interpreted to indic
ate normal HPA function, would probably have had disastrous consequenc
es. We conclude that a normal response to the rapid ACTH test can be d
angerously misleading, particularly in incomplete ACTH deficiency stat
es.