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From the Clinical Research Centers |
Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, State University of New York Health Science Center, Syracuse, New York 13210
Address all correspondence and requests for reprints to: David H. P. Streeten, Department of Medicine, SUNY Health Science Center, 750 East Adams Street, Syracuse, New York 13210.
Repeatedly normal cortisol suppressibility by dexamethasone in 2
patients with Cushings disease led to the present study of the
prevalence of this phenomenon in 58 patients with otherwise
incontrovertible evidence of Cushings disease. Because as many as
23% of these patients manifested this phenomenon, we investigated the
suppressibility of plasma ACTH: 1) during iv infusion of
hydrocortisone, after a priming dose (7 mg), at 3 mg/h in 8 patients
and 8 normal controls; and 2) for 2 h, after oral hydrocortisone,
0.25 mg/kg, in 13 patients and 16 controls. The data showed invariable
suppression of plasma ACTH to
10 pg/mL (
2.2 pmol/L) after 120 min
of the infusion or at 90 min after oral hydrocortisone in 16 fasting
normal subjects given oral hydrocortisone between 0800 and 0830 h.
Plasma ACTH exceeded 10 pg/mL (2.2 pmol/L) at the same times in 14/14
patients with active Cushings disease, including 3 patients whose
cortisol suppressibility by dexamethasone had been misleadingly normal
and in 4/7 patients with intermittent hypercortisolism. Occasional
variations in plasma cortisol elevations after the oral dose require
that plasma cortisol concentration be monitored at 60 min after the
oral hydrocortisone dose, because the present evidence supports the
validity of the conclusion that a plasma ACTH concentration below 10
pg/mL excludes Cushings disease only when plasma cortisol
concentration at 60 min lies between 16 and 38 µg/dL. Further
evaluation of ACTH suppressibility by cortisol would be worthwhile, to
confirm its potential value in facilitating positive diagnosis of
Cushings disease when dexamethasone suppressibility seems misleading.
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