Charles A. Nugent

Circadian Rhythm of Plasma Aldosterone Concentration in Patients with Primary Aldosteronism

Plasma aldosterone, cortisol, and renin activity were measured in nine recumbent patients with hyperaldosteronism, including seven with adenomas, one with idiopathic hyperplasia, and one with glucocorticoid suppressible hyperplasia. All had peak values of plasma aldosterone concentration from 3 a.m. to noon and lowest values at 6 p.m. or midnight. This rhythm was similar to the circadian pattern of plasma cortisol in the same patients. When these data were normalized to eliminate the wide variation in ranges of plasma aldosterone and cortisol between individuals, there was an excellent correlation (r = + 0.87, P < 0.005) between the two hormones. In contrast, plasma aldosterone concentrations did not correlate with plasma renin activity before or after normalization of data. Short term suppression of ACTH by administration of dexamethasone eliminated the circadian variation of plasma aldosterone in both patients with hyperplasia and in four of five patients with adenomas, while it markedly altered the rhythm in the fifth. Similar doses of dexamethasone were administered to four normal subjects and did not flatten the circadian rhythm of plasma aldosterone. These data suggest that patients with primary aldosteronism have a circadian rhythm of plasma aldosterone mediated by changes in ACTH.

Cushing's syndrome caused by bronchial adenomas

Abstract Two cases of Cushings syndrome caused by ACTH secreting bronchial adenomas are reported. In one ACTH was demonstrated in the tumor by bioassay and in the other by radioimmunoassay. In one patient the adenoma was found at autopsy, in the other the adenoma was discovered at the time Cushings syndrome was recognized. In this latter patient Cushings syndrome disappeared after resection of the tumor. Careful search for such a tumor should be made in every patient thought to have pituitary Cushings syndrome in order to select the most appropriate therapy. Presently available functional studies such as dexamethasone suppression and the response to metyrapone do not distinguish between these patients and those with Cushings syndrome due to excessive pituitary secretion of ACTH.

Laboratory tests in the diagnosis of hyperparathyroidism in hypercalcemic patients.

Abstract The results of tests of serum phosphate concentration or urine calcium or phosphate excretion, either under controlled conditions or after infusion of calcium or phosphate, were examined f...

Steroid laboratory tests in the diagnosis of Cushing's syndrome☆

Abstract The best steroid tests currently available for identifying patients with Cushings syndrome are the low dose dexamethasone suppression test with determination of urinary 17-hydroxycorticosteroid (17-OHCS) excretion and the single dose dexamethasone suppression test with determination of plasma 17-OHCS concentration. The results of steroid laboratory tests may be helpful in suggesting the lesion responsible for Cushings syndrome but no single test can be used to identify the cause with great confidence. (1) The high dose dexamethasone suppression test is best for guiding the physician in selecting therapy. In 82 per cent of the patients with Cushings syndrome due to adrenal hyperplasia from excessive pituitary secretion of ACTH unassociated with a pituitary tumor, urinary 17-OHCS excretion decreased to less than half the control value with this test. Suppression of this degree is very uncommon in patients with adrenal tumors. (2) Urinary 17-OHCS excretion increased with metyrapone administration in patients with Cushings syndrome caused by adrenal hyperplasia not associated with tumors whereas this response was infrequent in patients with other causes of Cushings syndrome. (3) In patients with Cushings syndrome, urinary 17-ketosteroids (17-KS) were elevated to values at least four times the upper limit of normal in 52 per cent of the patients with adrenal carcinoma, in 15 per cent of the patients with extrapituitary ACTH-secreting tumors and in only 3 per cent of the patients with adrenal hyperplasia not associated with tumor. Urinary 17-KS levels were normal or low in 69 per cent of the patients with adrenal adenomas and in only 10 per cent of the patients with adrenal carcinomas.

Glucocorticoid toxicity: Single contrasted with divided daily doses of prednisolone

Abstract The present study was designed to investigate whether single daily doses of prednisolone cause less glucocorticoid toxicity than divided daily doses while providing equal relief of the signs and symptoms of rheumatoid arthritis. By the use of placebo tablets, the nature of the dosage regimens was concealed from patients and physicians. The number of tablets taken was estimated by supplying a known number in excess of the amount prescribed and counting the tablets returned at each monthly visit. Large discrepancies were found between the dose of prednisolone advised and that taken by many of the patients. An equivalent degree of relief of the signs and symptoms of rheumatoid arthritis was attained on both dosage regimens. Although the amount of prednisolone taken was 20 per cent larger on the single- than on the divided-dosage regimen, the difference was not statistically significant. No significant difference in glucocorticoid toxicity was found between patients on the single- and on the divided-dose regimens.

Does Hispanic Identify a Race?-Reply

Dr de Junco raises a valid point in calling our attention to the incorrect description of Hispanics as a separate race. We regret this error and acknowledge that another term such as ethnic group would have been more accurate.

Clinical Endocrinology: Theory and Practice,

Textbook of Endocrinology, edited by Robert H. Williams, MD, ed 5, 1,138 pp, 527 illus,

Diurnal Variation in Suppression of Adrenal Function by Glucocorticoids

28, WB Saunders Co, 1974. The massive volume, edited by Alex Labhart and authored mainly by endocrinologists working in Zurich, is well organized and comprehensive in scope. Each major section in the book has a brief historical outline followed successively by a description of the embryology, gross anatomy, histology, biochemistry, pharmacology, physiology, and clinical aspects of the subjects. The diagrams and tables are well selected and the pictures illustrating clinical problems are outstanding. The detailed table of contents (23 pages long, with 72 items on separate lines on a typical page) makes it an easy book to use. The index and bibliographies are thorough. In addition to the discussion of general aspects of endocrinology and the usual hormone-secreting glands, there are separate sections on tissue hormones, growth and development, hormones of the thymus, and the