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Studies on Aldosterone, 17-Hydroxycorticosteroid, and 17-Ketosteroid Response to Corticotropin in Male Patients With Rheumatoid Arthritis

S. RICHARDSON HILL, JR., MD; ALEXANDER ULLOA, MD; WILLARD R. STARNES, MS; HOWARD L. HOLLEY, MD

Arch Intern Med. 1963;112(4):603-611.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The exact relationships between the secretory activity of the anterior pituitary-adrenal cortical system and the rheumatic disease states in man have not been completely delineated. Previous studies ¹ have shown that while the daily urinary excretion of 17-ketosteroids in patients with rheumatoid arthritis did not differ from that seen in normal subjects, the excretion of urinary 17-hydroxycorticosteroids was slightly diminished from the mean level observed in normal subjects, due to a lower output during the early morning hours. Although these mean urinary steroid values in patients with rheumatoid arthritis differed slightly from those found in normal subjects, they were not significantly different from those seen in patients with nonrheumatic chronic illnesses.

It has also been shown ^2,3 that glucocorticoid and mineralocorticoid hormones exert distinctly different effects on connective tissue; indeed the observed effects of these hormones on inflamed tissues may be opposite. A possible relationship between these two groups of . . . [Full Text PDF of this Article]

Author Affiliations
BIRMINGHAM, ALA

Professor, Department of Medicine, and Dean, University of Alabama Medical College (Dr. Hill); formerly Trainee of the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, USPHS, Instructor in Medicine, University of Alabama Medical Center, present address: Trujillo, Peru (Dr. Ulloa); Chief Biochemist of the Endocrine and Metabolic Laboratories, Birmingham Veterans Administration Hospital (Mr. Starnes); Professor and Director, Rheumatic Disease Division, Department of Medicine, University of Alabama Medical Center, and Birmingham Veterans Administration Hospital (Dr. Holley).

From the Department of Medicine and University Hospital, University of Alabama Medical Center, and the Medical Service, Veterans Administration Hospital.

Footnotes
Received for publication Dec 14, 1962; accepted May 6, 1963.

This investigation was supported in part by funds from grants No. A-1625 and A-3555 from the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, USPHS, the John R. Irby Fund, and the Upjohn Company.

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