@article{67debcc4976247929bc948850103585c,
title = "Androgen production in boys with sexual precocity and congenital adrenal hyperplasia",
abstract = "Plasma testosterone and testosterone production rates were studied in young boys with idiopathic sexual precocity and congenital adrenal hyperplasia (CAH). Four males with CAH and one with idiopathic sexual precocity underwent physiologic studies to delineate the source of testosterone. In young boys with idiopathic sexual precocity and CAH, plasma testosterone was increased over prepubertal levels although the increase was greater in the one patient with idiopathic sexual precocity than in those with CAH. Testosterone production rates (TPR) were increased to the same degree in both conditions. Physiologic studies of stimulation and suppression of gonads and adrenals delineate the glandular source of testosterone and provide a means of defining therapeutic measures of suppressing testosterone production.",
author = "Levine, {Lenore S.} and New, {Maria I.} and Paula Pitt and Peterson, {Ralph E.}",
note = "Funding Information: Testosterone production rates (TPR) determined from a urinary metabolitel and plasma testosterone2 were determined by methods previously described. Urinary 17-ketosteroids, 17-hydroxycorticosteroids, and pregnanetriol were measured by methods3 previously reported. The periods of study described in the illustrations and tables were as follows: base-line: control period, no medication; ACTH: 40 U ACTH i.v. for 8 hr; Glucocorticoid suppression [Meticorten (prednisone) : 15 mg/day or 7.5 mg orally daily for 3 mo; Decadron (dexamethasone) : z mg or more orally daily for 3 days or more]; Norlutin (norethindrone): 30 mg orally daily for 3 days; CGT: chorionic gonadotropin 4000 LJ i.m. daily for 3 days; when indicated, CGT or No&tin was administered simultaneously with From the Departments of Pediatrics and Medicine, Cornell University Medical College, New York, N.Y. Received for publication October 12, 1971. Supported in part by USPHS Research Grants HD 72 and AM 53.50 and USPHS Research Career Award K6-AM-14-241, National Institutes of Health; Health Research Council of the City of New York Career Scientist Award l-481; and NIH Division of Medical Sciences Grant RR4i{\textquoteright}. Lenore S. Levine, M.D.: Clinical Assistant Professor of Pediafrics, Department of Pediatrics, Cornell University Medical College, New York, N.Y. Maria I. New, M.D.: Professor of Pediatrics, Department of Pediatrics, Cornell University Medical College, New York, N.Y. Paula Pitt, M.D.: Research Assistant, Endocrine Research Unit, Cancer Institute, Melbourne, Australia. Ralph E. Peterson, M.D.: Professor of Medicine, Department of Medicine, Cornell University Medical College, New York, N.Y. The following trivial names and compounds are used in the text: Meticorten (predni-sane\ : 17~~2. x-Dihvdroxvpregna-1, 4-diene, 3, II, 2O-trione; Decadron (dexamethasonel : 9-Fluoro-1X/3, 17, 21-trihydroxy-%a-methyl-pregna-1, 4-diene-3, 20-dione; Norlutin (norethindrone) : 17-Hydroxy-19-nor-17czpregn-4-en-2o-yn+one; Provera (medroxyprogesterone) : 17-Hydroxy-6a-methylpregn-4-ene, 3, to-dione; and Depo-provera (medroxyprogesterone acetate) : 17a-Hydroxy-6n-methylprogesterone acetate.",
year = "1972",
month = may,
doi = "10.1016/0026-0495(72)90057-1",
language = "English",
volume = "21",
pages = "457--464",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "5",
}