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      Letter to the Editor: “Glucocorticoid Resistance in Premature Adrenarche and PCOS: From Childhood to Adulthood”

      letter
      Author(s): 1 , 2
      Publication date (Electronic):
      Journal: Journal of the Endocrine Society
      Publisher: Oxford University Press

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          Abstract

          The conclusion of Panayiotopoulos et al. that glucocorticoid resistance accounted for 57% to 67% of their premature adrenarche and polycystic ovary syndrome cases cannot be accepted from the data presented. This is because proper validation of their method for determining glucocorticoid sensitivity is not presented. Furthermore, the method seems insensitive to physiologic glucocorticoid concentrations.

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          Premature adrenarche--normal variant or forerunner of adult disease?

          N Potau, P Saenger, J DiMartino-Nardi … (2000)
          Adrenarche is the puberty of the adrenal gland. The descriptive term pubarche indicates the appearance of pubic hair, which may be accompanied by axillary hair. This process is considered premature if it occurs before age 8 yr in girls and 9 yr in boys. The chief hormonal product of adrenarche is dehydroepiandrosterone (DHEA) and its sulfated product DHEA-S. The well documented evolution of adrenarche in primates and man is incompatible with either a neutral or harmful role for DHEA and implies most likely a positive role for some aspect of young adult pubertal maturation and developmental maturation. Premature adrenarche has no adverse effects on the onset and progression of gonadarche in final height. Both extra- and intraadrenal factors regulate adrenal androgen secretion. Recent studies have shown that premature adrenarche in childhood may have consequences such as functional ovarian hyperandrogenism, polycystic ovarian syndrome, and insulin resistance in later life, sometimes already recognizable in childhood or adolescence. Premature adrenarche may thus be a forerunner of syndrome X in some children. The association of these endocrine-metabolic abnormalities with reduced fetal growth and their genetic basis remain to be elucidated.
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            Determination of the source of androgen excess in functionally atypical polycystic ovary syndrome by a short dexamethasone androgen-suppression test and a low-dose ACTH test.

            Elizabeth Littlejohn, Hannah R Rosenfield, Kristen Wroblewski … (2011)
            Polycystic ovary syndrome (PCOS) patients typically have 17-hydroxyprogesterone (17OHP) hyperresponsiveness to GnRH agonist (GnRHa) (PCOS-T). The objective of this study was to determine the source of androgen excess in the one-third of PCOS patients who atypically lack this type of ovarian dysfunction (PCOS-A). Aged-matched PCOS-T (n= 40), PCOS-A (n= 20) and controls (n= 39) were studied prospectively in a General Clinical Research Center. Short (4 h) and long (4-7 day) dexamethasone androgen-suppression tests (SDAST and LDAST, respectively) were compared in subsets of subjects. Responses to SDAST and low-dose adrenocorticotropic hormone (ACTH) were then evaluated in all. Testosterone post-SDAST correlated significantly with testosterone post-LDAST and 17OHP post-GnRHa (r = 0.671-0.672), indicating that all detect related aspects of ovarian dysfunction. An elevated dehydroepiandrosterone peak in response to ACTH, which defined functional adrenal hyperandrogenism, was similarly prevalent in PCOS-T (27.5%) and PCOS-A (30%) and correlated significantly with baseline dehydroepiandrosterone sulfate (DHEAS) (r = 0.708). Functional ovarian hyperandrogenism was detected by subnormal testosterone suppression by SDAST in most (92.5%) PCOS-T, but significantly fewer PCOS-A (60%, P< 0.01). Glucose intolerance was absent in PCOS-A, but present in 30% of PCOS-T (P < 0.001). Most of the PCOS-A cases with normal testosterone suppression in response to SDAST (5/8) lacked evidence of adrenal hyperandrogenism and were obese. Functional ovarian hyperandrogenism was not demonstrable by SDAST in 40% of PCOS-A. Most of these cases had no evidence of adrenal hyperandrogenism. Obesity may account for most hyperandrogenemic anovulation that lacks a glandular source of excess androgen, and the SDAST seems useful in making this distinction.
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              The pharmacokinetics of single high doses of dexamethasone in cancer patients.

              Emer Brady, Jonathan Rosenblum, G Sartiano … (1986)
              We have given single high doses of dexamethasone phosphate by intravenous infusion as an antiemetic to 15 cancer patients receiving regimens containing cisplatin and/or doxorubicin. The patients received graded doses of dexamethasone phosphate, in the range 40-200 mg, dependent upon nausea and vomiting scores, during up to three consecutive cycles of cancer chemotherapy. Plasma and urine concentrations of dexamethasone (dexamethasone alcohol) were measured by HPLC. The plasma concentration - time data were described by an open two-compartment model. The pharmacokinetic variables were independent of the dose of dexamethasone over the range studied. The terminal half-time was 4.0 +/- 0.4 h and the total body clearance was 3.5 +/- 0.4 ml X min-1 X kg-1. The volume of the central compartment and the total apparent volume of distribution were 0.23 +/- 0.03 and 1.0 +/- 0.1 l X kg-1 respectively. Approximately 8% of the dose was excreted into the urine as dexamethasone.
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                Author and article information

                Contributors
                Robert L Rosenfield:
                ORCID: http://orcid.org/0000-0001-8043-5693
                Journal
                Journal ID (nlm-ta): J Endocr Soc
                Journal ID (iso-abbrev): J Endocr Soc
                Journal ID (publisher-id): jes
                Title: Journal of the Endocrine Society
                Publisher: Oxford University Press (US )
                ISSN (Electronic): 2472-1972
                Publication date Collection: 01 January 2021
                Publication date (Electronic): 07 November 2020
                Publication date PMC-release: 07 November 2020
                Volume: 5
                Issue: 1
                Electronic Location Identifier: bvaa163
                Affiliations
                [1 ] The University of Chicago, Pritzker School of Medicine, Departments of Medicine and Pediatrics, Section of Endocrinology, Metabolism, and Diabetes , Chicago, Illinois
                [2 ] The University of California, San Francisco, Pediatric Endocrinology , San Francisco, California
                Author notes
                Correspondence : Robert L. Rosenfield, MD, University of Chicago, Chicago, IL 60637-1470, USA; or University of California, San Francisco, CA 94143, USA. E-mail: robros@ 123456peds.bsd.uchicago.edu .
                Author information
                http://orcid.org/0000-0001-8043-5693
                Article
                Publisher ID: bvaa163
                DOI: 10.1210/jendso/bvaa163
                PMC ID: 7747361
                SO-VID: b76c329a-63cd-4ba7-a981-4ab00a8143c7
                Copyright © © The Author(s) 2020. Published by Oxford University Press on behalf of the Endocrine Society.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com.

                History
                Date received : 18 September 2020
                Date: 02 October 2020
                Date: 18 December 2020
                Related
                Page count
                Pages: 2
                Categories
                Subject: Letter to the Editor
                Subject: AcademicSubjects/MED00250

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