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Naltrexone Does Not Affect Adrenal Steroidogenesis in Women with Hirsutism/Oligomenorrhea

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Naltrexone Does Not Affect Adrenal Steroidogenesis in Women with Hirsutism/Oligomenorrhea Henry Ford Hospital Medical Journal Volume 35 Number 4 Article 7 12-1987 Naltrexone Does Not Affect Adrenal Steroidogenesis in Women with Hirsutism/Oligomenorrhea Jeffrey A. Jackson Thomas J. Wincek Jose F. Pliego Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Jackson, Jeffrey A.; Wincek, Thomas J.; and Pliego, Jose F. (1987) "Naltrexone Does Not Affect Adrenal Steroidogenesis in Women with Hirsutism/Oligomenorrhea," Henry Ford Hospital Medical Journal : Vol. 35 : No. 4 , 194-197. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol35/iss4/7 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Naltrexone Does Not Affect Adrenal Steroidogenesis in Women with Hirsutism/ Oligomenorrhea Jeffrey A. Jackson, MD,* Thomas J. Wincek, MD, PhD,^ and Jose F. PHego, MD^ We studied the effects ofthe oral opiate receptor antagonist naltrexone on basal and ACTH-stimulated adrenal steroid levels in six women with hirsutism/oligomenorrhea and preexisting elevation of serum dehydroepiandrosterone sulfate. One ofthe stx patients met the criteria for partial 3-^-hydroxysteroid dehydrogenase deficiency. No statistical differences were detected in steroid levels or ratios before and after 14 days of 50 mg/day of naltrexone. Thus, we find no supportfor the hypothesis tfiat opioid peptides acting through opiate receptors (predominantly p. subtype) modulate the abnormal adrenal androgen secretion seen in these women with hirsutism/oligomenorrhea. (Henry Ford Hosp Med J 1987:35:194-7) onsiderable clinical and experimental evidence has sug­ mg orally, was given daily for 14 days (28 days for patient 2 Cgested that a non-ACTH pituitary factor may control only), with the final dose at 6 AM on the final day of ACTH adrenal androgen secretion (1-4). p-endorphin, a proopio- testing. melanocortin-derived opioid peptide, has been considered Serum gonadotropins (Leeco Diagnostics, Southfield, Ml), as a possible modulator of adrenal androgen synthesis (1). Ab­ prolactin (Serono Diagnostics, Inc, Randolph, MA), estradiol normal adrenal androgen levels occur frequently in patients with (Radioassay Systems, Carson, CA), testosterone and DHEA-S polycystic ovary syndrome (5-8), and elevated p-endorphin (Diagnostic Products Corp, Los Angeles, CA), and plasma levels have also been reported in this syndrome (9,10). Conse­ ACTH (edetic acid sample separated and stored at — 20°C prior to folficle-sl quently, we studied the effects of an oral opiate receptor antag­ to assay—Radioassay Systems) were measured by specific ra­ ovulation o onist, naltrexone, on basal and ACTH-stimulated adrenal dioimmunoassays prior to ACTH stimulation. Serum DHEA, two subjeci steroid levels in a group of women with hirsutism/oligomenor­ 17-hydroxypregnenolone, 17-hydroxyprogesterone, andro- respectively rhea and preexisting elevation of serum dehydroepiandrosterone stenedione (Endocrine Sciences, Tarzana, CA), and Cortisol Initial AC sulfate (DHEA-S). (Diagnostic Products Corp) were measured by specific radio­ partial defei immunoassays both before and after ACTH stimulation. Serum (Iroxyproges transaminases were measured by automated analyzer proposed c Materials and Methods Mean hormonal values prenaltrexone and postnaltrexone liydrogenase Six patients, aged 22 to 34, with at least three months of un­ were compared statistically by using paired t tests. The confi­ nenolone am treated hirsutism [mean Ferriman-Gallwey (11) index 10], prior dence intervals for correlations among various hormonal levels hydroxypro^ oligomenorrhea by history, and previously determined eleva­ and ratios were examined for indications of relationships. P-val­ •^HEA to an tions of serum DHEA-S (mean 4,646 ± 1,300 ng/mL; normal ues greater than 0.05 (one-tailed) were considered not statis­ 820 to 3,380 ng/mL) participated in the study after giving in­ tically significant. Mean values are expressed as mean ± SD- formed consent (Table I). All patients had previously demon­ strated suppressibility of serum DHEA-S by dexamethasone or prednisone and/or normal adrenal computed tomography to ex­ Results clude androgen-producing adrenal neoplasms. None had a his­ Baseline hormonal concentrations in the six subjects are tory of liver disease or narcotic abuse. Testing was performed in shown in Table 1. Prenaltrexone means (Table 2) for serum the early follicular phase for the patients who had a regular cycle DHEA-S and testosterone were above the reference range. All at the time of the study (patients 1 and 6); the other four subjects patients were normoprolactinemic; four had ratios of luteiniz'"^ were initiated randomly. Effective barrier contraception was rec­ ommended throughout the study period. Submitted for publication: April 30, 1987. Prenaltrexone and postnaltrexone blood sampling was Accepted for publication: June 5, 1987. performed by indwelling catheter between 8 AM and 9 AM and •Formerly Divisionof Endocrinology, Henry Ford Hospital. Currently tDivision ofb , crinology. Scott & White Ciinie, Scott & White Memorial Hospital. Scon. Sherwood one hour after intravenous administration of 0.25 mg of syn­ Brindley Foundation, Texas A .& M University College of Medicine. Temple. TX. theric I-24-ACTH (Cortrosyn™, Organon, West Orange, tDepartment of Obstetrics and Gynecology, Scott & White Clinic, Temple. TX- Address correspondence to Dr. Jackson, Division of Endocrinology, Scott & NJ). Naltrexone (Trexan™, Du Pont, Wilmington, DE), 50 Clinic, Scott & White Memorial Hospital. 2401 S 31st St, Temple, TX 76508. 194 Henry Ford Hosp Med J—Vol 35, No 4, 1987 Naltrexone and Steroidogenesis in Hirsutism— Jackson I Hti^p^^^ Hospi Table 1 ith Clinical Data and Baseline Hormonal Levels Age Height Weight Hirsutism ACTH PRL Patient (year) (cm) (kg) Index* Menses (pg/mL) (ng/mL) 1 23 158 55.7 7 Regular 32 13 2 23 158 73.0 9 Irregular 50 14 3 22 173 86.4 11 Irregular 58 11 4 22 163 100.5 1 1 Irregular 51 15 5 25 158 55.7 14 Irregular 37 10 6 34 170 83.2 9 Regular 28 15 Mean ± SD 43 ± 12 13 ± 2 Reference range < 100 < 16 Estradiol DHEA-S Testosterone 17-Preg 17-Prog DHEA Androstenedione Patient (pg/mL) (ng/mL) (ng/mL) (ng/mL) (ng/mL) (ng/mL) (ng/mL) 1 124t 3,663t 0.8t 4.3t 0.6 8.3t 2.9t 2 309t 3,899t 1.2t 3,2 1.9* 10.8t 5.0t 3 I48§ 4,286t 0.9t 3.4 1.4§ 5.6 3.0t 4 64 5,180t 1.2t 1.4 0.5 2.4 2.4 5 86 3,016 0.9t 1.1 I.6t 5.4 1.5 6 14t 3,091 0.8t 0.6 0.2 5.5 1.7 Mean ± SD 144 ± 119 3,856t ± 808 l.ot ± 0.2 2.3 ± 1.5 1.0 ± 0.7 6.3 ± 2.9 2.7 ± 1.3 Reference range: 25-12011 820-3,380 0.2-0.7 0.2-3.6 0.2-0.711 1.6-8.0 0.9-2.8 60-170§ 0.4-2.9§ *Ferriman-Gallwey index (11). tOutside reference range. tMid-cycle .spontaneous ovulation. for patient 2 §Luteal phase, IIFoilicular phase. lay of ACTH Note: PRL = prolacttn. DHEA-S ~ dehydroepiandrosterone sulfate, 17-Preg - 17-hydroxypregnenolone, and 17-Prog = 17-hydroxyprogesterone. ithfield, Ml), IA), estradiol and DHEA-S , and plasma : -20T prior to follicle-Stimulating hormone greater than 2.0. Coincidental controls) (12). All patients had normal Cortisol responses to )y specific ra- ovulation occurred just prior to and on day 1 of testing in ACTH. erum DHEA, two subjects who had oligomenorrhea (patients 3 and 2, Postnaltrexone means for ACTH, prolactin, gonadotropins, :rone, andro- respectively). and all of the steroid levels and ratios measured (Table 2) did not , and Cortisol Initial ACTH stimulation failed to uncover any patients with differ significantly from prenaltrexone values. Correlation ma­ pecific radio- partial defects in 21-hydroxylase activity (stimulated 17-hy­ trix examination showed no statistically significant relationships ilation. Serum droxyprogesterone levels. Table 2). Patient 4 met all previously between estradiol and A'-steroid levels or A-''-steroid A''-steroid ^zer. proposed criteria for suspected 3-p-hydroxysteroid de­ ratios. ostnaltrexone hydrogenase deficiency (Figure; stimulated 17-hydroxypreg­ Naltrexone treatment caused no alterations in liver trans­ its. The confi- nenolone and DHEA levels, and 17-hydroxypregnenolone to 17- aminase levels. Four subjects experienced mild nausea without •rmonal levels hydroxyprogesterone, 17-hydroxypregnenolone to Cortisol, and vomiting in the first three to seven days of therapy; prenaltrexone anships. P-vai- DHEA to androstenedione ratios > 2 SD above those of normal and postnaltrexone body weights did not differ statistically. ;red not statis- mean ± SD. X subjects ate Table 2 ; 2) for serum Baseline and ACTH-Stimulated Steroid Levels Before and After Naltrexone nee range. Al Steroid* Before Naltrexonet After Naltrexonet sof luteiniziDS DHEA-S (ng/mL) 3,856 ± 808 (3,016-5,180) 3,856 ± 1,385 (2,290-6,396) NS Testosterone (ng/mL) 1.0 0.2(0.8-1.2) 0.9 ± 0.2 (0.6-1.1) NS 17-Preg (ng/mL) 2.3 1.5(0.6-4.3) 1.9 ± 1.4 (0.5-4.3) NS 17-Prog (ng/mL) 1.0 0.7(0.2-1.9) 0.8 ± 0.8 (0.4-2.4) NS DHEA (ng/mL) 6.3 2.9(2.4-10.8) 6.9 ± 2.3 (4.8-9.8) NS ,Uy Division of En* Androstenedione (ng/mL) 2.7 ± 1.3(1.5-5.0) 2.8 ± 1.5 (1.8-5.7) NS Scott, Sherwood «» Stimulated 17-Preg (ng/mL) 12.2 6.1(5.9-20.6) 11.0 ± 3.9 (7.7-17.6) NS Femple, TX. Stimulated Cortisol (fi.g/dL) 37.3 8.3(27.1-48.9) 36.1 ± 4.9 (30.4-42.1)NS Temple.
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