Decreased inhibin B responses following recombinant human chorionic gonadotropin administration in normal women and women with polycystic ovary syndrome

To determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with polycystic ovary syndrome (PCOS) and in normal women. Prospective study. Academic medical center. Twenty women with PCOS and 16 normal women. Blood samples obt...

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Published in	Fertility and sterility Vol. 101; no. 1; pp. 275 - 279
Main Authors	Shayya, Rana F., Rosencrantz, Marcus A., Chuan, Sandy S., Cook-Andersen, Heidi, Roudebush, William E., Irene Su, H., Shimasaki, Shunichi, Chang, R. Jeffrey
Format	Journal Article
Language	English
Published	United States Elsevier Inc 01.01.2014
Subjects	Adult Biomarkers - blood Chorionic Gonadotropin - therapeutic use Female hCG Humans Inhibin B Inhibins - blood Internal Medicine Obstetrics and Gynecology polycystic ovary syndrome Polycystic Ovary Syndrome - blood Polycystic Ovary Syndrome - drug therapy Prospective Studies Recombinant Proteins - therapeutic use Treatment Outcome hCG Inhibin B polycystic ovary syndrome
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Abstract	To determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with polycystic ovary syndrome (PCOS) and in normal women. Prospective study. Academic medical center. Twenty women with PCOS and 16 normal women. Blood samples obtained before and 24 hours after injection of 25 μg recombinant hCG (r-hCG). Basal and stimulated Inh B, E2, androstenedione (A), and T responses after r-hCG administration. In normal and PCOS women, r-hCG induced a significant reduction of Inh B levels. Lowered Inh B responses were not related to body mass index, PCOS status, or age by multivariate regression. Recombinant hCG significantly increased serum A and E2 in both normal and PCOS women. In normal and PCOS women, Inh B production was decreased following r-hCG administration. These findings strongly suggest that in PCOS women androgen excess is not enhanced by LH-stimulated Inh B production. NCT00747617.
AbstractList	To determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with polycystic ovary syndrome (PCOS) and in normal women. Prospective study. Academic medical center. Twenty women with PCOS and 16 normal women. Blood samples obtained before and 24 hours after injection of 25 μg recombinant hCG (r-hCG). Basal and stimulated Inh B, E2, androstenedione (A), and T responses after r-hCG administration. In normal and PCOS women, r-hCG induced a significant reduction of Inh B levels. Lowered Inh B responses were not related to body mass index, PCOS status, or age by multivariate regression. Recombinant hCG significantly increased serum A and E2 in both normal and PCOS women. In normal and PCOS women, Inh B production was decreased following r-hCG administration. These findings strongly suggest that in PCOS women androgen excess is not enhanced by LH-stimulated Inh B production. NCT00747617. Objective To determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with polycystic ovary syndrome (PCOS) and in normal women. Design Prospective study. Setting Academic medical center. Patient(s) Twenty women with PCOS and 16 normal women. Intervention(s) Blood samples obtained before and 24 hours after injection of 25 μg recombinant hCG (r-hCG). Main Outcome Measure(s) Basal and stimulated Inh B, E2 , androstenedione (A), and T responses after r-hCG administration. Result(s) In normal and PCOS women, r-hCG induced a significant reduction of Inh B levels. Lowered Inh B responses were not related to body mass index, PCOS status, or age by multivariate regression. Recombinant hCG significantly increased serum A and E2 in both normal and PCOS women. Conclusion(s) In normal and PCOS women, Inh B production was decreased following r-hCG administration. These findings strongly suggest that in PCOS women androgen excess is not enhanced by LH-stimulated Inh B production. Clinical Trial Registration Number NCT00747617. To determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with polycystic ovary syndrome (PCOS) and in normal women.OBJECTIVETo determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with polycystic ovary syndrome (PCOS) and in normal women.Prospective study.DESIGNProspective study.Academic medical center.SETTINGAcademic medical center.Twenty women with PCOS and 16 normal women.PATIENT(S)Twenty women with PCOS and 16 normal women.Blood samples obtained before and 24 hours after injection of 25 μg recombinant hCG (r-hCG).INTERVENTION(S)Blood samples obtained before and 24 hours after injection of 25 μg recombinant hCG (r-hCG).Basal and stimulated Inh B, E2, androstenedione (A), and T responses after r-hCG administration.MAIN OUTCOME MEASURE(S)Basal and stimulated Inh B, E2, androstenedione (A), and T responses after r-hCG administration.In normal and PCOS women, r-hCG induced a significant reduction of Inh B levels. Lowered Inh B responses were not related to body mass index, PCOS status, or age by multivariate regression. Recombinant hCG significantly increased serum A and E2 in both normal and PCOS women.RESULT(S)In normal and PCOS women, r-hCG induced a significant reduction of Inh B levels. Lowered Inh B responses were not related to body mass index, PCOS status, or age by multivariate regression. Recombinant hCG significantly increased serum A and E2 in both normal and PCOS women.In normal and PCOS women, Inh B production was decreased following r-hCG administration. These findings strongly suggest that in PCOS women androgen excess is not enhanced by LH-stimulated Inh B production.CONCLUSION(S)In normal and PCOS women, Inh B production was decreased following r-hCG administration. These findings strongly suggest that in PCOS women androgen excess is not enhanced by LH-stimulated Inh B production.NCT00747617.CLINICAL TRIAL REGISTRATION NUMBERNCT00747617.
Author	Chuan, Sandy S. Cook-Andersen, Heidi Shayya, Rana F. Rosencrantz, Marcus A. Chang, R. Jeffrey Roudebush, William E. Irene Su, H. Shimasaki, Shunichi
AuthorAffiliation	b Department of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC a Department of Reproductive Medicine, University of California San Diego, La Jolla, CA
AuthorAffiliation_xml	– name: a Department of Reproductive Medicine, University of California San Diego, La Jolla, CA – name: b Department of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC
Author_xml	– sequence: 1 givenname: Rana F. surname: Shayya fullname: Shayya, Rana F. organization: Department of Reproductive Medicine, University of California San Diego, La Jolla, California – sequence: 2 givenname: Marcus A. surname: Rosencrantz fullname: Rosencrantz, Marcus A. organization: Department of Reproductive Medicine, University of California San Diego, La Jolla, California – sequence: 3 givenname: Sandy S. surname: Chuan fullname: Chuan, Sandy S. organization: Department of Reproductive Medicine, University of California San Diego, La Jolla, California – sequence: 4 givenname: Heidi surname: Cook-Andersen fullname: Cook-Andersen, Heidi organization: Department of Reproductive Medicine, University of California San Diego, La Jolla, California – sequence: 5 givenname: William E. surname: Roudebush fullname: Roudebush, William E. organization: Department of Biomedical Sciences, University of South Carolina School of Medicine, Greenville, South Carolina – sequence: 6 givenname: H. surname: Irene Su fullname: Irene Su, H. organization: Department of Reproductive Medicine, University of California San Diego, La Jolla, California – sequence: 7 givenname: Shunichi surname: Shimasaki fullname: Shimasaki, Shunichi organization: Department of Reproductive Medicine, University of California San Diego, La Jolla, California – sequence: 8 givenname: R. Jeffrey surname: Chang fullname: Chang, R. Jeffrey email: rjchang@ucsd.edu organization: Department of Reproductive Medicine, University of California San Diego, La Jolla, California
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Cites_doi	10.1210/jc.2006-0442 10.1677/joe.0.1670289 10.1016/0002-9378(73)90071-9 10.1677/joe.0.0730143 10.1210/jc.2007-2664 10.1073/pnas.84.14.5082 10.1677/joe.0.1260483 10.1016/S0015-0282(00)00421-0 10.1159/000182335 10.1210/endo.133.4.8404591 10.1210/endo-100-5-1341 10.1038/35006129 10.1016/S0015-0282(01)02968-5 10.1210/jc.2002-020546 10.1210/jc.2010-2200 10.1139/y83-072 10.1016/j.fertnstert.2007.03.086 10.1210/endo-124-4-1669 10.1056/NEJM199509283331307 10.1023/A:1022524516824 10.1111/j.1365-2265.1980.tb02132.x 10.1016/0303-7207(91)90234-J 10.1056/NEJMra041536 10.1210/jcem-33-6-917 10.1093/humrep/16.7.1359
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Snippet	To determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with polycystic ovary... Objective To determine whether granulosa cells contribute to excess androgen production, by assessing inhibin B (Inh B) responses to hCG in women with...
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SubjectTerms	Adult Biomarkers - blood Chorionic Gonadotropin - therapeutic use Female hCG Humans Inhibin B Inhibins - blood Internal Medicine Obstetrics and Gynecology polycystic ovary syndrome Polycystic Ovary Syndrome - blood Polycystic Ovary Syndrome - drug therapy Prospective Studies Recombinant Proteins - therapeutic use Treatment Outcome
Title	Decreased inhibin B responses following recombinant human chorionic gonadotropin administration in normal women and women with polycystic ovary syndrome
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