The role of LH and FSH in ovarian androgen secretion and ovarian follicular development

Clinical studies in a patient with isolated FSH deficiency and multicystic ovaries

Randall B. Barnes, Anne B. Namnoum, Robert L. Rosenfield, Lawrence C Layman

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Inactivating mutations have proven to be instructive in elucidating the role of FSH in human ovarian function. We performed a detailed reproductive endocrine evaluation of a patient with inactivating mutations in the FSH β-subunit gene who was hypo-estrogenic and had LH excess. The patient underwent a pelvic ultrasound and overnight frequent blood sampling followed by a human chorionic gonadotrophin (HCG) stimulation test. One month later she received human recombinant FSH, followed 24 h later by a second HCG stimulation test. Despite a mean LH serum concentration and LH pulse characteristics typical for polycystic ovaries (PCOS), baseline and dexamethasone-suppressed free testosterone were low-normal. The administration of HCG led to minimal stimulation of 17-hydroxyprogesterone and androgens. The patient had multicystic ovaries containing follicles 3-5 mm in diameter and responded to FSH with prompt increases in estradiol and inhibin B. There were no clinical or laboratory consequences of LH excess in this FSH-deficient woman. These findings support the hypothesis that excessive LH stimulation alone does not cause ovarian hyperandrogenism. We also found that follicular development was present in the absence of FSH. These antral follicles had apparently developed normally, since estradiol and inhibin B increased promptly after FSH administration.

Original languageEnglish (US)
Pages (from-to)88-91
Number of pages4
JournalHuman Reproduction
Volume17
Issue number1
StatePublished - Feb 18 2002

Fingerprint

Chorionic Gonadotropin
Human Follicle Stimulating Hormone
Androgens
Ovary
Estradiol
17-alpha-Hydroxyprogesterone
Hyperandrogenism
Mutation
Dexamethasone
Testosterone
Serum
Genes
Isolated Follicle-stimulating hormone deficiency
Clinical Studies
inhibin B

Keywords

  • Androgens
  • FSH deficiency
  • LH excess
  • Ovary

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology

Cite this

The role of LH and FSH in ovarian androgen secretion and ovarian follicular development : Clinical studies in a patient with isolated FSH deficiency and multicystic ovaries. / Barnes, Randall B.; Namnoum, Anne B.; Rosenfield, Robert L.; Layman, Lawrence C.

In: Human Reproduction, Vol. 17, No. 1, 18.02.2002, p. 88-91.

Research output: Contribution to journalArticle

@article{df992c1d432b4726b4b134392ae825a9,
title = "The role of LH and FSH in ovarian androgen secretion and ovarian follicular development: Clinical studies in a patient with isolated FSH deficiency and multicystic ovaries",
abstract = "Inactivating mutations have proven to be instructive in elucidating the role of FSH in human ovarian function. We performed a detailed reproductive endocrine evaluation of a patient with inactivating mutations in the FSH β-subunit gene who was hypo-estrogenic and had LH excess. The patient underwent a pelvic ultrasound and overnight frequent blood sampling followed by a human chorionic gonadotrophin (HCG) stimulation test. One month later she received human recombinant FSH, followed 24 h later by a second HCG stimulation test. Despite a mean LH serum concentration and LH pulse characteristics typical for polycystic ovaries (PCOS), baseline and dexamethasone-suppressed free testosterone were low-normal. The administration of HCG led to minimal stimulation of 17-hydroxyprogesterone and androgens. The patient had multicystic ovaries containing follicles 3-5 mm in diameter and responded to FSH with prompt increases in estradiol and inhibin B. There were no clinical or laboratory consequences of LH excess in this FSH-deficient woman. These findings support the hypothesis that excessive LH stimulation alone does not cause ovarian hyperandrogenism. We also found that follicular development was present in the absence of FSH. These antral follicles had apparently developed normally, since estradiol and inhibin B increased promptly after FSH administration.",
keywords = "Androgens, FSH deficiency, LH excess, Ovary",
author = "Barnes, {Randall B.} and Namnoum, {Anne B.} and Rosenfield, {Robert L.} and Layman, {Lawrence C}",
year = "2002",
month = "2",
day = "18",
language = "English (US)",
volume = "17",
pages = "88--91",
journal = "Human Reproduction",
issn = "0268-1161",
publisher = "Oxford University Press",
number = "1",

}

TY - JOUR

T1 - The role of LH and FSH in ovarian androgen secretion and ovarian follicular development

T2 - Clinical studies in a patient with isolated FSH deficiency and multicystic ovaries

AU - Barnes, Randall B.

AU - Namnoum, Anne B.

AU - Rosenfield, Robert L.

AU - Layman, Lawrence C

PY - 2002/2/18

Y1 - 2002/2/18

N2 - Inactivating mutations have proven to be instructive in elucidating the role of FSH in human ovarian function. We performed a detailed reproductive endocrine evaluation of a patient with inactivating mutations in the FSH β-subunit gene who was hypo-estrogenic and had LH excess. The patient underwent a pelvic ultrasound and overnight frequent blood sampling followed by a human chorionic gonadotrophin (HCG) stimulation test. One month later she received human recombinant FSH, followed 24 h later by a second HCG stimulation test. Despite a mean LH serum concentration and LH pulse characteristics typical for polycystic ovaries (PCOS), baseline and dexamethasone-suppressed free testosterone were low-normal. The administration of HCG led to minimal stimulation of 17-hydroxyprogesterone and androgens. The patient had multicystic ovaries containing follicles 3-5 mm in diameter and responded to FSH with prompt increases in estradiol and inhibin B. There were no clinical or laboratory consequences of LH excess in this FSH-deficient woman. These findings support the hypothesis that excessive LH stimulation alone does not cause ovarian hyperandrogenism. We also found that follicular development was present in the absence of FSH. These antral follicles had apparently developed normally, since estradiol and inhibin B increased promptly after FSH administration.

AB - Inactivating mutations have proven to be instructive in elucidating the role of FSH in human ovarian function. We performed a detailed reproductive endocrine evaluation of a patient with inactivating mutations in the FSH β-subunit gene who was hypo-estrogenic and had LH excess. The patient underwent a pelvic ultrasound and overnight frequent blood sampling followed by a human chorionic gonadotrophin (HCG) stimulation test. One month later she received human recombinant FSH, followed 24 h later by a second HCG stimulation test. Despite a mean LH serum concentration and LH pulse characteristics typical for polycystic ovaries (PCOS), baseline and dexamethasone-suppressed free testosterone were low-normal. The administration of HCG led to minimal stimulation of 17-hydroxyprogesterone and androgens. The patient had multicystic ovaries containing follicles 3-5 mm in diameter and responded to FSH with prompt increases in estradiol and inhibin B. There were no clinical or laboratory consequences of LH excess in this FSH-deficient woman. These findings support the hypothesis that excessive LH stimulation alone does not cause ovarian hyperandrogenism. We also found that follicular development was present in the absence of FSH. These antral follicles had apparently developed normally, since estradiol and inhibin B increased promptly after FSH administration.

KW - Androgens

KW - FSH deficiency

KW - LH excess

KW - Ovary

UR - http://www.scopus.com/inward/record.url?scp=0036165848&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036165848&partnerID=8YFLogxK

M3 - Article

VL - 17

SP - 88

EP - 91

JO - Human Reproduction

JF - Human Reproduction

SN - 0268-1161

IS - 1

ER -