help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Catargi, B.
Right arrow Articles by Tabarin, A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Catargi, B.
Right arrow Articles by Tabarin, A.
The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 9 3404
Copyright © 1999 by The Endocrine Society


Letters to the Editor

Comment on Gonadotroph Adenoma Causing Ovarian Hyperstimulation

B. Catargi, E. Felicie-Dellan and A. Tabarin

Centre Hospitalier Universitaire de Bordeaux Hopital Haut-Leveque Bordeaux, France 33604

Gonadotropin overproduction by gonadotroph adenomas is not usually responsible for a specific and clinically recognizable syndrome (1). Only two cases of ovarian hyperstimulation in the setting of gonadotroph adenoma have been reported so far. One of these was recently published in JCEM (2) and was remarkable with regard to the severity of the clinical presentation. We report herein a milder form of the disease that emphasizes, as has been suggested (3), the importance of measuring E2 and gonadotrophin levels in the presence of multicystic ovaries in premenopausal women.

A 41-yr-old obese woman (body mass index: 36 kg/m2), with a long history of hypertension and noninsulin dependent diabetes melitus presented with an hemorrhagic stroke. Magnetic resonance imaging of the brain showed a huge pituitary adenoma with suprasellar extension (Fig. 1Go). The patient had been spontaneously pregnant 8 and 10 yr before admission. Her menses became irregular and occurred approximately at 3-month intervals since the second delivery. Hormonal evaluation revealed elevated plasma E2 level of 1487 pmol/L (normal range, 100–400). Plasma FSH and LH were 15.3 and 0.9 IU/L respectively (normal ranges: 2–10 IU/L and 2–14 IU/L), and these increased to 35 and 3 IU/L respectively, after i.v. injection of GnRH. The {alpha}-subunit level was normal (0.49 mIU/mL) and did not increase after TRH injection. The prolactine level was 261 ng/mL. The remaining anterior pituitary functions were intact. Transvaginal ultrasound showed enlarged ovaries (6 and 3 cm in diameter) with multiple cysts (Fig. 2Go).



View larger version (191K):
[in this window]
[in a new window]
 
Figure 1.
 


View larger version (121K):
[in this window]
[in a new window]
 
Figure 2.
 
Transsphenoidal surgery was performed. Immunostaining of the tumor was positive for FSHß (65%) and LHß (40%) subunits but not for PRL. Despite incomplete surgical resection, plasma E2 and FSH levels fell to 188 pmol/L and 5.5 IU/L, 3 months postoperatively. Transvaginal ultrasound showed ovaries of normal size (2 and 2.4 cm) without cyst.

Although the pituitary tumor was incidentally discovered, the endocrinological symptoms displayed by our patient before presentation were milder than those described by Christin-Maitre et al., as she complained only of spaniomenorrhea and had no previous history of metrorragia. Accordingly, she displayed lower (although elevated) plasma E2 levels than those recently reported (2). In the setting of obesity, hypertension, and noninsulin dependent diabetes melitus presented by our patient, the association of anovulation, hyperestrogenism, and multiple ovarian cysts would rather suggest polycystic ovary syndrome (3). However, the marked elevation of E2 and FSH together with low LH plasma levels ruled out this hypothesis and was strongly suggestive of a pituitary gonadotroph adenoma.

Footnotes

Address correspondence to: B. Catargi, Hopital Haut-Leveque, Avenue de Magellau, Pessac, France 33604.

Received November 30, 1998.

References

  1. Snyder PJ. 1985 Gonadotroph cell adenomas of the pituitary. 1985 Endocr Rev. 6:552–563.[Abstract/Free Full Text]
  2. Christin-Maitre S, Rongière-Bertrand C, Kottler ML, et al. 1998 A spontaneous and severe hyperstimulation of the ovaries revealing a gonadotroph adenoma. J Clin Endocrinol Metab. 83:3450–3453.[Abstract/Free Full Text]
  3. Djerassi A, Coutifaris C, West VA, et al. 1995 Gonadotroph adenoma in a premenopausal woman secreting follicle-stimulating hormone and causing ovarian hyperstimulation. J Clin Endocrinol Metab. 80:591–594.[Abstract]




This Article
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Catargi, B.
Right arrow Articles by Tabarin, A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Catargi, B.
Right arrow Articles by Tabarin, A.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals