Hum. Reprod. Advance Access originally published online on April 20, 2007
Human Reproduction 2007 22(6):1562-1566; doi:10.1093/humrep/dem060
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
The excess in 2–5 mm follicles seen at ovarian ultrasonography is tightly associated to the follicular arrest of the polycystic ovary syndrome
1 Department of Endocrine Gynaecology and Reproductive Medicine, Hôpital Jeanne de Flandre, C.H.R.U., 59037 Lille, France 2 Department of Radiology, Hôpital Jeanne de Flandre, C.H.R.U., 59037 Lille, France 3 Laboratory of Endocrinology, Parc Eurasanté, C.H.R.U., 59037 Lille, France
4 Correspondence address. Tel: 33-3-20-44-69-03; Fax: 33-3-20-44-64-07; E-mail: ddewailly{at}chru-lille.fr
BACKGROUND: We previously hypothesized that the excess of 2–5 mm follicles seen at ovarian ultrasonography might be involved in the follicular arrest (FA) of polycystic ovary syndrome (PCOS), independently from the main putative contributors of FA, namely hyperandrogenism and hyperinsulinism.
METHODS: A multivariate statistical analysis was applied retrospectively to clinical, biological and ultrasound data that were consecutively collected during 5 years in 457 patients with polycystic ovaries and in 188 age-matched non-hyperandrogenic and regularly cycling controls without PCO at ultrasound.
RESULTS: Stepwise discriminant analysis indicated that in PCOS the 2–5 mm follicle number (FN) gave the strongest correlation to severity of the FA, followed by age and then by fasting insulin level. The other variables [waist circumference (WC), 6–9 mm FN, serum testosterone, FSH, LH and ovarian area] were rejected by the analysis. Multiple linear regression indicated a significant and independent negative relationship between the 2–5 and 6–9 mm FN in the PCOS (r = – 0.186, P < 0.01) and control groups (r = – 0.281, P < 0.01). In PCOS only, the 6–9 mm FN was negatively and independently related to the WC (r = – 0.108, P < 0.05).
CONCLUSIONS: The size of the 2–5 mm follicle pool is an independent and important contributor to the FA of PCOS. This result could be explained by an exaggerated physiological inhibitory effect from this pool on the terminal follicle growth. The metabolic derangement of PCOS that also contributes to the FA would act through a different mechanism.
Key words: androgens/anovulation/follicular arrest/insulin/polycystic ovary syndrome
Submitted on December 4, 2006; resubmitted on February 7, 2007; accepted on February 13, 2007.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
S. Catteau-Jonard, P. Pigny, A.-C. Reyss, C. Decanter, E. Poncelet, and D. Dewailly Changes in Serum Anti-Mullerian Hormone Level during Low-Dose Recombinant Follicular-Stimulating Hormone Therapy for Anovulation in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., November 1, 2007; 92(11): 4138 - 4143. [Abstract] [Full Text] [PDF] |
||||
