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Human Reproduction, Vol. 14, No. 3, 611-617, March 1999
© 1999 European Society of Human Reproduction and Embryology

Changes in luteinizing hormone and insulin secretion in polycystic ovarian syndrome

A.M. Fulghesu, F. Cucinelli, V. Pavone, F. Murgia, M. Guido, A. Caruso, S. Mancuso and A. Lanzone1

Department of Obstetrics and Gynecology, Catholic University of Sacred Heart, L.go A. Gemelli 8, 00168 Rome, Italy

Uncertainties regarding the pathogenetic changes underlying the polycystic ovarian syndrome (PCOS) have been reported. The aim of this study was to investigate the endocrine and metabolic features of PCOS patients in relation to luteinizing hormone (LH) secretion. Androgen assays, oral glucose tolerance tests, hyperinsulinaemic euglycaemic clamps and gonadotrophin releasing hormone (GnRH) tests were performed in 100 patients. Sixty-six patients scheduled as hyperinsulinaemic and 34 as normoinsulinaemic showed similar concentrations of LH, follicle stimulating hormone (FSH), LH/FSH ratio, and LH response to GnRH testing. Hyperinsulinaemic subjects showed higher body mass index (BMI), insulin resistance, testosterone and free androgen index levels compared with those of normoinsulinaemic subjects; when clustered in relation to their LH basal concentrations, the two groups obtained differed only in androstenedione concentrations. Considering both insulin and LH plasma concentrations, four groups were obtained. Hyperinsulinaemia and hyper-LH secretion were not related in 54% and coexisted in the same subjects in 26% of cases. Hyperinsulinaemia as well as hyper-LH secretion affected the expression of the syndrome; the insulinaemia was directly correlated with testosterone concentrations and all metabolic parameters that affected the free androgen index. The LH concentrations were related to androgen production and were independent of BMI and insulin concentrations. It is concluded that the degree of hormonal alteration is the final sum of such pathogenetic factors.

Key words: androgen/insulin/LH/obesity/PCOS

1 To whom correspondence should be addressed


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