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Reproductive Endocrinology |
Reproductive Endocrine Unit and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114
Address correspondence and requests for reprints to: Ann E. Taylor, Reproductive Endocrine Unit, National Center for Fertility Research, Massachusetts General Hospital, Bartlett Hall Extension, Fruit Street, Boston, Massachusetts 02114.
Polycystic ovary syndrome (PCOS) is a heterogeneous disorder of reproductive age women characterized in its broadest definition by the presence of oligoamenorrhea and hyperandrogenism and the absence of other disorders. Defects of gonadotropin secretion, including an elevated LH level, elevated LH to FSH ratio, and an increased frequency and amplitude of LH pulsations have been described, but the prevalence of these defects in a large, unbiased population of PCOS patients has not been determined.
Sixty-one women with PCOS defined by oligomenorrhea and hyperandrogenism and 24 normal women in the early follicular phase had LH samples obtained every 10 min for 8–12 h. Pool LH levels from the frequent sampling studies were within the normal range in the 9 PCOS patients (14.8%) who were studied within 21 days after a documented spontaneous ovulation. Excluding these post-ovulatory patients, 75.0% of the PCOS patients had an elevated pool LH level (above the 95th percentile of the normal controls), and 94% had an elevated LH to FSH ratio.
In the anovulatory PCOS patients, pool LH correlated positively with 17-OH progesterone (R = 0.30, P = 0.03), but not with estradiol, estrone, testosterone, androstenedione, or DHEA-S. Pool LH and LH to FSH ratio correlated positively with LH pulse frequency (R = 0.40, P = 0.004 for pool LH, and R = 0.39; P = 0.005 for LH/FSH). There was also a strong negative correlation between pool LH and body mass index (BMI) (R = -0.59, P < 10-5). The relationship between BMI and LH secretion in the PCOS patients appeared to be strongest with body fatness, as pool LH was correlated inversely with percent body fat, whether measured by skinfolds (R = -0.61, P < 10-5), bioimpedance (R = -0.55, P < 10-4), or dual energy x-ray absorptiometry (DEXA) (R = -0.70, P = 0.001; n = 18 for DEXA only). By DEXA, the only body region that was highly correlated with pool LH was the trunk (R = -0.71, P = 0.001).
The relationship between body fatness and LH secretion occurred via a decrease in LH pulse amplitude (R = -0.63, P < 10-5 for BMI; R = -0.58, P < 10-4 for bioimpedance; and R = -0.64, P = 0.004 for whole body DEXA), with no significant change in pulse frequency with increasing obesity (R = -0.17, P = 0.23 for BMI).
In conclusion: 1) the prevalence of gonadotropin abnormalities is very high in women with PCOS selected on purely clinical grounds, but is modified by recent spontaneous ovulation; 2) the positive relationship between LH pulse frequency and both pool LH and LH to FSH ratio supports the hypothesis that a rapid frequency of GnRH secretion may play a key etiologic role in the gonadotropin defect in PCOS patients; 3) pool LH and LH pulse amplitude are inversely related to body mass index and percent body fat in a continuous fashion; and 4) the occurrence of a continuous spectrum of gonadotropin abnormalities varying with body fat suggests that nonobese and obese patients with PCOS do not represent distinct pathophysiologic subsets of this disorder.
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L. Bilo, R. Meo, R. Valentino, C. Di Carlo, S. Striano, and C. Nappi Characterization of Reproductive Endocrine Disorders in Women with Epilepsy J. Clin. Endocrinol. Metab., July 1, 2001; 86(7): 2950 - 2956. [Abstract] [Full Text] [PDF]
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P.M. Spritzer, M. Poy, D. Wiltgen, L.S. Mylius, and E. Capp Leptin concentrations in hirsute women with polycystic ovary syndrome or idiopathic hirsutism: influence on LH and relationship with hormonal, metabolic, and anthropometric measurements Hum. Reprod., July 1, 2001; 16(7): 1340 - 1346. [Abstract] [Full Text] [PDF]
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S. Gill, A. E. Taylor, K. A. Martin, C. K. Welt, J. M. Adams, and J. E. Hall Specific Factors Predict the Response to Pulsatile Gonadotropin-Releasing Hormone Therapy in Polycystic Ovarian Syndrome J. Clin. Endocrinol. Metab., June 1, 2001; 86(6): 2428 - 2436. [Abstract] [Full Text] [PDF]
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J. D. Veldhuis, S. M. Pincus, M. C. Garcia-Rudaz, M. G. Ropelato, M. E. Escobar, and M. Barontini Disruption of the Joint Synchrony of Luteinizing Hormone, Testosterone, and Androstenedione Secretion in Adolescents with Polycystic Ovarian Syndrome J. Clin. Endocrinol. Metab., January 1, 2001; 86(1): 72 - 79. [Abstract] [Full Text]
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C. A. Eagleson, M. B. Gingrich, C. L. Pastor, T. K. Arora, C. M. Burt, W. S. Evans, and J. C. Marshall Polycystic Ovarian Syndrome: Evidence that Flutamide Restores Sensitivity of the Gonadotropin-Releasing Hormone Pulse Generator to Inhibition by Estradiol and Progesterone J. Clin. Endocrinol. Metab., November 1, 2000; 85(11): 4047 - 4052. [Abstract] [Full Text]
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M. H. A. van Hooff, F. J. Voorhorst, M. B. H. Kaptein, R. A. Hirasing, C. Koppenaal, and J. Schoemaker Insulin, Androgen, and Gonadotropin Concentrations, Body Mass Index, and Waist to Hip Ratio in the First Years after Menarche in Girls with Regular Menstrual Cycles, Irregular Menstrual Cycles, or Oligomenorrhea J. Clin. Endocrinol. Metab., April 1, 2000; 85(4): 1394 - 1400. [Abstract] [Full Text]
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M. P. Rose, R. E. Gaines Das, and A. H. Balen Definition and Measurement of Follicle Stimulating Hormone Endocr. Rev., February 1, 2000; 21(1): 5 - 22. [Abstract] [Full Text]
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H. J. H. M. T. van Dessel, P. D. K. Lee, G. Faessen, B. C. J. M. Fauser, and L. C. Giudice Elevated Serum Levels of Free Insulin-Like Growth Factor I in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., September 1, 1999; 84(9): 3030 - 3035. [Abstract] [Full Text]
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L. Poretsky, N. A. Cataldo, Z. Rosenwaks, and L. C. Giudice The Insulin-Related Ovarian Regulatory System in Health and Disease Endocr. Rev., August 1, 1999; 20(4): 535 - 582. [Abstract] [Full Text] [PDF]
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M.H.A. van Hooff, M. van der Meer, C.B. Lambalk, and J. Schoemaker Variation of luteinizing hormone and androgens in oligomenorrhoea and its implications for the study of polycystic ovary syndrome Hum. Reprod., July 1, 1999; 14(7): 1684 - 1689. [Abstract] [Full Text] [PDF]
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S. B. Seminara, J. E. Hall, A. E. Taylor, W. F. Crowley Jr., and K. A. Martin The Reproductive Endocrine Associates of the Massachusetts General Hospital: Fifteen Years of Integrated Clinical Practice and Investigation J. Clin. Endocrinol. Metab., June 1, 1999; 84(6): 1912 - 1918. [Full Text]
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M. Nagamani, C. Osuampke, and M. E. Kelver Increased Bioactive Luteinizing Hormone Levels and Bio/Immuno Ratio in Women with Hyperthecosis of the Ovaries: Possible Role of Hyperinsulinemia J. Clin. Endocrinol. Metab., May 1, 1999; 84(5): 1685 - 1689. [Abstract] [Full Text]
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A. E. Taylor, J. Hubbard, and E. J. Anderson Impact of Binge Eating on Metabolic and Leptin Dynamics in Normal Young Women J. Clin. Endocrinol. Metab., February 1, 1999; 84(2): 428 - 434. [Abstract] [Full Text]
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F. J. Hayes, A. E. Taylor, K. A. Martin, and J. E. Hall Use of a Gonadotropin-Releasing Hormone Antagonist as a Physiologic Probe in Polycystic Ovary Syndrome: Assessment of Neuroendocrine and Androgen Dynamics J. Clin. Endocrinol. Metab., July 1, 1998; 83(7): 2343 - 2349. [Abstract] [Full Text]
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C. L. Pastor, M. L. Griffin-Korf, J. A. Aloi, W. S. Evans, and J. C. Marshall Polycystic Ovary Syndrome: Evidence for Reduced Sensitivity of the Gonadotropin-Releasing Hormone Pulse Generator to Inhibition by Estradiol and Progesterone J. Clin. Endocrinol. Metab., February 1, 1998; 83(2): 582 - 590. [Abstract] [Full Text]
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E. W. C. M. Van Dam, F. Roelfsema, J. D. Veldhuis, F. M. Helmerhorst, M. Frolich, A. E. Meinders, H. M. J. Krans, and H. Pijl Increase in daily LH secretion in response to short-term calorie restriction in obese women with PCOS Am J Physiol Endocrinol Metab, April 1, 2002; 282(4): E865 - E872. [Abstract] [Full Text] [PDF]
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