The significance of a single serum LH measurement in women with cycle disturbances: discrepancies between immunoreactive and bioactive hormone estimates*

Fauser, Bart C.J.M.; Pache, Thierry D.; Hop, Wim C. J.; Jong, Frank H. de; Dahl, Kristine D.

doi:10.1111/j.1365-2265.1992.tb02357.x

Cited by 32 publications

(9 citation statements)

References 27 publications

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“…58,59 On the other hand, an increased LH bioactivity is an almost invariable feature of PCOS, but the mechanism responsible for this alteration still remains unclear. 60 It is a matter of debate whether the increase of gonadotrophins, when present, may be attributed to a primary abnormality of the hypothalamic -pituitary axis or may be secondary to alterations in peripheral signaling. As reported in the previous paragraph, the elevation of circulating LH concentration may be due to inappropriate estrogen feed-back to neuroendocrine centers.…”

Section: Neuroendocrine Factorsmentioning

confidence: 99%

Obesity and the polycystic ovary syndrome

et al. 2002

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The polycystic ovary syndrome (PCOS) is a condition characterized by hyperandrogenism and chronic oligo-anovulation. However, many features of the metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are overweight or obese and most of them have the abdominal phenotype. Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and, possibly, high dietary lipid intake, may be additional mechanisms by which obesity favours the development of hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype.Body weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and=or antiandrogens to weight reduction programmes. These obviously emphasize the role of obesity in the pathophysiology of PCOS.

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Section: Neuroendocrine Factorsmentioning

confidence: 99%

Obesity and the polycystic ovary syndrome

et al. 2002

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“…This is consistent with an abnormal diurnal pattern of LH secretion that has been reported both in adolescent girls with PCOS (Apter et al, 1994) and in adults with PCOS (Yen et al, 1993), with the highest LH values occurring in late afternoon rather than at night. Finally, there is evidence that bioactive LH is elevated in many patients with PCOS, in whom immunoactive LH is normal (Fauser et al, 1992;Imse et al, 1992). Marshall et al (1991;Marshall & Eagleson, 1999) have focused on pulsatile patterns of LH secretion as an indicator of altered hypothalamic secretion of GnRH.…”

Section: Neuroendocrine Defectmentioning

confidence: 99%

The pathophysiology of polycystic ovary syndrome

Tsilchorozidou

Overton

Conway

2003

Clinical Endocrinology

230

167

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“…The primary purpose of this study was to assess the pituitary-ovarian response to GnRHa in hyperandrogenic women with polycystic ovaries and regular menses and to compare it to results in anovulatory women with PCOS and control subjects. In view of reported disparities between immunoreactive and bioactive measurements of LH in PCOS (Lobo et al, 1983;Jaakolla et al, 1990;Fauser et al, 1992), we compared values obtained by radioimmunoassay and in-vitro bioassay. The diagnostic value of the androstenedione and 170HP responses to GnRHa was evaluated.…”

mentioning

confidence: 99%

Gonadotrophin and gonadal steroid response to a single dose of a long‐acting agonist of gonadotrophin‐releasing hormone in ovulatory and anovulatory women with polycystic ovary syndrome

White

Leigh

Wilson

et al. 1995

Clinical Endocrinology

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These data provide evidence for ovarian hypersecretion of androgens in ovulatory, as well as anovulatory women with PCO, supporting the concept of abnormal regulation of 17-hydroxylase and (17,20-lyase activity in the ovary. The finding of an equal degree of hyperandrogenaemia in ovPCO and anovPCO groups, even though LH levels were much higher in the latter, suggests that hypersecretion of LH is not the primary cause of ovarian hyperandrogenism. Hyperandrogenism in PCOs may therefore represent an intrinsic abnormality of ovarian theca-interstitial cell function.

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The significance of a single serum LH measurement in women with cycle disturbances: discrepancies between immunoreactive and bioactive hormone estimates*

Cited by 32 publications

References 27 publications

Obesity and the polycystic ovary syndrome

Obesity and the polycystic ovary syndrome

The pathophysiology of polycystic ovary syndrome

Gonadotrophin and gonadal steroid response to a single dose of a long‐acting agonist of gonadotrophin‐releasing hormone in ovulatory and anovulatory women with polycystic ovary syndrome

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