Abstract
Most patients with polycystic ovarian disease (PCOD) have inappropriately elevated LH re-lease and low or a low normal FSH secretion, namely, an elevated LH/FSH ratio (24,39,74, 138, 202, 203, 242, 302, 327, 332, 434, 443, 529, 530, 647, 711, 733, 742, 830, 934, 973, 998,1015,1028,1029). The mean normal mid- follicular LH/FSH ratio is 1.3 (1.0–1.6) (24, 39,332). The high circulating LH level is maintained by exaggerated pulsatile LH discharge, either in the form of enhanced amplitude or increased frequency (oscillations) (Fig. 6-1) (39, 742,973). The serum LH has no consistent pat-tern in magnitude or interval in PCOD (473). Daily LH excursions are frequently so great that they may resemble those of normal cycling women, or to the magnitude seen in a spontaneous mid-cycle LH surge (1015). It has been demonstrated that surges of LH in patients with polycystic ovaries may be preceded by a rapid increase of endogenous circulating E2 (1015).
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© 1984 Springer-Verlag New York Inc
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Futterweit, W. (1984). Pathophysiology of Polycystic Ovarian Disease. In: Polycystic Ovarian Disease. Clinical Perspectives in Obstetrics and Gynecology. Springer, New York, NY. https://doi.org/10.1007/978-1-4613-8289-8_6
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DOI: https://doi.org/10.1007/978-1-4613-8289-8_6
Publisher Name: Springer, New York, NY
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