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Curr Opin Obstet Gynecol. 1991 Oct;3(5):641-8.

Luteal phase defect: a review of pathophysiology.

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  • 1Jones Institute for Reproductive Medicine, Eastern Virginia Medical School, Norfolk.


Corpus luteum function depends on normal granulosa and theca cell components, which in turn are stimulated by an adequate luteinizing hormone (LH) surge in both duration and amplitude of pulses with LH residual pulses of adequate amplitude during the 14-day luteal span. The granulosa component must be competent to 1) synergize with thecal androgen production for increased estrogen production, 2) develop LH receptors for progesterone production, and 3) mature the egg cytoplasmically. The theca component must be capable of inducing angiogenesis factor to increase follicular blood supply and must be responsive to an LH pulse and human chorionic gonadotropin for corpus luteum rescue. The corpus luteum defect with a normal 14-day span is related either to an inadequate granulosa cell or to an inadequate LH surge, but a fairly normal LH pulse and theca cell response. The short luteal phase defect is related to a poor LH surge and an absent or extremely poor LH pulse. Diagnostic studies have indicated that the endometrial biopsy is the most efficient diagnostic method. Severe luteal defects can be diagnosed by a progesterone assay if the entire cycle is assayed, but single or even multiple progesterone assays are unreliable. The etiology is multifactorial and usually is related to the hypothalamic-pituitary factors influencing the LH surge, rather than to ovarian factors. Factors may vary from cycle to cycle, making it important to determine that the defect is repetitive. The specific etiology is often difficult to determine; substitution progesterone therapy is the most satisfactory treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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