Luteal Phase Deficiency: Characterization of Reproductive Hormones over the Menstrual Cycle*

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Abstract
The recurrent deficiency of progesterone (P) secretion by the corpus luteum has been associated with infertility and habitual abortion and given the clinical diagnosis of luteal phase deficiency (LPD). There is evidence that both follicular and luteal phase abnormalities can result in LPD cycles. In this study we have examined reproductive hormone levels and preovulatory follicular size in women with LPD (n = 10). For the purposes of this study, LPD was determined by an endometrial biopsy in the studied cycle that was more than 2 days out of phase. These biopsies were performed in women with infertility or habitual abortion who exhibited an out of phase biopsy in a prior cycle. The control group consisted of 28 normal women. Daily serum levels of the following hormones were determined in each subject: LH and FSH [immuno- and bioactive (LH-immuno and LH-bio)], P, estradiol (E2), and inhibin. The LPD women exhibited significant decreases in integrated luteal phase levels of inhibin [10,615 .+-. 898 vs. 13,560 .+-. 662 (U/L) .cntdot. days; P < 0.02] and E2 [5,015 .+-. 275 vs. 6,435 .+-. 393 (pmol/L) .cntdot. days (1366 vs. 1753 (pg/mL) .cntdot. days); P < 0.05] in addition to the expected decrease in P [280 .+-. 23 vs. 420 .+-. 23 (nmol/L) .cntdot. days (88 vs. 132 (ng/mL) .cntdot. days); P < 0.01]. On days 6-11 after the LH surge (day 0), there was a significant (P < 0.05) decrease in mean LH-bio levels in LPD compared with those in normal women (146 .+-. 26 vs. 212 .+-. 24 .mu.g/L). The midcycle LH surge was deficient in LPD when both LH-immuno [482 .+-. 30 vs. 672 .+-. 43 (.mu.g/L) .cntdot. days; P < 0.01] and LH-bio [1711 .+-. 179 vs. 2248 .+-. 226 (.mu.g/L) .cntdot. days; P < 0.05] levels were compared with normal values. When comparing the follicular phase in LPD with that in normal women, similar follicle size, peak and integrated E2 levels, and mean LH and FSH (immuno and bio) levels were found. The only follicular phase abnormality noted in this study was decreased mean levels of serum inhibin in the early and midfollicular phases (221 .+-. 19 vs. 308 .+-. 25 U/L; P < 0.01). In this group of women with LPD, low levels of inhibin in the follicular phase were consistent with the concept of a defect in function of the preovulatory follicle, possible as a result of previously described defects in gonadotropin secretion in this condition. Our findings of decreased LH levels by both immunoand bioassay at midcycle and in the luteal phase may also be causal in the deficiencies of corpus luteal function. We conclude that 1) the corpus luteum in LPD exhibits multiple hormone deficiencies, and 2) the pathogenesis of LPD is complex and includes decreased inhibin levels in the follicular phase, a subnormal midcycle LH surge, and abnormal levels of LH-bio in the luteal phase.