Soules, M. R., Clifton, D. K., Cohen, N. L., Bremner, W. J., & Steiner, R. A. (1989). Luteal phase deficiency: abnormal gonadotropin and progesterone secretion patterns. The Journal of Clinical Endocrinology and Metabolism, 69(4), 813-820. https://doi.org/10.1210/jcem-69-4-813
Soules, M. R., et al. "Luteal phase deficiency: abnormal gonadotropin and progesterone secretion patterns." The Journal of Clinical Endocrinology and Metabolism, vol. 69, no. 4, 1989, pp. 813-820.
Luteal phase deficiency linked to faster early follicular LH pulses
A 1989 study of 21 women with normal cycles and 20 women with luteal phase deficiency found that women with luteal phase deficiency had faster luteinizing hormone (LH) pulses early in the follicular phase. The authors conclude that this may lead to weak LH support of the corpus luteum.
Key Findings
Early in the follicular phase, women with luteal phase deficiency had more LH pulses: 12.8 +/- 1.4 (+/- SE) against 8.2 +/- 0.7 pulses/12 h in normal women (P less than 0.05).
Among women with luteal phase deficiency, LH pulse frequency was similar early and late in the follicular phase. Normal women showed a higher frequency late in that phase.
In the luteal phase, progesterone pulse amplitude and mean serum progesterone were significantly lower in the deficiency group (P less than 0.01).
Mean serum follicle-stimulating hormone (FSH) did not differ between the groups in the early or late follicular phase.
Interpretation
The source is the abstract of a case-control study. It compared normal women with women who had luteal phase deficiency, found by two out of phase endometrial biopsies, and drew their blood every 10 minutes for 12 hours. The authors conclude that weaker progesterone pulses explain the low progesterone. They also say that matching FSH levels give no support to poor follicle growth as a cause.
RRM Context
Restorative reproductive medicine looks for the source of a low progesterone phase. The pulse findings point to one possible source: the hormone signal sent before ovulation. Studying the whole cycle comes before choosing a treatment.
Our editorial summary of this paper, not the article's abstract.
Abstract
Luteal phase deficiency (LPD) is a reproductive disorder associated with infertility and spontaneous abortion. This study was undertaken to determine whether LPD might be related to an abnormal pattern of gonadotropin secretion. We tested this hypothesis by evaluating the pattern of pulsatile LH secretion in both the follicular and luteal phases of the menstrual cycle in normal women (n = 21) and women with LPD (n = 20), which was diagnosed on the basis of two out of phase endometrial biopsies. In addition, we sought to determine whether changes in progesterone (P) pulse patterns could account for the decrease in average serum P levels in women with LPD. To this end, we examined the pulse patterns of P and compared these patterns between normal women and those with LPD. Frequent blood sampling was performed in both groups to determine their respective hormone secretion patterns. In the follicular phase, blood samples were obtained every 10 min for 12 h; in the luteal phase the samples were obtained every 10 min for 12 h; in the luteal LH, FSH, and P were assayed in each sample. Pulse detection was performed by an adaptive threshold method of pulse analysis. The LH pulse frequency was significantly higher in the women with LPD than in the normal women in the early follicular phase [P less than 0.05; LPD, 12.8 +/- 1.4 (+/- SE); normal, 8.2 +/- 0.7 pulses/12 h]. LH pulse frequency was similar in the early and late follicular phases in the women with LPD, whereas it was higher in the late follicular phase in normal women. Mean serum FSH levels were not different between groups in both the early and late follicular phases. In the luteal phase the P pulse amplitude and mean serum P level were significantly lower in the LPD group than in the normal women (P less than 0.01). We conclude that 1) a too rapid LH pulse pattern in the early follicular phase may lead to inadequate LH support of the corpus luteum and become manifest as LPD; 2) the mechanism for inadequate P secretion in LPD is decreased P pulse amplitude; 3) the finding of similar serum FSH levels in the two groups in both the early and late follicular phases did not support compromised folliculogenesis as an etiological factor for LPD.
