Luteal phase deficiency: abnormal gonadotropin and progesterone secretion patterns.
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.
Soules
M R
MR
Department of Obstetrics, University of Washington, Seattle 98195.
Clifton
D K
DK
Cohen
N L
NL
Bremner
W J
WJ
Steiner
R A
RA
D000026:Abortion, Habitual / Q000097:blood / Q000503:physiopathology*; D000328:Adult; D001706:Biopsy; D003338:Corpus Luteum / Q000503:physiopathology*; D004717:Endometrium / Q000473:pathology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000378:metabolism; D005687:Galactorrhea / Q000503:physiopathology; D006801:Humans; D007247:Infertility, Female / Q000097:blood / Q000503:physiopathology*; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D008597:Menstrual Cycle; D011247:Pregnancy; D011374:Progesterone / Q000097:blood / Q000378:metabolism*; D011388:Prolactin / Q000097:blood
D011374:Progesterone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone