Luteal phase deficiency: abnormal gonadotropin and progesterone secretion patterns
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Date
Authors
Bremner, William J.
Cohen, Nancy L.
Steiner, Robert A.
Soules, Michael R.
Clifton, Donald K.
Journal Title
Journal ISSN
Volume Title
Publisher
Endocrine Society
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.
Description
Citation
J Clin Endocrinol Metab. 1989 Oct;69(4):813-20
