Lipoprotein-cholesterol levels in infertile women with luteal phase deficiency.
OBJECTIVE
To determine if reductions in plasma progesterone (P) secretion seen in luteal phase deficiency (LPD) might be because of reduced availability of circulating low-density lipoprotein (LDL) or high-density lipoprotein (HDL), known substrates for corpus luteum P synthesis.


METHODS
We measured plasma lipoproteins in the luteal phase of the menstrual cycle in 39 infertile women. These women were divided into two groups on the basis of endometrial biopsies; the LPD group had biopsies that were greater than or equal to 3 days out-of-phase.


METHODS
All participants were recruited from the Reproductive Endocrinology and Infertility Clinic at the University of Washington, an institutional tertiary care center.


METHODS
Eighteen women had in-phase and 21 had out-of-phase LPD biopsies.


METHODS
Lipoprotein levels were obtained in a fasted state on the day of the luteal phase on which the biopsy was performed.


RESULTS
No difference in covariates that affect lipoprotein levels such as obesity, age, and alcohol use were observed between the two groups. No significant differences between groups were found for triglycerides, total cholesterol, very low density lipoprotein, LDL, HDL, HDL2, and HDL3 concentrations. However, LPD was associated with a reduction in the extent to which: age and obesity are associated with higher triglycerides; obesity is associated with a lower HDL2; and alcohol is associated with a higher HDL3-cholesterol.


CONCLUSIONS
Lipoproteins on average are not different in LPD, suggesting reasons other than a deficient plasma lipoprotein cholesterol source as the explanation for decreased P secretion. A lesser interaction between LDL or HDL and obesity, age, and alcohol in LPD could signify an influence of the altered hormonal milieu of LPD on the way lipoproteins interact with covariates and could lead to differences in lipoproteins between normal and LPD subjects at the extremes of the lipoprotein distribution.
Hansen
K K
KK
Department of Obstetrics and Gynecology, University of Washington, Seattle 98195.
Knopp
R H
RH
Soules
M R
MR
D001706:Biopsy; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood*; D003338:Corpus Luteum / Q000378:metabolism; D004717:Endometrium / Q000473:pathology; D005260:Female; D006801:Humans; D007247:Infertility, Female / Q000473:pathology / Q000503:physiopathology*; D008075:Lipoproteins, HDL / Q000097:blood; D053439:Lipoproteins, HDL2; D053440:Lipoproteins, HDL3; D008183:Luteal Phase / Q000502:physiology*; D011374:Progesterone / Q000172:deficiency*; D014280:Triglycerides / Q000097:blood
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008075:Lipoproteins, HDL; D053439:Lipoproteins, HDL2; D053440:Lipoproteins, HDL3; D014280:Triglycerides; D011374:Progesterone