Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Luteal Phase”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1985

Hormonal profiles in the follicular phase, luteal phase and first trimester of pregnancies arising from in-vitro fertilization.

The hormonal profiles for oestradiol-17 beta, progesterone, prolactin and beta-human chorionic gonadotrophin (beta-hCG) are documented for the first 24 pregnancies arising from in-vitro fertilization during a collaborative project between the University of Western Australia and PIVET Laboratory. All patients had ovarian follicle stimulation with clomiphene citrate, sometimes combined with human menopausal gonadotrophin and all had oocyte recovery undertaken 36 h after injection of 5000 i.u. hCG. The follicular phase profile indicated that patients were admitted for the hCG injection when oestradiol-17 beta levels were around 1500 pmol/l per follicle with a dimension of greater than or equal to 1.6 cm on ultrasound. Luteal phase data indicated that oestradiol-17 beta and progesterone levels were two to three times higher than that expected during spontaneous conception cycles and those pregnancies which subsequently aborted had significantly lower levels in the late luteal phase. During pregnancy elevated oestradiol-17 beta and progesterone levels were maintained through the early weeks during organogenesis while the beta-hCG profile was similar to that reported for spontaneous pregnancies arising without ovarian stimulation. Six women aborted and the other 18 pregnancies have generated 22 infants.

Chorionic Gonadotropin↗
PubMed1989

Luteal phase deficiency after completely normal follicular and periovulatory phases.

Luteal phase defect (LPD) accounts for a significant proportion of reproductive disorders, however its etiology is still debated. A prospective study was performed on 37 ovulatory women to determine whether LPD can occur in cycles characterized by completely normal folliculogenesis. Criteria for normal folliculogenesis included: a gradual rise of serum estradiol, a luteinizing hormone (LH) surge, the presence of a dominant follicle that disappeared, an increase of serum progesterone, and normal serum levels of prolactin, testosterone, dehydroepiandrosterone sulfate, follicle-stimulating hormone, and LH. Thirty of 37 women fulfilled the above mentioned strict criteria and underwent endometrial biopsy in the late luteal phase. Seven of 30 (23%) demonstrated a delay in endometrial development and all had normal hormonal and ultrasonographic parameters of folliculogenesis and ovulation. Women with delayed endometrial development demonstrated slightly longer follicular phases (17.0 +/- 1.1 versus 14.5 +/- 0.3 days). Perfectly normal follicular and periovulatory events may be followed by deficient luteal phases.

Adult↗
PubMed1985

Prolactin production by explants of normal, luteal phase defective, and corrected luteal phase defective late secretory endometrium.

The production of prolactin by explants of late secretory endometrium has been correlated with the extent of decidual differentiation. This correlation is strengthened by the observation that luteal phase defective endometrium produces less prolactin than normal control endometrium in a 24-hour in vitro culture system. In the present study the prolactin production by explants of normal, luteal phase defective, progesterone-corrected luteal phase defective, and clomiphene- or follicle-stimulating hormone/luteinizing hormone-corrected luteal phase defective late secretory endometrium was measured over 96 hours at 24-hour intervals. Progesterone in physiologic concentrations was added to the culture medium to maintain tissue integrity and prolactin synthesis. The prolactin production of normal late secretory endometrium rose over 96 hours under progesterone stimulation. The luteal phase defective endometrium produced significantly less prolactin under the same conditions. Histologically proven corrected luteal phase defective endometrium, regardless of treatment method, produced prolactin not different from the normal controls of the same dates. From these results it is concluded that histologic correction of luteal phase defective endometrium is associated with a corresponding biochemical correction with use of prolactin as a metabolic marker. The findings also strongly support timed endometrial biopsy as the method of diagnosis and evaluation of treatment of luteal phase defect.

Biopsy↗
PubMed1986

Immunoperoxidase localization of prolactin in endometrium during normal menstrual, luteal phase defect, and corrected luteal phase defect cycles.

An avidin-biotin immunoperoxidase staining technique for human prolactin (hPRL) was developed for determination of the location of PRL-producing cells in the endometrium of women with normal menstrual cycles (NMC), luteal phase defects (LPD), and corrected LPD cycles (CLPD). One hundred eight biopsy specimens were studied. Fifty-six patients had NMC, 29 had LPD, and 23 had CLPD. Only decidualized stromal cells stained specifically for hPRL. There was no specific staining in specimens dated earlier than day 25. All specimens dated later than day 25 exhibited decidual cell staining. In specimens dated day 25, 15 of 20 NMC, 5 of 11 CLPD, and 6 of 10 LPD demonstrated decidual staining (P greater than 0.1). These findings suggest that decidual cells are responsible for hPRL production in late secretory endometrium and that the ability of decidual cells to stain for hPRL is dependent on the histologic date of the endometrium and not on the diagnosis of LPD or CLPD.

Bromocriptine↗
PubMed1981

Follicular phase treatment of luteal phase dysfunction.

Previously, we demonstrated that selective suppression of serum follicle-stimulating hormone (FSH) in monkeys treated with charcoal-extracted porcine follicular fluid (pFF) in the early follicular phase induced luteal defects resembling those which occur spontaneously in women and monkeys. Here, we assessed whether luteal phase defects arising in association with induced FSH deficiencies during the early follicular phase can be treated by early FSH therapy. Rhesus monkeys were treated with pFF and human menopausal gonadotropin (hMG) (FSH:luteinizing hormone [LH], 3:1) on cycle days 1 to 3 or day 4, respectively. Daily femoral blood samples were analyzed for LH, FSH, and estradiol by radioimmunoassay. In the monkeys treated with the pFF-hMG combination, a single ovulation was uniformly noted at laparoscopy, and initial luteal phase elevations in serum progesterone levels were nearer those of normal ovulatory cycles than after pFF alone. These results suggest that FSH/LH treatment in the early follicular phase compensated, in part, for the pFF-induced deficiency in endogenous FSH levels.

Animals↗
PubMed1988

Sustained effects of opioid antagonism during the normal human luteal phase.

The luteal phase of the menstrual cycle is characterized by a progressive decrease in LH pulse frequency. Short term administration of opiate receptor antagonists during the luteal phase increases the release of both LH and PRL. However, the effects of prolonged opioid antagonism throughout the luteal phase are unknown and, hence, the precise role of endogenous opioid peptides in the reproductive cycle remains to be elucidated. In this study, we examine the ability of longer term opioid antagonism during the luteal phase to alter pulsatile LH and PRL release. Naltrexone (NTX), a long-acting oral opioid antagonist, at a dose of 50 mg, was administered daily for 7 days during the luteal phase in five women. Blood samples were obtained at intervals of 10 min starting at 0800 h for 11-12 h on matched days of the luteal phase of both a control and the experimental cycle. LH and PRL pulse frequencies were significantly increased at the end of the 7-day NTX administration period compared to those in the control cycle [LH, 0.22 +/- 0.04 (+/- SE) vs. 0.07 +/- 0.03 pulse/h (P less than 0.01); PRL, 0.20 +/- 0.02 vs. 0.13 +/- 0.02 pulse/h (P less than 0.05)]. The concordance between LH and PRL pulses increased from 50% in the control cycle to 70% in the NTX cycle, and there was a significant positive correlation between the amplitudes of the concomitant LH and PRL pulses (r = 0.72; P = 0.01). In conclusion, prolonged oral opioid antagonism increased pulsatile LH and PRL secretion during the luteal phase in normal women. The results underscore the important role of endogenous opioid peptides in controlling LH pulse frequency during the luteal phase of the cycle.

Adult↗
PubMed1984

Abnormal patterns of pulsatile luteinizing hormone in women with luteal phase deficiency.

Luteal phase deficiency is usually a problem of inadequate progesterone production associated with inadequate ovarian follicular development. The hypothesis that luteal phase deficiency results from an abnormal secretion pattern of luteinizing hormone (LH) was tested in these women. To this end, the early follicular LH secretion pattern in four women with luteal phase deficiency was characterized and compared with patterns in normal women. Blood samples were obtained through indwelling catheters every ten minutes for eight hours (10 AM to 6 PM), and plasma levels of LH and FSH were measured. Luteinizing hormone and FSH secretion profiles were analyzed for pulse frequency, amplitude, and mean plasma level. A significantly greater LH pulse frequency in women with luteal phase deficiency was observed when compared with the frequency in normal controls (luteal phase deficiency, 10.5 pulses/eight hours; normal, 5.2 pulses/eight hours; P less than or equal to .05). The mean FSH concentration was less in the women with luteal phase deficiency, but the level was not significant. These data suggest that the abnormal LH secretion pattern observed in women with luteal phase deficiency is responsible for their inadequate luteal phase progesterone secretion and their infertility.

Adult↗
PubMed1982

Could aspiration of the Graafian follicle cause luteal phase deficiency?

Luteal phase quality was evaluated in 32 patients wih nonstimulated cycles after laparoscopic oocyte recovery for in vitro fertilization. A luteal phase deficiency occurred in two cases (6.2%), the mean duration of the luteal phase was 13.5 +/- 1.3 days in 30 patients, and two patients developed amenorrhea of 23 and 43 days respectively after laparoscopy in spite of normal progesterone values 7 and 9 days after oocyte recovery. Six embryo transfers were performed after fertilization and regular cleavage of the obtained oocytes. No pregnancy resulted from the embryo transfers, although the patients had apparently normal luteal phases. In one patient there was a transient beta-subunit human chorionic gonadotropin (beta-hCG) elevation in serum. Luteal phase deficiency should not be main cause of a nonsuccessful embryo transfer. However, a prophylactic luteal phase support after oocyte recovery and embryo transfer in nonstimulated cycles is proposed.

Chorionic Gonadotropin↗
PubMed1984

Follicular phase treatment of luteal phase defect with follicle-stimulating hormone in infertile women.

Fifteen infertile women diagnosed by endometrial dating to have a luteal phase defect were treated with human pituitary follicle-stimulating hormone (hFSH) for 45 cycles. Human follicle-stimulating hormone was administered intramuscularly in a dose of 50 IU/day (group 1) for 35 cycles and 100 IU/day (group 2) for ten cycles from either the third or fifth day of the cycle for five days. Plasma estrogen was measured daily during drug injection. Plasma progesterone was measured on the fourth, seventh, and tenth days after ovulation by basal body temperature during 11 pretreatment control cycles and 39 treatment cycles. Endometrial biopsies were performed on the seventh day after ovulation. The daily estrogen levels increased gradually during hFSH treatment. There was no significant difference between the two dosage groups. The mean progesterone levels were: 1) significantly (P less than .02) greater in the treatment cycles than in the control cycles, 2) significantly (P less than .05) greater in the pregnancy cycles than in the nonpregnancy cycles, 3) significantly (P less than .01) greater in the cycles with normal endometrial dating than in the cycles with abnormal endometrial dating after treatment, and 4) significantly (P less than .05) greater in group 1 than in group 2. After treatment, the endometrial biopsy specimens were improved to normal in 20 of 38 cycles. Five patients became pregnant during the treatment. The authors have concluded that hFSH may be useful in treatment of luteal phase defect.

Adult↗
PubMed1984

Normal variation in the length of the luteal phase of the menstrual cycle: identification of the short luteal phase.

Normal probability plots were used to assess the homogeneity of a population of 327 luteal phases from apparently ovulatory menstrual cycles. The length of the luteal phase was defined as the interval (in days) following but not including, the luteinizing hormone peak, up to and including the day before onset of menstruation. A small sub-set of the population consisted of cycles with abnormally short luteal phases but the majority of the data followed a normal frequency distribution which gave a mean (+/- SD) for normal luteal phase length of 14.13 (+/- 1.41) days. It was estimated that all cycles with a luteal phase less than or equal to 9 days were abnormal, and that 74%, 22% and 2% respectively of cycles with luteal phases of 10, 11 and 12 days were also abnormal. The total incidence of short luteal phases defined as above was 5.2%.

Adolescent↗
PubMed1987

Effect of clomiphene citrate administration during the early luteal phase on the luteal function and pregnancy rate of women.

To study the effect of clomiphene citrate (clomiphene) administration during the early luteal phase of the menstrual cycle on the luteal function and the pregnancy rate in women, 75 infertile women who ovulated but did not conceive after clomiphene treatment during the early follicular phase and 6 normal cycling women were chosen. Clomiphene was administered orally to 35 of the 75 infertile women at a dose of 50 mg per day for 5 days from the second day of the rise in the basal body temperature (BBT) as well as during the follicular phase, while 40 control patients received clomiphene only during the follicular phase. In the test patients, the rate of pregnancy (25.7%) was significantly (p less than 0.05) higher than that of control patients (10.0%). On the 7th of the rise of BBT, the mean serum progesterone levels of the test patients and normal cycling women treated with clomiphene were significantly (p less than 0.05) higher than those of the control patients. However, the levels of serum estradiol, LH and FSH, the gonadotropin pulsatilities, and the pituitary responses to LH-RH in the test women were not significantly different from those of the control. These data suggest that, when administered during the early luteal phase, clomiphene may act directly on the ovary, enhancing the secretion of progesterone from the corpus luteum, and thereby increasing the rate of pregnancy in infertile women with clomiphene-induced ovulation.

Adult↗
PubMed1991

Prolactin secretion and corpus luteum function in women with luteal phase deficiency.

Luteal phase deficiency (LPD) as a clinical infertility problem is considered to have a heterogeneous etiology. Hyperprolactinemia has long been considered a causative factor of LPD. In this context we investigated PRL secretion in 18 women with LPD. All of the subjects were infertile with 2 out of phase (greater than 2 days) endometrial biopsies; 10 of the women also had daily blood samples, this latter subgroup had significantly decreased integrated luteal phase progesterone (P) levels compared to normal women with in-phase biopsies. PRL secretion was investigated as follows: 1) daily blood levels; 2) pulsatile secretion patterns in 3 cycle phase [early follicular (12 h); late follicular (12 h); midluteal (24 h)], 3) LH-PRL coupling, and 4) nocturnal patterns. Results were compared to findings in 36 normal women. The mean daily levels of PRL over the menstrual cycle were not different between the two groups (LPD, 12.1 +/- 1.5; normal, 13.8 +/- 0.8 microgram/L; P = 0.3). There was no correlation between luteal phase integrated P and PRL levels for either group. There was a small difference in the PRL pulse amplitude in the early follicular phase between the LPD and normal women (2.6 +/- 0.3 vs. 5.5 +/- 1.3 micrograms/L; P less than 0.05). There were no significant differences between groups in PRL pulse frequency or mean level during the 12 or 24 h in any cycle phase. There was an equivalent amount of LH-PRL pulse coupling in both groups in all three cycle phases. Diurnal and nocturnal PRL secretion was studied by breaking the 24 h data (midluteal) into day (0700-2300 h) and night (2300-0700) segments. Mean PRL levels were higher at night in both groups (LPD, 15.9 vs. 12.6; normal, 15.4 vs. 9.3 micrograms/L; P less than 0.05), as expected. There were no differences in nocturnal PRL secretory patterns between the two groups. In summary, we have serious reservations whether abnormalities in PRL secretion are a common or integral part of the pathophysiology of LPD. From previous work we know these subtle abnormalities in PRL secretion in LPD are associated with definite abnormalities in gonadotropin secretion. We believe these gonadotropin abnormalities are probably more significant in terms of decreased P secretion.

Adult↗
PubMed1991

Hormonal and histological evaluation of the luteal phase after combined GnRH-agonist/gonadotrophin treatment for superovulation and luteal phase support in in-vitro fertilization.

A hormonal and histological study of the luteal phase was performed in 21 stimulated in-vitro fertilization (IVF) patients not undergoing embryo transfer. Ovarian stimulation was carried out with gonadotrophins [follicle stimulating hormone (FSH) + human menopausal gonadotrophin (HMG)] under pituitary suppression with buserelin. Ovulation was induced with 5000 IU human chorionic gonadotrophin (HCG) and additional doses of 5000, 2500 and 2500 IU were given on the day of follicular aspiration, and 2 and 5 days later respectively, to support the luteal phase. Supraphysiological levels of oestradiol (E2) and progesterone in plasma were found in the midluteal phase of all women, while prolactin was in the normal range. An endometrial biopsy taken in the late luteal phase was normal in 90.5% (19/21) of patients, most of them (15/19, 79%) having E2 greater than 1500 pg/ml on the day of HCG. Conversely, both patients with defective endometrial biopsies had E2 levels less than 1500 pg/ml.

Adult↗
PubMedDate not supplied

Luteal phase defects in assisted reproduction: the role of luteal phase supplementation.

Data from literature show that whereas in non-GnRH-a controlled ovarian hyperstimulation cycles luteal phase supplementation is not crucial, its use in GnRH-a/gonadotropins protocols seems to lead to a definite reduction of the negative effects of such drugs. The most important side effect of the hCG use as luteal support is the increased rate of the ovarian hyperstimulation syndrome (OHSS). Therefore its use should be reserved for very selected patients, for those subjects with preovulatory levels of E2 < 2500 pg/ml. As regard the use of progesterone, most authors agree that it has less efficacy than hCG but this depends on the administration route.

Chorionic Gonadotropin↗
PubMed1979

Gonadotropin in follicular phase in women with luteal phase defect.

Serum FSH and LH in women with luteal phase defect were measured. Their serum FSH and LH were lower than those in normal women and higher than those in women with amenorrhea. Administration of clomiphene citrate to the women with luteal phase defect were effective in 2/3 of the cases. These results are consistent with the hypothesis that a relative deficiency of FSH during the follicular phase results in diminished follicular development and subsequent inadequate corpus luteum maintenance.

Adult↗
PubMed1979

Clomiphene citrate in the management of infertility associated with shortened luteal phases.

Repetitively short luteal phases were found in eight infertile women. The short luteal phase was defined as 10 days or less from the presumed time of ovulation (as assessed by basal body temperature recording) to the onset of menses. Clomiphene citrate (Clomid) therapy resulted in pregnancy in two patients and lengthened the luteal phase in the other six. Ultimately, seven of eight patients conceived during Clomid therapy. Clomid therapy can lengthen the luteal phase in patients with luteal temperature elevation of 10 days or less. The occurrence of short luteal phases may be associated with infertility.

Anovulation↗