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The luteal phase is the second half of your cycle, beginning after ovulation and ending when you get your next period. But the luteal phase is an important part of not just your fertility, but your overall health. But this is a particularly important part of the cycle. The luteal phase is the latter half of your cycle, after the dramatic and exciting stuff has already happened. If you were planning a surprise party for your husband, the follicular phase would be the part where you bake a cake, gather all your friends together, and hang streamers all over the living room. The luteal phase would be the part where everyone sits quietly, the tension building as you all wait for him to get home.

Once the follicle has released its egg, the egg travels down the fallopian tube, where it may come in contact with sperm and be fertilized. The follicle itself then changes. The empty sac closes off, turns yellow, and transforms into a new structure called the corpus luteum.

The corpus luteum releases progesterone and some estrogen. Progesterone thickens the lining of your uterus so that a fertilized egg can implant. Blood vessels grow inside the lining. These vessels will supply oxygen and nutrients to the developing embryo.

If you get pregnant, your body will also start to produce human gonadotropin hCG. This hormone maintains the corpus luteum. HCG enables the corpus luteum to keep producing progesterone until around the 10th week of your pregnancy. Then the placenta takes over progesterone production. Your progesterone levels will drop. The uterine lining will shed during your period. Then the entire cycle will repeat. A normal luteal phase can last anywhere from 11 to 17 days.

In most womenthe luteal phase lasts 12 to 14 days. Your luteal phase is considered to be short if it lasts less than 10 days. In other words, you have a short luteal phase if you get your period 10 days or less after you ovulate.

As a result, it can be harder to get pregnant or it might take you longer to conceive. A long luteal phase may be due to a hormone imbalance like polycystic ovary syndrome PCOS.

All About the Luteal Phase of the Menstrual Cycle

But your progesterone levels during this phase may drop as you get closer to menopause. A short luteal phase can be a sign of a condition called luteal phase defect LPD. In LPD, the ovary produces less progesterone than usual. LPD can lead to infertility and miscarriage.

Certain lifestyle factors might also be behind a short luteal phase. In one studywomen with a short luteal phase were more likely to smoke than those with a longer phase. The first and likely more common cause relates to the impaired function of the CL resulting in insufficient progesterone and estradiol secretion. Both mechanisms result in a CL with deficiencies in progesterone production.

The second theory suggests an inability of the endometrium to mount a proper response to appropriate estradiol and progesterone exposure. Because the CL originates from the dominant follicles, it is logical to infer that abnormal development of the dominant follicle could result in an abnormal CL. Multiple studies have found a correlation between low follicular follicle-stimulating hormone FSH and LPD as defined by luteal phase progesterone secretion or luteal phase biopsy. Experiments by Soules and colleagues 43 found some women with LPD have a fixed and increased LH pulse frequency throughout the early follicular phase compared with women with normal luteal function who have an accelerating LH pulse frequency approaching ovulation.

It is suggested that an earlier increase in LH pulse frequency in the early follicular phase leads to decreased LH bioactivity in the luteal phase, decreasing progesterone secretion. These medications can cause suppression of pituitary LH secretion for 2 to 3 weeks after discontinuation, resulting in decreased CL progesterone production and necessitating progesterone supplementation for optimal outcomes.

Another potential form of LPD is an abnormal endometrial response to adequate levels of progesterone exposure. Usadi and colleagues 39 investigated normal, young research subjects who underwent modeled cycles, highly similar to endometrial preparation for donor oocyte recipience, except that progesterone levels were reduced to simulate LPD.

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These subjects underwent pituitary downregulation with a GnRH agonist and were supplemented with estradiol, to mimic the follicular phase, followed by estradiol and varying doses of progesterone to mimic the effects of the luteal phase on the endometrium.

These investigators found that unequivocally low levels of progesterone produced a completely normal appearing endometrium on histologic evaluation. The findings suggest that lower levels of progesterone might not be the sole culprit in LPD and there may be other molecular mechanisms affecting abnormal responses to progesterone and, therefore, abnormal endometrial development and receptivity.

Due to the incomplete understanding of the pathophysiology and lack of an accurate method to diagnose LPD, empiric treatment of suspected LPD cannot be completely evidence-based.

Clinical studies of treatment regiments are faced with a catch how to evaluate treatment in a disease that cannot be accurately diagnosed. Most studies have used improvements in surrogate markers, such as endometrial biopsy and progesterone level, to show treatment effect. Unfortunately all attempts to link these surrogate outcomes to fertility outcomes have been unsuccessful.

Instead, this is an area in which many treating physicians believe that the art of medicine plays a role and they continue to treat patients they suspect to be affected by a LPD.

In this scenario, the risk of the treatment must be exceptionally small. Before considering treatment of LPD, it is important to evaluate and treat underlying conditions, such as hypothyroidism and hyperprolactinemia, which can alter the hypothalamic-pituitary-ovary axis function, causing abnormalities in hormone production.

LUTEAL PHASE DEFICIENCY. Luteal phase deficiency (LPD) is a condition of insufficient progesterone exposure to maintain a normal secretory endometrium and allow for normal embryo implantation and growth. 19 The condition was first described as a possible cause of infertility by Georgiana Seegar Jones 20 in This early, elegant study investigated the luteal phase of ovulatory women Cited by: Endometrial dating luteal phase defect - Register and search over 40 million singles: chat. Join the leader in rapport services and find a date today. Join and search! Want to meet eligible single woman who share your zest for life? Indeed, for those who've tried and failed to . Luteal phase defect (LPD) or sometimes termed inadequate luteal phase is defined as secretory maturation that is at least 2 days earlier than the expected chronological dating in two, preferably consecutive, cycles. 17 In the past decade, the endometrial biopsy as a tool to access the adequacy of the luteal phase has come under fire. Those.

If clinical suspicion over multiple cycles points to LPD as a cause of infertility or miscarriage, it is reasonable to consider empiric treatment to correct LPD. Two strategies, improving the follicular development and supplementing progesterone, have been used to correct suspected LPD and treat infertility or recurrent miscarriage.

Extrapolating from studies showing impaired luteal progesterone secretion with lower gonadotropins in the follicular phase, it is inferred that more robust or numerous mature follicles will improve luteal progesterone secretion from the CL, correcting LPD. Therefore, many clinicians treat suspected LPD by attempting to optimize follicular development and number using ovulation induction agents, including clomiphene citrate CCletrozole, or injectable gonadotropins.

However, how many would have had the same without CC cannot be determined. Progesterone supplementation is suggested as a treatment of LPD. Although frequently used, there is no published evidence that it improves pregnancy outcomes in natural cycles.

Given reports of teratogenicity associated with synthetic progestins 48 that have since been disproven 49natural micronized progesterone has been the treatment of choice. Micronized progesterone can be potentially supplied orally, sublingually, rectally, as an oil-based vaginal suppository, an aqueous vaginal cream, or intramuscularly see later discussion.

A meta-analysis evaluated 3 underpowered controlled trails that failed to show a positive effect of progesterone treatment of recurrent pregnancy loss in patients with LPD. Well-designed randomized trials are needed to definitively answer whether ovulation induction or luteal progesterone supplementation is beneficial for patients with LPD.

We typically treat with ovulation induction agents 50 mg CC or 2. In patients with recurrent loss, the progesterone supplementation is often given after the first positive pregnancy test.

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We do not treat suspected LPD with injectable gonadotropins, given the high cost and unacceptable risk of twins or higher order multiples. We acknowledge these treatments are not based on strong evidence; however, they are based on clinical interpretation of underlying physiology and come with few risks.

These treatments frequently result in either the transfer of an embryo into a woman who has undergone controlled ovarian hyperstimulation with subsequent oocyte retrieval or a woman receiving an embryo in a nonovulatory cycle FET or fresh embryo transfer of embryos from donor eggs into a recipient.

In both situations, there is an effective LPD.

IVF Protocols and Procedures - Kathleen Brennan, MD - UCLA OBGYN/Fertility Clinic

In the patients who are receiving embryos in nonovulatory cycles, the need for progesterone supplementation is easy to understand given the absent CL.

These are cycles in which the natural cyclicity is absent or suppressed, and the endometrial effects of the follicular phase are mimicked with estradiol supplementation to cause a proliferative endometrium.

To prepare the endometrium for implantation of the embryo, the luteal phase is mimicked by exposing the endometrium to progesterone. Timing the transfer of an embryo to the appropriate duration of progesterone exposure allows for successful implantation.

It is also clear that the luteal phase following controlled ovarian hyperstimulation and oocyte aspiration is dysfunctional, a fact that has been recognized since the infancy of IVF. This theory was questioned after no changes in progesterone levels or luteal phase length were seen after aspiration of the single mature follicle in a natural, unstimulated cycle. Currently, the most widely accepted theory of LPD after IVF states the supraphysiologic steroid hormones secreted by the multiple CL in the early luteal phase of an IVF cycle causes direct inhibition of LH secretion via negative feedback on the hypothalamic-pituitary axis.

The optimization of ART success rates relies not only on the creation of high-quality embryos but also on the establishment of a receptive endometrium. During the past 35 years, since the first IVF pregnancy and subsequent first pregnancy from frozen embryos, significant research has been directed toward establishing the optimum supplementation of the luteal phase in both IVF and FET cycles, with a goal to maximize live births while minimizing patient discomfort and inconvenience.

A recent Cochrane systematic review has evaluated many of these options and will be referred to in the remainder of this article. Progesterone supplementation is available in multiple preparations, including intramuscular, vaginal, oral, or in a newly developed subcutaneous preparation.

Subcutaneous progesterone is still in the trial phase. Oral micronized progesterone was the luteal support progesterone of choice in the s; however, it has since proven to be a poor treatment option.

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Although the most convenient form of progesterone, micronized progesterone, has poor and inconsistent bioavailability. In a randomized, controlled trial, users of oral micronized progesterone had a significantly decreased implantation rate compared with users of intramuscular progesterone Given the allure of an oral agent for luteal support, other oral agents have been studied to replace oral micronized progesterone.

Dydrogestrone, is an oral progestin with improved bioavailability compared with oral micronized progesterone. Intramuscular progesterone was first described as a form of luteal supplementation during IVF in Vaginal preparations of progesterone have become the mainstay of luteal supplementation during IVF because of their relative ease of use and equivalence to intramuscular progesterone.

Vaginal progesterone benefits from a first-pass uterine effect in which endometrial tissue concentrations are typically much greater than would be expected based on serum levels. Recently, a water-soluble injectable progesterone complex Prolutex has been developed for subcutaneous administration. There is currently no consensus on when to begin progesterone supplementation during an IVF cycle.

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The first dose of progesterone is typically administered between the between the day of retrieval to 2 days after retrieval with no obvious changes in pregnancy rates. Most surveyed clinics A recent meta-analysis of 6 eligible studies and randomized subjects concluded there may be no additional benefit of progesterone supplementation beyond the first positive HCG value, showing no difference in live birth risk ratio [RR]: 0.

Effect of days of progesterone exposure on implantation and pregnancy rates after cleavage-stage embryo transfer from donor oocytes.

The window for embryo transfer in oocyte donation cycles depends on the duration of progesterone therapy. Hum Reprod ;13 3 Adjuvants to progesterone supplementation to increase IVF pregnancy rates have been widely discussed in the literature. The CL is not only a source of progesterone but also produces estradiol, along with many nonsteroidal hormones.

Therefore, it has been suggested luteal support should include estradiol supplementation. However, when a subgroup analysis of clinical pregnancy was performed, progesterone alone performed worse then progesterone plus transdermal estradiol OR: 0.

Another suggested adjuvant to progesterone supplementation is a single dose of GnRH agonist 5 to 6 days after oocyte retrieval. It is hypothesized the GnRH agonist may support the CL by stimulating LH secretion for the pituitary but also may have effects on the endometrial GnRH receptors or direct effects on the embryo. When data were pooled, there was an increased pregnancy rate in cycles in which a single dose of luteal GnRH agonist was given 5 to 6 days after oocyte retrieval A subgroup analysis was performed and pregnancy rate was significantly higher with luteal GnRH agonist used in a GnRH antagonist stimulation compared with the long protocol.

Similarly, the recent Cochrane review showed increased pregnancy, ongoing-pregnancy, and live birth rates in subjects receiving luteal GnRH agonists. In these cycles, exogenous estradiol is typically used to proliferate the endometrium, then exogenous progesterone is added to induce secretory changes in preparation for implantation.

Intramuscular progesterone is typically used for this purpose in the United States, whereas in Europe vaginal progesterone is preferred. Two small, prospective, randomized trials from the same group showed no difference in ongoing pregnancy rate when comparing intramuscular progesterone to vaginal progesterone in recipients of donor oocytes.

However, 2 other retrospective studies of women undergoing FET illustrated a deceased live birth rate in subjects receiving vaginal progesterone In the clinical studies mentioned above, 97 - cleavage-stage embryos were transferred on the fourth day of progesterone exposure and blastocyst were transferred on the sixth day of progesterone exposure.

Progesterone production from the CL is critical for natural reproduction and progesterone supplementation seems to be an important ct of any ART treatment. LPD in natural cycles is a plausible cause of infertility and pregnancy loss, although there is no adequate diagnostic test.

Future research should concentrate on establishing thresholds of progesterone dose and timing for fertile and infertile women, as well as on a precise and accurate diagnostic test. Luteal phase deficiency is a disease without a reliable diagnostic test, impairing clinical research and patient care. Exogenous progesterone is the primary agent for luteal support during assisted reproductive technology treatment; however, the best delivery method, protocol, and formulation are not yet known.

Vaginal or intramuscular progesterone seem to be equivalent in terms of pregnancy outcomes after in vitro fertilization. The best route of progesterone supplementation after frozen embryo transfer is not yet established. The authors have nothing to disclose. National Center for Biotechnology InformationU. Obstet Gynecol Clin North Am. Author manuscript; available in PMC Mar 1.

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Tolga B. YoungMD, PhD. Author information Article notes Copyright and License information Disclaimer. Copyright notice.

See other articles in PMC that cite the published article. Pathophysiologic theories of luteal phase deficiency Two mechanisms have been proposed as causes of clinical LPD. Treatment of luteal phase deficiency Due to the incomplete understanding of the pathophysiology and lack of an accurate method to diagnose LPD, empiric treatment of suspected LPD cannot be completely evidence-based. Open in a separate window. Footnotes The authors have nothing to disclose.

References 1. Fritz MA, Speroff L. Clinical gynecologic endocrinology and infertility. An immunohistochemical study of the vascularization of the human Graafian follicle. Hum Reprod. Human follicle fluid vascular endothelial growth factor concentrations are correlated with luteinization in spontaneously developing follicles. Barbieri RL. The endocrinology of the menstrual cycle.

Methods Mol Biol. Chapter 7 [ PubMed ] [ Google Scholar ]. Functional differentiation in steroidogenesis of two types of luteal cells isolated from mature human corpora lutea of menstrual cycle.

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J Clin Endocrinol Metab. A differentiation antigen of human large luteal cells in corpora lutea of the menstrual cycle and early pregnancy.

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Biol Reprod. Progesterone production by monkey luteal cell sub-populations at different stages of the menstrual cycle: changes in agonist responsiveness. Morpho-functional study of human luteal cell subpopulations. The rhesus monkey corpus luteum is dependent on pituitary gonadotropin secretion throughout the luteal phase of the menstrual cycle. Mechanisms regulating the menstrual cycle in women. Recent Prog Horm Res.

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Neuroendocrine regulation of the corpus luteum in the human. Evidence for pulsatile progesterone secretion. J Clin Invest. Ellinwood WE. Changing frequency of pulsatile luteinizing hormone and progesterone secretion during the luteal phase of the menstrual cycle of rhesus monkeys. Normal variation in the length of the luteal phase of the menstrual cycle: identification of the short luteal phase.

Br J Obstet Gynaecol. Philadelphia: Elsevier; Characterization of the physiological pattern of episodic gonadotropin secretion throughout the human menstrual cycle.

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Lopata A, Hay DL. The surplus human embryo: its potential for growth, blastulation, hatching, and human chorionic gonadotropin production in culture.


Fertil Steril. The significance of the human corpus luteum in pregnancy maintenance. Am J Obstet Gynecol. Effects of luteectomy and progesterone replacement therapy in early pregnant patients.

The clinical relevance of luteal phase deficiency: a committee opinion. Jones GS. Some newer cts of the management of infertility. Luteal phase defect. Curr Opin Obstet Gynecol.

Sonntag B, Ludwig M.

A meta-analysis of randomized controlled trials of IVF cycles using GnRH agonists observed that all luteal phase support regimens (IM or vaginally administered P and hCG) yield significantly higher pregnancy rates (PR), compared with placebo or no treatment (11 x 11 Pritts, E.A. and Atwood, A.K. Luteal phase support in infertility. Oct 08,   Dating has low interobserver agreement, and may not have accuracy to diagnose luteal phase deficiency or to guide clinical management of women with reproductive failure (Fertil Steril ;) Difficult to date endometrium of patients with IUD or on hormones or if . Aug 20,   A normal luteal phase can last anywhere from 11 to 17 days. In most women, the luteal phase lasts 12 to 14 days. Your luteal phase is considered to be short if it lasts less than 10 days. In Author: Stephanie Watson.

An integrated view on the luteal phase: diagnosis and treatment in subfertility. Clin Endocrinol Oxf ; 77 4 Luteal phase deficiency in regularly menstruating women: prevalence and overlap in identification based on clinical and biochemical diagnostic criteria. Superovulation of habitual aborters with subtle luteal phase deficiency. Int J Fertil. The inadequate luteal phase. Am J Ob-stet Gynecol.

Unexplained infertility: evaluation of the luteal phase; results of the National Center for Infertility Research at Michigan. Swyer GI, Daley D. Progesterone implantation in habitual abortion. Br Med J. Endocrinology and recurrent early pregnancy loss.

Semin Reprod Med. The short luteal phase and infertility.

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