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Luteal Phase Deficiency: What We Now Know

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Luteal Phase Deficiency: What We Now Know ■ OBGMANAGEMENT BY LAWRENCE ENGMAN, MD, and ANTHONY A. LUCIANO, MD Luteal phase deficiency: What we now know Disagreement about the cause, true incidence, and diagnostic criteria of this condition makes evaluation and management difficult. Here, 2 physicians dissect the data and offer an algorithm of assessment and treatment. espite scanty and controversial sup- difficult to definitively diagnose the deficien- porting evidence, evaluation of cy or determine its incidence. Further, while Dpatients with infertility or recurrent reasonable consensus exists that endometrial pregnancy loss for possible luteal phase defi- biopsy is the most reliable diagnostic tool, ciency (LPD) is firmly established in clinical concerns remain about its timing, repetition, practice. In this article, we examine the data and interpretation. and offer our perspective on the role of LPD in assessing and managing couples with A defect of corpus luteum reproductive disorders (FIGURE 1). progesterone output? PD is defined as endometrial histology Many areas of controversy Linconsistent with the chronological date of lthough observational and retrospective the menstrual cycle, based on the woman’s Astudies have reported a higher incidence of LPD in women with infertility and recurrent KEY POINTS 1-4 pregnancy losses than in fertile controls, no ■ Luteal phase deficiency (LPD), defined as prospective study has confirmed these find- endometrial histology inconsistent with the ings. Furthermore, studies have failed to con- chronological date of the menstrual cycle, may be firm the superiority of any particular therapy. caused by deficient progesterone secretion from the corpus luteum or failure of the endometrium Once considered an important cause of to respond appropriately to ovarian steroids. infertility, LPD has become the subject of debate, with some experts questioning its very ■ Wide variation in the reported incidence of LPD— existence. Unclear terminology describing 3.7% to 20% in infertile women—reflects lack of this disorder is part of the problem, making it agreement about its diagnostic criteria. ■ Dr. Engman is a fellow in reproductive endocrinology and ■ Histologic dating of an endometrial sample is the infertility, University of Connecticut School of Medicine, gold standard for evaluation of the corpus luteum. Farmington, Conn. Dr. Luciano is professor of obstetrics and gynecology, University of Connecticut School of Medicine, ■ Two main treatment strategies have been and director, Center for Fertility and Women’s Health, New suggested: improving follicular dynamics using Britain General Hospital, New Britain, Conn. follicle-maturing drugs such as clomiphene, and use of supplemental progesterone during the August 2003 • OBG MANAGEMENT 41 luteal phase and first trimester of pregnancy. Luteal phase deficiency: What we now know FIGURE 1 of the corpus luteum steroidogenic function. Diagnosis and treatment of luteal phase deficiency Normal embryonic implantation depends on a Infertility properly functioning luteal phase, which, in turn, Luteal phase length* requires optimal secretion of follicle-stimulating hor- <12 days 12 to 16 days mone (FSH) and adequate follicular development dur- ing the follicular phase. Measurement of midluteal serum progesterone levels and endometrial stripe by transvaginal Other requirements are a ultrasound satisfactory luteinizing hor- mone (LH) surge during ovulation and continuous Progesterone >9 Progesterone tonic LH pulses during the ng/mL, endometrial <10 ng/mL and/or stripe ≥8 mm with endometrial stripe luteal phase of the cycle. diffuse pattern <8 mm LH secretion from the pituitary occurs in a pul- 7 Endometrial biopsy satile fashion, which is between cycle days essential for corpus 24 and 27 luteum function.8 During the follicular phase the Normal Abnormal in pulse frequency is high, 3 consecutive cycles occurring at a rate of Clomiphene approximately 1 pulse per or No luteal phase defect gonadotropins 90 minutes. However, dur- ing the luteal phase and under the influence of * In 3 consecutive cycles progesterone, the pulse frequency is significantly next menses. It was first described by Jones in diminished, occurring approximately every 1949.5 One year later, Noyes et al6 published 3 to 6 hours, depending on the age of the criteria on endometrial dating that became corpus luteum.7,9 The corpus luteum is the gold standard for LPD diagnosis. unresponsive to LH pulses during the early Pathophysiology. LPD may be caused by luteal phase; sensitivity develops about 4 to deficient progesterone secretion from the 6 days after ovulation.7,9 corpus luteum or failure of the endometri- The luteal phase thus involves creation of um to respond appropriately to ovarian an optimal hormonal environment as well as steroids (TABLE). Most experts believe LPD adequate endometrial transformation. Alter- is a defect of corpus luteum progesterone ation of any of the factors that contribute to a output—both in amount and duration— normally functioning corpus luteum may resulting in inadequate stimulation of the thus deleteriously affect the endometrium endometrium for implantation of the blas- and embryonic implantation. tocyst (FIGURE 2).5 Thus, the endometrial Epidemiology. The reported prevalence of histologic pattern is an important bioassay LPD ranges from 3.7% to 20% among patients 42 OBG MANAGEMENT • August 2003 Luteal phase deficiency: What we now know with infertility.10,11 When an out-of-phase TABLE endometrium is the diagnostic criterion, Etiology of luteal phase deficiency prevalence estimates range from 3.5% to 12,13 31%. A short luteal phase is thought to FOLLICULAR PHASE EVENTS 14 occur in 5% of ovulatory cycles. Some reports Trophic alterations suggest that LPD accounts for 25% to 40% of • Inadequate FSH stimulation 15 recurrent pregnancy losses. – Increased inhibin The wide variation in reported incidence • Alterations in LH secretion of LPD reflects the lack of agreement about its Intrinsic ovarian defects definition and diagnostic criteria. Further, • Defective granulosa cells some studies evaluating prevalence have not – Decreased inhibin levels concurrently tested controls—an important – Decreased follicular phase diameter omission since endometrial histology sugges- – Decreased primordial follicles tive of LPD occurs in up to 50% of single men- Intrinsic endometrial defects strual cycles and 25% of sequential cycles.16 • Inadequate estrogen priming Thus, the true incidence of the defect may LUTEAL PHASE EVENTS never be known. Trophic alterations • Alterations in LH secretion Seeking a reliable diagnostic tool – Decreased LH surge and luteal levels lthough significant progress has been – Systemic factors Amade in recent years, LPD diagnosis is • Factors acting upon corpus luteum neither straightforward nor completely accu- rate. Approaches include measuring the luteal Intrinsic corpus luteum defects phase duration, taking basal body temperature • Specific cellular defects – Large and small cell abnormalities (BBT), and assessing single or multiple serum progesterone levels, as well as using sono- Intrinsic secretory endometrial defect graphic imaging and endometrial biopsy. • Deficient number of progesterone receptors Luteal phase duration. An abnormally LUTEAL RESCUE EVENTS short luteal phase—defined as less than 10 Trophic alterations days17,18—occurs in approximately 5% of ovu- • Defective hCG stimulus 19 latory cycles. Research has shown such Intrinsic corpus luteum defects in early pregnancy cycles to have low peak serum progesterone • Defective progesterone synthesis levels, suggestive of poor corpus luteum func- Intrinsic endometrial defects tion.18 The relationship between an abnor- FSH = follicle-stimulating hormone, hCG = human chorionic gonadotropin, mally short luteal phase and infertility is LH = luteinizing hormone unclear, however. Smith and colleagues,20 for example, evaluated women with known fer- tility and women with unexplained infertility increases at midcycle. A rise of approximately and found the prevalence of a short luteal 2.5 ng/mL of progesterone will result in a phase to be the same in both groups. temperature elevation of nearly 1ºF. Our own practice is to measure luteal Interpretation of the BBT is based on this phase parameters in infertile patients. When thermogenic shift. Unfortunately, although the luteal phase is shorter than 12 days, we BBT may be a sensitive indicator of ovula- usually treat it. tion, it is a poor indicator of the quality of the Basal body temperature. A rise in BBT luteal phase. Neither the rate nor the magni- occurs when progesterone production tude of rise of the postovulatory temperature August 2003 • OBG MANAGEMENT 45 Luteal phase deficiency: What we now know curve correlates with endometrial histology. and conception cycles. However, as men- Overall correlation varies between 25%21 and tioned earlier, the cutoff level for normal 81%.22 Further, an abnormal BBT may occur progesterone is not standard in the literature. in 12% of women with normal endometrial Single midluteal serum values between 2.5 histologic dating.23 Because of this lack of ng/mL and 15 ng/mL have been used by var- specificity and sensitivity, BBT is not an ade- ious investigators to distinguish normal from quate diagnostic tool. abnormal luteal phase levels.14,29 Measuring progesterone and its Using 95% confidence intervals, metabolites. Because progesterone is the Landgren et al30 and Olive11 considered prog- principal product of the corpus luteum, its esterone levels abnormal
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