Luteal Phase Dysfunction

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1 (advertisement) Home Specialties CME PDA Contributor Recruitment Patient Education November 4, 2003 Articles Images CME Patient Education Advanced Search Link to this site Back to: emedicine Specialties > Medicine, Ob/Gyn, Psychiatry, and Surgery > Obstetrics/gynecology Luteal Phase Dysfunction Last Updated: October 17, 2002 Rate this Article to a Colleague Synonyms and related keywords: LPD, luteal phase deficiency, luteal phase defect, progesterone, infertility, recurrent pregnancy loss AUTHOR INFORMATION Section 1 of 10 Author: Thomas L Alderson, DO, Program Director, Assistant Professor, Department of Obstetrics and Gynecology, Mount Clemens General Hospital, Michigan State University College of Osteopathic Medicine Editor(s): Ronald Levine, MD, Director, Section of Gynecologic Endoscopy, Professor, Department of Obstetrics and Gynecology, University of Louisville School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, emedicine; A David Barnes, MD, PhD, Clinical Assistant Professor, Department of Obstetrics and Gynecology, Jackson Memorial Hospital, University of Miami; Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Lake Hospital; and Lee P Shulman, MD, Professor of Obstetrics and Gynecology, Head, Section of Reproductive Genetics, Feinberg School of Medicine, Northwestern University; Distinguished Physician, Department of Obstetrics and Gynecology, Northwestern Memorial Hospital INTRODUCTION Section 2 of 10 Quick Find Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Click for related images. Related Articles Hyperprolactinemia Continuing Education CME available for this topic. Click here to take this CME. Patient Education Click here for patient education. Background: In 1949, Georgeanna Jones, MD, first described luteal phase deficiency (LPD). The inadequate secretory transformation of the endometrium, resulting from deficient progesterone production, has been implicated in both infertility and recurrent pregnancy loss. LPD has been the subject of much debate among specialists in the field of reproductive endocrinology since Jones' introduction of this condition into the medical literature. LPD has been diagnosed in 3-20% of patients who are infertile and in 5-60% of patients experiencing recurrent pregnancy loss. However, data show that 6-10% of women who are fertile demonstrate an inadequate luteal phase, which confirms the need for a better understanding of normal variations in the menstrual cycle and in variations Page 1 of 10

2 that could be pathologic. This article addresses healthy menstrual physiology, the proposed pathophysiology of LPD, current methods available for diagnosis and treatment, and reasons for the controversy surrounding this subject. Healthy menstrual physiology Following ovulation, the mature ovarian follicle forms the corpus luteum, which becomes a blood-filled structure that allows the precursor cholesterol to be obtained, initiating steroidogenesis and resulting in progesterone production. Whereas the follicular phase of the menstrual cycle can vary in length, the secretory phase lasts approximately 14 days, correlating with the life span of the corpus luteum. Presumably, progesterone prepares the endometrium for implantation and maintenance of a pregnancy. If pregnancy occurs, the production of progesterone from the corpus luteum continues for 7 weeks because of the tonic release of luteinizing hormone (LH) from the pituitary gland. Studies show that after 7 weeks, the placenta takes over this function. If pregnancy does not occur, menses begins with the demise of the corpus luteum. Pathophysiology: The following mechanisms can cause an inadequate endometrial response to hormonal stimulation during the luteal phase. Abnormal follicular development Abnormal follicular development results from inadequate follicle-stimulating hormone (FSH) and LH secretion from the anterior pituitary gland. FSH stimulates the granulosa cells of the developing follicle to produce estradiol from the conversion of its substrate androstenedione. A decrease in FSH release results in reduced granulosa cell growth and lower estradiol levels. Because the corpus luteum is not a de novo structure but is a direct result of the follicle, it shows the effects of abnormal folliculogenesis with decreased progesterone production. Abnormal luteinization An inadequate LH release can cause a decrease in androstenedione from the theca cells. Less substrate results in a decrease in estradiol and, subsequently, lower progesterone levels. Additionally, a suboptimal LH surge at ovulation causes deficient progesterone because of inadequate luteinization of the granulosa cells. Uterine abnormalities Uterine abnormalities cause changes in vascularization of the endometrium despite normal progesterone levels. Myomas, uterine septa, and endometritis are responsible for poor secretory changes in the endometrium. Hypocholesterolemia Hypocholesterolemia is the substrate responsible for initiation of the steroid pathway. A deficiency results in low-to-absent progesterone production and a luteal phase defect. Frequency: Page 2 of 10

3 In the US: No consensus has been achieved regarding frequency; however, a 1991 symposium hypothesized that LPD occurs in 3-10% of infertile patients, and healthy women have deficient luteal phase production of progesterone on a sporadic basis. Internationally: Presumably, international frequency is similar to that in the United States. See above. Mortality/Morbidity: condition. Race: LPD effects women of all races. Sex: This condition affects only women. No morbidity or mortality has been associated with this Age: LPD primarily affects women during their reproductive years. CLINICAL Section 3 of 10 History: The patient may report menstrual cycles of less than 26 days or a luteal phase of less than 11 days by basal body temperatures; however, neither of these circumstances can alone be used to diagnose LPD. Physical: Physical findings that might aid in the diagnosis of luteal phase dysfunction are those associated with abnormal endocrine function. An enlarged thyroid gland is indicative of hypothyroidism. Expression of milk from the breasts (galactorrhea) is indicative of hyperprolactinemia. An enlarged, irregularly shaped uterus is indicative of uterine myomas. Causes: See Pathophysiology for a full discussion of the causes. DIFFERENTIALS Section 4 of 10 Hyperprolactinemia WORKUP Section 5 of 10 Lab Studies: Serum progesterone levels have been studied as a means to diagnose LPD. Early data showed that peak progesterone production occurred in the mid-luteal phase. Later studies confirmed that progesterone is released in a pulsatile fashion, suggesting that a single sample is nondiagnostic. Page 3 of 10

4 The use of multiple samples to overcome the pulsatile nature of progesterone is expensive and inconvenient. Urinary LH kits provide a useful test to estimate the appropriate timing of an endometrial biopsy (EB). Following a positive test finding, ovulation occurs within hours. The EB should be performed on the 12th day of a 14-day luteal phase. Studies measuring progestin endometrial protein (PEP) have not been conclusive in diagnosing LPD. Studies regarding cell adhesion molecules or integrins, growth factors, and cytokines are all in the experimental phase. Imaging Studies: Ultrasound documentation of ovulation from follicular growth to collapse of the follicle is very accurate; however, this procedure is too expensive and time consuming to be realistic in all patients. Ultrasound measurement of endometrial thickness has not been shown to be effective in the prediction of LPD. Procedures: Biopsy In 1950, Noyes, Hertig, and Rock established that the diagnosis of LPD is centered on histologic dating of the endometrium. However, the location and time of the biopsy can greatly influence EB findings. Some authors believe that mid-luteal phase biopsy is the best for accurate diagnosis of LPD. Biopsies from the fundus of the uterus yield improved histologic samples compared to those taken from the lower uterine segment. Specimens taken approximately 1-2 days prior to menses provide better specimens for interpretation. For example, women with cycles of 28 days should have an EB performed on the 26th day. Histologically, a luteal phase defect provides a biopsy that lags behind the date of actual endometrial sampling by 3 days or more. To confirm that such a result is not a variance within the reference range, the biopsy should be performed in 2 consecutive cycles; however, the discomfort associated with the biopsy causes difficulty in convincing the patient to have the procedure performed twice. Several methods can be used to time the EB just prior to menses. The basal body temperature (BBT) chart is one such method. The BBT chart can aid in determining the length of the luteal phase. A luteal phase of less than 11 days may be associated with LPD. The BBT chart can also assist in timing the EB by observing the patient's cycle length and performing the biopsy 2 days prior to the expected menses. Although the BBT chart is easy and inexpensive, interpretation can be difficult and frustrating with a woman who is infertile or has suffered multiple pregnancy losses. TREATMENT Section 6 of 10 Medical Care: Hyperprolactinemia and hypothyroidism cause LPD through hypothalamic-pituitary dysfunction. Page 4 of 10

5 Bromocriptine and levothyroxine, respectively, are used to treat LPD in women with these conditions. In women without hyperprolactinemia and hypothyroidism, vaginal progesterone is advocated to supplement endogenous progesterone production. The vaginal suppository or gel is preferred over both the oral and intramuscular forms because of superior endometrial progesterone concentrations. Vaginal suppositories are less expensive but are messier than the vaginal gel. Progesterone should be continued for 8-10 weeks to cover the time of the ovarian-placental shift. Clomiphene citrate corrects LPD by improving folliculogenesis and the resultant luteal phase following ovulation. Successful treatment with gonadotropins and human chorionic gonadotropins (HCGs) probably results from superovulation rather than from a correction of LPD. Following any of these treatments, the patient should have a repeat EB to determine that LPD has been corrected. MEDICATION Section 7 of 10 The goals of pharmacotherapy are to restore ovarian function, reduce morbidity, and prevent complications. Drug Category: Hormone replacements -- Medical treatment centers on hormonal support of the patient's luteal phase. Bromocriptine (Parlodel) -- Used if hyperprolactinemia is the underlying pathology causing LPD. Tablets can be used vaginally in patients who cannot tolerate adverse GI effects mg (ie, half of 2.5-mg tab) PO qd; increase to 2.5 mg/d after 2 wk; repeat EB after a prolactin level in the reference range is achieved to document correction of LPD Pediatric Dose Not established Documented hypersensitivity; ischemic heart disease; peripheral vascular disorders Toxicity may increase with ergot alkaloids; amitriptyline, butyrophenones, imipramine, methyldopa, phenothiazines, and reserpine may decrease bromocriptine effects C - Safety for use during pregnancy has not been established. Precautions Caution in renal or hepatic disease Levothyroxine (Levoxyl, Synthroid) -- If LPD is caused by hypothyroidism, correction of endocrine disease results in normal luteal phase mcg/kg of ideal body weight PO; repeat TSH and T4 in 6-8 wk to determine if dose adjustment is needed; once normalization is achieved, a repeat EB Page 5 of 10

6 Pediatric Dose Precautions Pediatric Dose Precautions Pediatric Dose should be performed to confirm correction of LPD Not established Documented hypersensitivity; uncorrected adrenal insufficiency Cholestyramine may decrease liothyronine absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; effect of anticoagulants increased when administered with liothyronine; activity of some beta-blockers may decrease when patients who have hypothyroidism are converted to a euthyroid state A - Safe in pregnancy Caution in angina pectoris or cardiovascular disease; monitor thyroid status periodically Clomiphene citrate (Clomid, Serophene) -- Stimulates release of pituitary gonadotropins. Improves folliculogenesis and, therefore, the luteal phase. Works best in biopsies that are lagging 1 week behind the date of endometrial sampling. Initial: 50 mg PO qd from days 5-9 of menstrual cycle; if repeat EB does not confirm correction of LPD, then increase in 50-mg doses (ie, 100 mg, 150 mg); no increment in dosage is necessary once correction of LPD is accomplished Not established Documented hypersensitivity; liver disease; abnormal uterine bleeding; uncontrolled thyroid or adrenal dysfunction Danazol may reduce response to clomiphene X - Contraindicated in pregnancy Visual symptoms and abdominal pain may occur Cabergoline (Dostinex) -- Long-acting dopamine receptor agonist with high affinity for D2 receptors. Prolactin secretion by anterior pituitary predominates under hypothalamic inhibitory control exerted through dopamine mg PO 2 times/wk; once prolactin level is within the reference range, a repeat EB should be performed to confirm correction of LPD Not established Documented hypersensitivity; uncontrolled hypertension May increase effects of antihypertensive medications (adjust dose accordingly); dopamine agonists may reduce effects of cabergoline C - Safety for use during pregnancy has not been established. Page 6 of 10

7 Precautions Pediatric Dose Precautions Pediatric Dose Concomitant use with hypertensives; do not use to inhibit physiologic lactation due to relatively high incidence of stroke, seizures, and hypertension; monitor prolactin levels monthly; caution in hepatic impairment Progesterone (Crinone Vaginal Gel, Progestasert) -- Progesterone supplementation may be administered PO, IM, or vaginally. Oral progesterone is metabolized rapidly in the liver, and the metabolites have little effect on endometrial activity. When administered IM, fails to achieve adequate levels of endometrial progesterone compared with the vaginal forms. Vaginal progesterone is DOC for LPD; this is because of the proximity of the uterus to where the medication is delivered. Vaginal gel 8%, either qd or bid, is better tolerated compared to suppository form. Gel also provides increased receptor sites in the endometrium compared with suppository. Treatment begins 2 days after ovulation as determined by an ovulation predictor kit. Correction of LPD can be confirmed by repeat EB. Vaginal gel: Apply qd/bid Suppository: 100 mg bid Oil: 25 mg IM bid Not established Documented hypersensitivity; thrombophlebitis, carcinoma of the breast, undiagnosed vaginal bleeding Aminoglutethimide may decrease effects X - Contraindicated in pregnancy Fluid retention may occur; caution in patients with history of depression, impaired liver function, diabetes, and epilepsy; monitor for loss of vision, proptosis, diplopia, migraine, signs of embolic disorders Follitropins (Follistim, Gonal-F, Fertinex) -- Improve folliculogenesis, which increases total progesterone. This remains an expensive method associated with increased patient discomfort because medication is administered SC. 75 IU IM increase to desired follicular response Not established Documented hypersensitivity; ovarian failure, uncontrolled thyroid or adrenal dysfunction, tumor of the ovary, breast, uterus, hypothalamus, or pituitary; undiagnosed vaginal bleeding; ovarian cystic enlargement not due to polycystic ovarian disease None reported X - Contraindicated in pregnancy Page 7 of 10

8 Precautions Ovarian enlargement may be accompanied by abdominal distention; serious respiratory distress, thromboembolic events, atelectasis may occur FOLLOW-UP Section 8 of 10 Further Inpatient Care: Luteal phase dysfunction does not require hospitalization and therefore no inpatient diagnostic workup or treatment. Further Outpatient Care: All diagnostic testing and treatment can be performed in an outpatient setting. In/Out Patient Meds: Medications used to treat luteal phase dysfunction include dopamine receptor agonists to treat elevated serum prolactin levels. Thyroid replacement treats hypothyroidism. Supplemental progesterone increases the lower levels in the luteal phase observed with this condition. Clomiphene citrate enhances follicular development and thus increases luteal-phase progesterone levels. Human menopausal gonadotropins enhance follicular development and increase luteal-phase progesterone levels. Deterrence/Prevention: No methodology prevents luteal phase defect. Maintain a high level of clinical suspicion that such a condition exists when seeing a patient with infertility or recurrent pregnancy loss. Complications: Complications are associated with the EB. Be cautious when performing the biopsy in order to avoid perforating the uterus. Advise patients to take a nonsteroidal anti-inflammatory drug (NSAID) prior to the procedure to alleviate uterine cramping. No antibiotic prophylaxis is needed. Prognosis: The lack of double-blinded placebo-controlled studies prevents an accurate prognosis for this condition. Patient Education: Patients should keep an accurate menstrual cycle calendar. Abnormal cycle length may heighten the physician's suspicion that a luteal phase dysfunction exists. Page 8 of 10

9 MISCELLANEOUS Section 9 of 10 Medical/Legal Pitfalls: Failure to consider the diagnosis when seeing a patient with infertility or recurrent pregnancy loss Special Concerns: The best treatment is not yet established because of the lack of double-blinded placebo-controlled studies with an adequate number of patients from whom appropriate conclusions can be made. Until investigators can resolve these issues, the decision to treat patients with LPD occurs through an open and honest discussion between the physician and patient. BIBLIOGRAPHY Section 10 of 10 Behrman HR, Endo T, Aten RF: Corpus luteum function and regression. Reprod Med Rev 1993; 2: Cicinelli E, de Ziegler D, Bulletti C, et al: Direct transport of progesterone from vagina to uterus. Obstet Gynecol 2000 Mar; 95(3): [Medline]. Cooke ID: The corpus luteum. Hum Reprod 1988 Feb; 3(2): [Medline]. Csapo AI, Pulkkinen MO, Ruttner B et al: The significance of the human corpus luteum in pregnancy maintenance. I. Preliminary studies. Am J Obstet Gynecol 1972 Apr 15; 112(8): [Medline]. Giudice LC: Growth factors and growth modulators in human uterine endometrium: their potential relevance to reproductive medicine. Fertil Steril 1994 Jan; 61(1): 1-17 [Medline]. Healy DL, Schenken RS, Lynch A, et al: Pulsatile progesterone secretion: its relevance to clinical evaluation of corpus luteum function. Fertil Steril 1984 Jan; 41(1): [Medline]. Jones GES: Some newer aspects of management of infertility. JAMA 1949; 141: Jones GS: The luteal phase defect. Fertil Steril 1976 Apr; 27(4): [Medline]. Karamardian LM, Grimes DA: Luteal phase deficiency: effect of treatment on pregnancy rates. Am J Obstet Gynecol 1992 Nov; 167(5): [Medline]. Li TC, Nuttall L, Klentzeris L, Cooke ID: How well does ultrasonographic measurement of endometrial thickness predict the results of histological dating? Hum Reprod 1992 Jan; 7(1): 1-5 [Medline]. McNeely MJ, Soules MR: The diagnosis of luteal phase deficiency: a critical review. Fertil Steril 1988 Jul; 50(1): 1-15 [Medline]. Murray DL, Reich L, Adashi EY: Oral clomiphene citrate and vaginal progesterone suppositories in the treatment of luteal phase dysfunction: a comparative study. Fertil Steril 1989 Jan; 51(1): [Medline]. Noyes RW, Hertig AW, Rock J: Dating the endometrial biopsy. Fertil Steril 1950; 1: Peters AJ, Lloyd RP, Coulam CB: Prevalence of out-of-phase endometrial biopsy specimens. Am J Obstet Gynecol 1992 Jun; 166(6 Pt 1): ; discussion [Medline]. Peters AJ, Wentz AC: Luteal phase inadequacy. Seminars in Reprod Endo 1995; 13: Sherman BM, Korenman SG: Measurement of plasma LH, FSH, estradiol and progesterone in disorders of the human menstrual cycle: the short luteal phase. J Clin Endocrinol Metab 1974 Jan; 38(1): [Medline]. Shoupe D, Mishell DR Jr, Lacarra M, et al: Correlation of endometrial maturation with four methods of estimating day of ovulation. Obstet Gynecol 1989 Jan; 73(1): [Medline]. Page 9 of 10

10 Soules MR (ed.): Luteal phase deficiency. Pitkin RM (ed.): Clinical Obstetrics and Gynecology. Vol 34, pp Philadelphia. JB Lippincott, 1991). Yen SC, Jaffe RB, Barbieri RL: Luteal Phase Defects. In: Reproductive Endocrinology. 4th ed. 1999: NOTE: Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER Luteal Phase Dysfunction excerpt Copyright 2003, emedicine.com, Inc. About Us Privacy Terms of Use Contact Us Advertise Institutional Subscribers Page 10 of 10

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