Luteal Phase Dysfunction Medication
- Author: Thomas L Alderson, DO; Chief Editor: Richard Scott Lucidi, MD, FACOG more...
The goals of pharmacotherapy in luteal phase deficiency are to restore ovarian function, reduce morbidity, and prevent complications.
Medical treatment centers on hormonal support of the patient's luteal phase.
Used if hyperprolactinemia is the underlying pathology causing LPD. Tablets can be used vaginally in patients who cannot tolerate adverse GI effects.
If LPD is caused by hypothyroidism, correction of endocrine disease results in normal luteal phase.
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.
Long-acting dopamine receptor agonist with high affinity for D2 receptors. Prolactin secretion by anterior pituitary predominates under hypothalamic inhibitory control exerted through dopamine.
Progesterone supplementation may be administered PO, IM, or vaginally. Oral progesterone is metabolized rapidly in liver, and the metabolites have little effect on endometrial activity. When administered IM, fails to achieve adequate levels of endometrial progesterone compared with 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 ovulation predictor kit. Correction of LPD can be confirmed by repeat EB.
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.
Jones GES. Some newer aspects of management of infertility. JAMA. 1949. 141:1123-1129.
Siklósi GS, Bánhidy FG, Ács N. Fundamental role of folliculo-luteal function in recurrent miscarriage. Arch Gynecol Obstet. 2012 Nov. 286(5):1299-305. [Medline].
Sonntag B, Ludwig M. An integrated view on the luteal phase: diagnosis and treatment in subfertility. Clin Endocrinol (Oxf). 2012 Oct. 77(4):500-7. [Medline].
Boutzios G, Karalaki M, Zapanti E. Common pathophysiological mechanisms involved in luteal phase deficiency and polycystic ovary syndrome. Impact on fertility. Endocrine. 2013 Apr. 43(2):314-7. [Medline].
Hajishaiha M, Ghasemi-Rad M, Karimpour N, Mladkova N, Boromand F. Transvaginal sonographic evaluation at different menstrual cycle phases in diagnosis of uterine lesions. Int J Womens Health. 2011. 3:353-7. [Medline].
van der Linden M, Buckingham K, Farquhar C, Kremer JA, Metwally M. Luteal phase support for assisted reproduction cycles. Cochrane Database Syst Rev. 2011 Oct 5. CD009154. [Medline].
Taylor HS, Bagot C, Kardana A, et al. HOX gene expression is altered in the endometrium of women with endometriosis. Hum Reprod. 1999 May. 14(5):1328-31.
Behrman HR, Endo T, Aten RF. Corpus luteum function and regression. Reprod Med Rev. 1993. 2:153-80.
Cermik D, Selam B, Taylor HS. Regulation of HOXA-10 expression by testosterone in vitro and in the endometrium of patients with polycystic ovary syndrome. J Clin Endocrinol Metab. 2003 Jan. 88(1):238-43. [Medline].
Cicinelli E, de Ziegler D, Bulletti C, et al. Direct transport of progesterone from vagina to uterus. Obstet Gynecol. 2000 Mar. 95(3):403-6. [Medline].
Cooke ID. The corpus luteum. Hum Reprod. 1988 Feb. 3(2):153-6. [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):1061-7. [Medline].
Daftary GS, Taylor HS. Hydrosalpinx fluid diminishes endometrial cell HOXA10 expression. Fertil Steril. 2002 Sep. 78(3):577-80. [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):114-21. [Medline].
Jones GS. The luteal phase defect. Fertil Steril. 1976 Apr. 27(4):351-6. [Medline].
Karamardian LM, Grimes DA. Luteal phase deficiency: effect of treatment on pregnancy rates. Am J Obstet Gynecol. 1992 Nov. 167(5):1391-8. [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):35-41. [Medline].
Noyes RW, Hertig AW, Rock J. Dating the endometrial biopsy. Fertil Steril. 1950. 1:3-25.
Peters AJ, Lloyd RP, Coulam CB. Prevalence of out-of-phase endometrial biopsy specimens. Am J Obstet Gynecol. 1992 Jun. 166(6 Pt 1):1738-45; discussion 1745-6. [Medline].
Peters AJ, Wentz AC. Luteal phase inadequacy. Seminars in Reprod Endo. 1995. 13:162-171.
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):89-93. [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):88-92. [Medline].
Soules MR. Luteal phase deficiency. Pitkin RM, ed. Clinical Obstetrics and Gynecology. Philadelphia, PA: JB Lippincott; 1991. Vol 34: 123-126.
Yen SC, Jaffe RB, Barbieri RL. Luteal phase defects. Reproductive Endocrinology. 4th ed. 1999. 244-5.