Luteal Phase Dysfunction

Updated: Jul 12, 2021
  • Author: Thomas L Alderson, DO; Chief Editor: Richard Scott Lucidi, MD, FACOG  more...
  • Print

Practice Essentials

In luteal phase dysfunction (LPD), the inadequate secretory transformation of the endometrium results from deficient progesterone production. LPD has been implicated in both infertility and recurrent pregnancy loss. [1, 2]

Signs and symptoms

The patient may report menstrual cycles of less than 26 days or a luteal phase of less than 11 days by basal body temperatures. Physical findings that might aid in the diagnosis of LPD are those associated with abnormal endocrine function, such as the following:

  • An enlarged thyroid gland – Hypothyroidism
  • Galactorrhea – Hyperprolactinemia
  • An enlarged, irregularly shaped uterus – Uterine myomas

See Presentation for more detail.


Serum progesterone levels have been studied as a means to diagnose luteal phase deficiency. Endometrial biopsy has been used for histologic dating of the endometrium. Urinary luteinizing hormone kits provide a useful test to estimate the appropriate timing of an endometrial biopsy.

See Workup for more detail.


Hyperprolactinemia and hypothyroidism cause LPD through hypothalamic-pituitary dysfunction. 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.

See Treatment and Medication for more detail.




In 1949, Georgeanna Jones, MD, first described LPD. [3] 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 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.

For related information, see Medscape's Pregnancy Resource Center.



The following mechanisms can cause an inadequate endometrial response to hormonal stimulation during the luteal phase. [4]

Abnormal follicular development

Abnormal follicular development results from inadequate follicle-stimulating hormone (FSH) and luteinizing hormone (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 is the substrate responsible for initiation of the steroid pathway. A deficiency results in low-to-absent progesterone production and a luteal phase defect.



United States statistics

No consensus has been achieved regarding frequency; however, a 1991 symposium hypothesized that luteal phase deficiency (LPD) occurs in 3-10% of infertile patients, and healthy women have deficient luteal phase production of progesterone on a sporadic basis.

International statistics

Presumably, international frequency is similar to that in the United States.

Race-, sex-, and age-related demographics

Luteal phase deficiency affects women of all races. Only women are affected. Luteal phase deficiency primarily affects women during their reproductive years.



The lack of double-blinded placebo-controlled studies prevents an accurate prognosis for this condition. A report by the Practice Committee of the American Society for Reproductive Medicine concluded that there is no significant evidence that LPD alone can cause infertility. [5]


No morbidity or mortality has been associated with this condition.


Complications are associated with the endometrial biopsy. Be cautious when performing the biopsy 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.


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.