Luteal Phase Defects – The Basics
The menstrual cycle (the interval of time from the first day of one period to the first day of the next) is generally broken down into two parts, the first or follicular phase, and the second part usually termed the luteal phase. During the follicular phase, the follicles or egg bearing parts of the ovary are acted upon by pituitary control hormones termed FSH (follicle stimulating hormone) and to a more limited extent, LH (luteinizing hormone). In a typical 28-day menstrual cycle, the follicular phase may last 14 days during which time the dominant follicle, which is destined to produce the mature egg for that cycle, is growing rapidly and the egg within the follicle is undergoing maturation. The cells that line the inside of the follicle large amounts of estrogen which has many effects, one of which is to thicken and begin preparing the uterine lining for implantation of the embryo later in the cycle. If a woman has longer cycles (i.e. 35 days), it is likely that the follicular phase will be lengthened to approximately 21-23 days, while the phase after release of the egg (luteal phase), is more stable and likely to last 12-14 days normally. The luteal phase is that part of the menstrual cycle which begins at the time of ovulation and ends with the onset of menstruation. The term “luteal” refers to the corpus luteum, which is actually the dominant follicle that has released its egg and undergone a transition to progesterone production. The luteal phase therefore refers to the time of the menstrual cycle when progesterone is being produced in progressively increasing amounts in preparation for implantation of the embryo.
One of the earliest methods of diagnosing luteal phase deficiencies was the endometrial biopsy. During the luteal phase the lining of the uterus undergoes daily microscopic changes that have been carefully described in the literature. The clinician obtains a biopsy of the uterine lining late in the luteal phase (i.e. post ovulatory day 8, 9, 10, or 11). This was accomplished using the basal body temperature chart as a guide. The biopsy was then stained and examined by an experienced examiner to determine if the biopsy was “in phase”, or “out of phase”. For example, if the endometrium was obtained on post ovulatory day number 10, but appeared under the microscope as having come from endometrium that appeared as post ovulatory day number 6, this would indicate a luteal phase deficiency. This technique proved to be unreliable primarily because of variability from examiner to examiner with respect to dating the emdometrium.
Another diagnostic approach, which was studied, consisted of using “pooled” serum taken from the patient on various days during the luteal phase. For example, blood might be obtained on postovulatory days 4, 6, 8, and 10. By mixing all of these samples together, a single “averaged” progesterone level could be obtained for that patient in that particular cycle. Determination of the critical value of pooled progesterone that established the diagnosis of a luteal phase deficiency proved elusive, and this approach to diagnosing luteal phase deficiencies lost traction.
One of the simplest approaches that can establish the diagnosis in many situations is the basal body temperature chart. Although this technique is cumbersome, and not in common use today, recording the body temperature each morning for a complete menstrual cycle can give very strong indicators of luteal phase deficiency. Because progesterone is a “thermogenic hormone”, body temperature rises by .4 to .6 degrees during the luteal phase. When body temperature does not remain elevated for at least 12-14 days following the initial temperature rise, luteal phase deficiency is strongly suspected.
Pre-menstrual spotting is highly suggestive of luteal phase deficiency. It is important to recognize that each menstrual cycle is hormonally unique and although some patients may be prone to have frequent cycles demonstrating luteal phase deficiency, that same patient may have cycles with normal hormonal function.
There are many satisfactory treatments for luteal phase deficiency, the simplest of which is luteal phase progesterone supplementation. Vaginal progesterone offers the best combination of excellent absorption and ease of administration. However, intra-muscular administration of progesterone is also highly effective. Treatment should begin 1-2 days after ovulation and continue for at least 14 days before a sensitive blood pregnancy test is done to determine if pregnancy had occurred. If the blood test confirms pregnancy, progesterone is usually continued through 8 weeks of gestation.
Luteal phase deficiencies may also be corrected with either clomiphene citrate (Clomid), or pituitary gonadotropins (FSH and LH). These medications stimulate follicular development leading to increased secretion of estrogen from cells lining the follicles early in the menstrual cycle. Later in the menstrual cycle, during the luteal phase, the same cells that had earlier been producing estrogen, convert to progesterone secretion, and in this way provide improved preparation of the uterine lining for implantation.
Luteal phase defects may be obvious or subtle. In some situations they may be diagnosed with relative certainty while in other circumstances they may be merely strongly suspected. Once other causes for infertility or recurrent miscarriage have been ruled out or corrected, my approach is to correct obvious as well as subtle luteal phase deficiencies.