Luteal phase defect. Etiology, diagnosis, and management

Luteal phase defect is an ovulatory disorder of considerable clinical importance that is implicated in infertility and recurrent spontaneous abortion. As a subtle disruption of ovulatory or luteal function, it may be the most common ovulatory disorder in women. Pathophysiologic alterations of the complex reproductive process that lead to delayed endometrial maturation characteristic of LPD include disordered folliculogenesis, defective corpus luteum function, and abnormal luteal rescue by the early pregnancy. A variety of clinical conditions, such as hyperprolactinemia, hyperandrogenic states, weight loss, stress, and athletic training may result not in overt oligo- or anovulation, but rather may be manifest as LPD. Reasonable consensus exists regarding the use of endometrial biopsy for diagnosis of LPD, although issues regarding timing, number of samples needed, method of interpretation, and the adjunctive use of hormone assay and ultrasonography are still not settled. Other tests, including assay of progesterone-associated endometrial protein, analysis of decidual steroid receptors, or determination of decidual prolactin production, may in the future contribute to the accurate diagnosis of this condition. In the absence of an identifiable correctable underlying cause of LPD, progesterone replacement and clomiphene citrate are the usual treatment options for consideration. Combination therapy, gonadotropins, and other treatments are reserved for refractory cases. No data at present suggest a difference in efficacy between progesterone and clomiphene. When abnormal luteal endometrial biopsy is corrected, conception and live birth rates are high.