Analysis of Clinical Backgrounds and Pathogenesis of Luteal-Phase Defect

Abstract

To elucidate the clinical background of the luteal-phase defect (LPD), 201 LPD cycles were studied in 753 infertile women. One hundred and twenty-one cases (62.2%) of LPD showed transient hyperprolactinemia. In transient hyperprolactinemia, there was a significant inverse correlation between serum prolactin (PRL) 30 min after the 500-µg intravenous loading of thyrotropin-releasing hormone TRH (PRL₃₀) and progesterone (P₄) in the luteal phase (r=-0.67, p < 0.005). Mature follicles (diameter > 20 mm as determined by ultrasonography) were observed in 74 cases (61.2% of the transient hyperprolactinemia cases). On the contrary, in 25 (12.4%) of the 121 LPD cases who showed the hyper-luteinizing hormone (LH) syndrome (LH/FSH ratio > 1), only 9 (36%) had mature follicles. Of the remaining 55 cases who showed neither transient hyperprolactinemia nor the hyper-LH syndrome, 27 cases (49.1%) had mature follicles. Five of these patients indicated a significantly higher LH pulse amplitude despite depressed P₄ secretion in the luteal phase. From these results, it was concluded that the most common cause of LPD was transient hyperprolactinemia. The second cause of LPD was suspected to be disturbed follicle development due to the inappropriate ratio of LH/FSH in the hyper-LH syndrome. Another cause was speculated to be the primary failure of a response from the corpus luteum to LH. Treatments based on the conclusions mentioned above resulted in a 48.3% pregnancy success rate.

The Effect of Prolactin on Gene Expression and the Secretion of Reproductive Hormones in Ewes during the Estrus Cycle

“…P4 is mainly produced by the CL [50] and its concentration 44 could be due to an increased number of CLs [51]. The inhibition of PRL increased the P4 concentration in heifer [52], which is consistent with our research; PRL has also been significantly negatively correlated with P4 levels during the luteal phase [53]. Therefore, PRL inhibition can regulate the production of recruiting follicles and ovulation by increasing GnRH and E2 in the proestrus and estrus stages and increasing P4 in the diestrus stage.…”

Vitex agnus-castus (Chaste Tree): Pharmacological and Clinical Data

“…In a considerable number of women with anovulatory (no ovum discharged) cycles and sterility, increased basal prolactin levels were found. Subsequently, hyperprolactinernia turned out to be rather widespread in women and to be one of the most common reasons for infertility (5). In women with manifest hyperprolactinernia, often a correlation between the severity of the clinical findings and the prolactin levels is found (4).…”

“…In 50% of the patients suffering from luteal phase defects, a manifest or only a latent hyperprolactinernia is diagnosed. In a study from 1992, Aisaka et aL diagnosed in 62% of 753 infertile women a latent hyperprolactinernia identified by a diminished progesterone phase of the cycle, an augmented prolactin increase following TRH application, or an increased nocturnal prolactin rise (5).…”