Some randomized studies have suggested a significant beneficial effect of 17-hydroxyprogesterone caproate in the prevention of preterm labor [1, 2], The therapy in both studies was initiated at approximately 12-16 weeks and continued until labor. We considered the possibility that a deficient proges terone effect during the first trimester may lead to a higher rate of preterm deliveries. A retrospective study was thus performed comparing the incidence of preterm versus full-term pregnancies in women with luteal phase defects who were either treated or not treated with proges terone supplementation during the first trimester.
PMID 1612531 1612531 DOI 10.1159/000294877 10.1159/000294877
Cite this article
Check, J. H., Lee, G., Epstein, R., & Vetter, B. (1992). Increased rate of preterm deliveries in untreated women with luteal phase deficiencies. Preliminary report. Gynecologic and obstetric investigation, 33(3), 183-184. https://doi.org/10.1159/000294877
Check JH, Lee G, Epstein R, Vetter B. Increased rate of preterm deliveries in untreated women with luteal phase deficiencies. Preliminary report. Gynecol Obstet Invest. 1992;33(3):183-184. doi:10.1159/000294877
Check, J. H., et al. "Increased rate of preterm deliveries in untreated women with luteal phase deficiencies. Preliminary report." Gynecologic and obstetric investigation, vol. 33, no. 3, 1992, pp. 183-184.
Twenty-four women with luteal phase defects who were ovulatory on clomiphene therapy with or without human chorionic gonadotropin (hCG) at midcycle for three to eight cycles yet failed to produce a live birth were treated with a short course of menotropin (hMG-S), one to two ampules for five days in the early follicular phase followed or not followed by hCG at midcycle for three to eight cycles. The luteal phase defect was diagnosed with repeat endometrial biopsies with a lag time of three or more days prior to clomiphene therapy. A complete infertility workup revealed only eight patients (33%) with a purely endocrine factor (luteal phase defect). The rest (16 patients, or 67%) had one or two additional infertility factors. Two abortions occurred in this group during clomiphene therapy, while five pregnancies (four live births and one spontaneous abortion) occurred during hMG-S therapy. The ovulation rates were similar for hMG-S (89%) and clomiphene (91%) therapy, but the frequency of a normal ovulatory cycle was significantly greater (P = .026) for hMG-S therapy (71%) than for clomiphene therapy (57%). The midluteal mean serum progesterone level was lower and the mean luteal length shorter in the cycles with less than 130 ng/mL/d of total integrated luteal progesterone. The postcoital test results showed better cervical mucus, with increased mucus volume and better fluidity and spinnbarkeit, in hMG-S cycles than in clomiphene cycles. It appears that hMG-S treatment can improve ovarian function and achieve successful pregnancy in patients with luteal phase defects who fail to produce a live birth during clomiphene treatment.
EndometriosisPrevalencePelvic Pain and DyspareuniaCross-Sectional Survey
To estimate the prevalence of diagnosed endometriosis (DE) in women in the United States and assess the associated symptomatic burden. An online, cross-sectional survey of women aged 18-49 years was conducted from August 6, 2012, through November 14, 2012. Survey data (weighted by age, race, education, income, geographical distribution, and propensity score) were used to estimate the prevalence and symptomatic burden of DE in women in the United States. Weighted logistic regressions were used to assess differences in symptom burden between women with and without endometriosis. The prevalence of DE was estimated at 6.1% (2,922 of 48,020 women surveyed); 52.7% of women were 18-29 years of age when they were diagnosed with endometriosis. Most (86.2%) women experienced symptoms before diagnosis. More women with (vs. without) DE had menstrual pelvic pain/cramping (52.7 vs. 45.2%), non-menstrual pelvic pain/cramping (36.7 vs. 14.3%), infertility (11.6 vs. 3.4%), and dyspareunia (29.5 vs. 13.4%). Women with endometriosis were also more likely to report severe symptoms (OR (95% CI) 2.7 (2.3-3.1) for menstrual pelvic pain/cramping, 2.2 (1.7-2.9) for non-menstrual pelvic pain/cramping, and 2.4 (1.8-3.2) for dyspareunia). The prevalence of DE among US women is notable, and affected women experience a substantial symptom burden.
EndometriosisGenetic MechanismsLoss of Heterozygosity and PTENEndometriosis-Associated Ovarian Cancer
We analyzed 81 ovarian cancers for loss of heterozygosity (LOH) on 10q23 and for mutations in PTEN. LOH was common among the endometrioid (43%) and serous (28%) cancers, but was infrequent among the other histological subtypes. Somatic PTEN mutations were detected in seven (21%) endometrioid cancers and the mutation in all informative cases was accompanied by loss of the wild-type allele. One mucinous cancer without 10q23 LOH was shown to harbor two somatic PTEN mutations. Frequent LOH was observed on chromosome 6q (60.0%) and chromosome 10q (40.0%) in ovarian atypical endometriosis, but no PTEN mutations were observed. These findings support the hypothesis that endometrioid and clear cell ovarian carcinomas may arise through malignant transformation of endometriotic lesions.
EndometriosisClinical EvidenceInvasion and Metastatic BehaviorEndometriosis Cancer Risk
It is well known that certain aspects of endometriosis are similar to those of malignant disease. For example, like cancer, endometriosis can be both locally and distantly metastatic; it attaches to other tissues, invades, and damages them. Endometriosis is a common disease that does not create a cachectic or catabolic state, and is rarely fatal. There are, however, numerous reported cases of malignancy arising from endometriotic deposits and substantial histologic evidence that endometriosis is associated with endometrioid carcinoma and clear cell carcinoma of the ovary. A large review article by Mostoufizadeh and Scully investigated the association between endometriosis and endometrioid carcinoma, noting that women who had both diseases tended to be younger [1]. They found no association between endometriosis and serous or mucinous carcinoma of the ovary, and reported that malignant transformation of endometriosis was rare and associated with the use of exogenous estrogens. An epidemiological study of Swedish women reported a higher incidence of breast and ovarian cancer and non-Hodgkin's lymphoma in women with endometriosis compared with controls [2]. Vercellini and colleagues also reported a higher incidence of endometrioid and clear cell carcinoma in women with endometriosis compared with controls [3]. Mutations in genes associated with galactose metabolism have been identified as one possible mechanism for this association. These mutations are more common in ovarian cancer and have been reported to be more common in women with endometriosis. We compared 78 women with endometriosis with 248 controls and were unable to demonstrate an increased frequency of these mutations in any of these groups.