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Importance: Long-term sleep disturbances in menopausal women are closely related to cardiovascular disorders, metabolic disorders, and cognitive impairment. At present, hormone therapy (HT) is a standard treatment for menopausal symptoms. However, it remains unclear whether HT can improve sleep quality. Objective: We did a systematic review and meta-analysis to assess the effects of different HT regimens on menopausal sleep quality. Evidence Review: We systematically searched MEDLINE, Embase, the Cochrane Central Register of Controlled Trials, PsycINFO, CINAHL, and Web of Science for randomized controlled trials of menopausal HT on sleep disturbances up to June 14,2021. Information about ongoing and unpublished trials was collected by searching WHOICTRP and ClinicalTrials.gov. Our primary outcome was sleep quality with objective measurements. We estimated the standardized mean difference (SMD) using random-effects models. Findings: We identified a total of 3,059 studies and finally included 15 studies in the meta-analysis. Compared with placebo, HT improved self-reported sleep outcomes (SMD = –0.13; 95% CI, –0.18 to -0.08, P < 0.00001 and I 2 = 41%), but not sleep parameters measured by polysomnography. Subgroup analyses according to the regimen of HT showed that 17β-estradiol (17β-E 2 ) (SMD = –0.34; 95% CI, –0.51 to -0.17, P < 0.0001, and I 2 = 0%) and conjugated equine estrogens (SMD = –0.10; 95% CI, −0.12 to −0.07, P < 0.00001, and I 2 = 0%) improved sleep quality. Moreover, transdermal administration (SMD = −0.35; 95% CI, −0.64 to −0.06, and P = 0.02) was more beneficial than oral (SMD = −0.10; 95% CI, −0.14 to −0.07, and P < 0.00001). In addition, the combination of estrogen and progesterone had a positive effect on sleep disturbance (SMD = −0.10; 95% CI, −0.13 to −0.07, P < 0.00001, and I 2 = 0%), while estrogen monotherapy did not. The results showed that estrogen/micronized progesterone (SMD = −0.22; 95% CI, −0.37 to −0.06, P = 0.007, and I 2 = 0%) and estrogen/medroxyprogesterone acetate (SMD = −0.10; 95% CI, −0.13 to −0.07, P < 0.00001, and I 2 = 0%) could alleviate sleep disturbance. Conclusions and Relevance: HT has a beneficial effect on sleep disturbance to some extent, and the formulations and routes of administration of hormonal agents influence the effect s...

Background The optimal management of patients in reproductive endocrinology relies on the accuracy and validity of sex hormone assays. Endogenous or exogenous substances can compete with the analyte. This competition can result in interfering errors and falsely indicate elevated serum levels. Obvious interference in estradiol assays appears to occur rarely. Consequently, clinicians who are not familiar with the potential of interference could be misled. In addition to unnecessary investigations and interventions and severe mental stress, falsely elevated estradiol results can result in missed or delayed fertility opportunities. Case A 28-year-old female with pregnancy demand was diagnosed with polycystic ovary syndrome, Hashimoto’s thyroiditis and subclinical hypothyroidism. She was found to have persistently elevated levels of serum estradiol in the early follicular phase (between 527 and 642 pg/mL). Screening workup was performed for nearly 11 months to find the causes. Serum tumor biomarkers were normal. Abdominal and pelvic computed tomography were negative for adrenal or adnexal masses. A left mesosalpinx cyst and benign pathological results were achieved by laparoscopic surgery. Hormonal substances and dietary supplements were absent, as determined by dietary records. Ultrasound confirmed follicles could grow slowly and eventually ovulate. Falsely elevated estradiol levels were suspected due to the discrepancy among high estradiol levels, follicle growth and normal gonadotropin levels. Immunological interference by heterophile antibody was finally verified by two competitive chemiluminescent immunoassay platforms (estradiol levels in the early follicle phase: 619 pg/mL, Siemens ADVIA CENTAUR and 60 pg/mL, Beckman, DxI 800). Successful clinical pregnancy was eventually achieved by combining induced ovulation, ultrasound monitoring and intercourse guidance. Conclusions Analytical interference and laboratory error should be suspicious at first when the clinical characteristics contradict the laboratory results of serum hormones. Measuring serum estradiol with another immunoassay platform is an easy and non-time-consuming method to exclude the heterophile interfering.

Monozygotic triplet pregnancies are very rare in assisted reproductive technology, and the relationship between monozygotic multiple pregnancies and several assisted reproductive techniques, including blastocyst transfer, remains unclear. Here, the case of a 28-year-old female patient with dichorionic quadruplet pregnancy following intracytoplasmic sperm injection and transfer of two day-3 fresh embryos, without assisted hatching, is reported. At 7 weeks following embryo transfer, the dichorionic quadruplet pregnancy, comprising monozygotic monochorionic triamniotic (MCTA) triplets plus a singleton, was detected by a transabdominal ultrasound scan. After counselling, the patient underwent selective reduction of the MCTA triplet pregnancy at 7 weeks after embryo transfer. The remaining singleton pregnancy was uneventful, resulting in a live birth at 38+ weeks. As the predictors of monozygotic multiple gestations remain poorly characterized, clinicians and patients should give great consideration to the risks associated with monozygotic multiple pregnancies, even if the patient has not undergone blastocyst transfer.

Background Recent literature has reported that the higher obstetric and perinatal complications in FET may be associated with endometrial preparation protocols. To date, the specific mechanism behind these higher complications is unknown and probably multifactorial. Multiple data indicate that blastocyst transfer led to a better live birth rate than cleavage-stage embryo transfer. Therefore, does the embryo stage at the time of transfer play a role in obstetric and perinatal complications in FET? Methods This is a systematic review with meta-analysis. The PubMed, MEDLINE, and EMBASE databases and the Cochrane Central Register of Controlled Trials (CCRT) were searched from 1983 to October 2022. Studies were included only if at least two cohorts underwent programmed-cycle FET versus natural FET cycles and if obstetric and/or perinatal outcomes following programmed cycle FET versus natural FET cycle were reported. The primary outcomes were hypertensive disorders of pregnancy (HDPs), gestational hypertension and preeclampsia (PE). The secondary outcomes were gestational diabetes mellitus (GDM), placenta previa, postpartum haemorrhage (PPH), placental abruption, preterm premature rupture of membranes (PPROM), large for gestational age (LGA), small for gestational age (SGA), macrosomia, and preterm delivery (PTD). Results The risk of HDP (14 studies, odds ratio (OR) 2.17; 95% confidence interval (CI) 1.95–2.41; P < 0.00001; I2 = 43%), gestational hypertension (11 studies, OR 1.38; 95% CI 1.15–1.66; P = 0.0006; I2 = 19%), PE (12 studies, OR 2.09; 95% CI 1.88–2.32; P < 0.00001; I2 = 0%), GDM (20 studies, OR 1.09; 95% CI 1.02–1.17; P = 0.02; I2 = 8%), LGA (18 studies, OR 1.11; 95% CI 1.07–1.15; P < 0.00001; I2 = 46%), macrosomia (12 studies, OR 1.15; 95% CI 1.07–1.24; P = 0.0002; I2 = 31%), PTD (22 studies, OR 1.21; 95% CI 1.15–1.27; P < 0.00001; I2 = 49%), placenta previa (17 studies, OR 1.2; 95% CI 1.02–1.41; P = 0.03; I2 = 11%), PPROM (9 studies, OR 1.19; 95% CI 1.02–1.39; P = 0.02; I2 = 40%), and PPH (12 studies, OR 2.27; 95% CI 2.02–2.55; P < 0.00001; I2 = 55%) were increased in programmed FET cycles versus natural FET cycles with overall embryo transfer. Blastocyst transfer had a higher risk of HDP (6 studies, OR 2.48; 95% CI 2.12–2.91; P < 0.00001; I2 = 39%), gestational hypertension (5 studies, OR 1.87; 95% CI 1.27–2.75; P = 0.002; I2 = 25%), PE (6 studies, OR 2.23; 95% CI 1.93–2.56; P < 0.00001; I2 = 0%), GDM (10 studies, OR 1.13; 95% CI 1.04–1.23; P = 0.005; I2 = 39%), LGA (6 studies, OR 1.14; 95% CI 1.07–1.21; P < 0.0001; I2 = 9%), macrosomia (4 studies, OR 1.15; 95% CI 1.05–1.26; P < 0.002; I2 = 68%), PTD (9 studies, OR 1.43; 95% CI 1.31–1.57; P < 0.00001; I2 = 22%), PPH (6 studies, OR 1.92; 95% CI 1.46–2.51; P < 0.00001; I2 = 55%), and PPROM (4 studies, OR 1.45; 95% CI 1.14–1.83; P = 0.002; I2 = 46%) in programmed FET cycles than in natural FET cycles. Cleavage-stage embryo transfers revealed no difference in HDPs (1 study, OR 0.81; 95% CI 0.32–2.02; P = 0.65; I2 not applicable), gestational hypertension (2 studies, OR 0.85; 95% CI 0.48–1.51; P = 0.59; I2 = 0%), PE (1 study, OR 1.19; 95% CI 0.58–2.42; P = 0.64; I2 not applicable), GDM (3 study, OR 0.79; 95% CI 0.52–1.20; P = 0.27; I2 = 21%), LGA (1 study, OR 1.15; 95% CI 0.62–2.11; P = 0.66; I2 not applicable), macrosomia (1 study, OR 1.22; 95% CI 0.54–2.77; P = 0.64; I2 not applicable), PTD (2 studies, OR 1.05; 95% CI 0.74–1.49; P = 0.79; I2 = 0%), PPH (1 study, OR 1.49; 95% CI 0.85–2.62; P = 0.17; I2 not applicable), or PPROM (2 studies, OR 0.74; 95% CI 0.46–1.21; P = 0.23; I2 = 0%) between programmed FET cycles and natural FET cycles. Conclusions The risks of HDPs, gestational hypertension, PE, GDM, LGA, macrosomia, SGA, PTD, placenta previa, PPROM, and PPH were increased in programmed FET cycles versus natural FET cycles with overall embryo transfer and blastocyst transfer, but the risks were not clear for cleavage-stage embryo transfer.

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