Oteseconazole versus fluconazole for the treatment of severe vulvovaginal candidiasis: a multicenter, randomized, double-blinded, phase 3 trial.

Vulvovaginal candidiasis (VVC) is a common condition among women. Fluconazole remains the dominant treatment option for VVC. Oteseconazole is a highly selective inhibitor of fungal CYP51. This randomized, double-blinded, phase 3 trial was conducted to evaluate the efficacy and safety of oteseconazole compared with fluconazole in treating severe VVC. Female subjects presenting with vulvovaginal signs and symptoms score of ≥7 and positive Candida infection determined by potassium hydroxide test or Gram staining were randomly assigned to receive oteseconazole (600 mg on D1 and 450 mg on D2) or fluconazole (150 mg on D1 and D4) in a 1:1 ratio. The primary endpoint was the proportion of subjects achieving therapeutic cure [defined as achieving both clinical cure (absence of signs and symptoms of VVC) and mycological cure (negative culture of Candida species)] at D28. A total of 322 subjects were randomized and 321 subjects were treated. At D28, a statistically significantly higher proportion of subjects achieved therapeutic cure in the oteseconazole group than in the fluconazole group (66.88% vs 45.91%; P = 0.0002). Oteseconazole treatment resulted in an increased proportion of subjects achieving mycological cure (82.50% vs 59.12%; P < 0.0001) and clinical cure (71.25% vs 55.97%; P = 0.0046) compared with fluconazole. The incidence of treatment-emergent adverse events was similar between the two groups. No subjects discontinued study treatment or withdrew study due to adverse events. Oteseconazole showed statistically significant and clinically meaningful superiority over fluconazole for the treatment of severe VVC and was generally tolerated.

RBM24 controls cardiac QT interval through CaMKIIδ splicing.

Calcium/calmodulin-dependent kinase II delta (CaMKIIδ) is the predominant cardiac isoform and it is alternatively spliced to generate multiple variants. Variable variants allow for distinct localization and potentially different functions in the heart. Dysregulation of CaMKIIδ splicing has been demonstrated to be involved in the pathogenesis of heart diseases, such as cardiac hypertrophy, arrhythmia, and diastolic dysfunction. However, the mechanisms that regulate CaMKIIδ are incompletely understood. Here, we show that RNA binding motif protein 24 (RBM24) is a key splicing regulator of CaMKIIδ. RBM24 ablation leads to the aberrant shift of CaMKIIδ towards the δ-C isoform, which is known to activate the L-type Ca current. In line with this, we found marked alteration in Ca2+ handling followed by prolongation of the ventricular cardiac action potential and QT interval in RBM24 knockout mice, and these changes could be attenuated by treatment with an inhibitor of CaMKIIδ. Importantly, knockdown of RBM24 in human embryonic stem cell-derived cardiomyocytes showed similar electrophysiological abnormalities, suggesting the important role of RBM24 in the human heart. Thus, our data suggest that RBM24 is a critical regulator of CaMKIIδ to control the cardiac QT interval, highlighting the key role of splicing regulation in cardiac rhythm.

One case report and literature review of arrhythmia caused by pituitrin.

Arrhythmias are perceived as a complication of pituitrin. However, injecting a standard dose of pituitrin via vein causes different arrhythmias. In our case, a 35-year-old female patient was admitted to the hospital due to a productive cough with sputum for 5 days and two occasions of massive hemoptysis. After 1 day of treatment using 500 ml normal saline with 10u pituitrin, the sputum was filled with small amounts of kermesinus bloodstains. When pituitrin was stopped without any other treatment, all presenting symptoms gradually subsided after half an hour, and the ECG returned to normal. Therefore, when treating massive hemoptysis by administering pituitrin intravenously, it is necessary to exercise great precaution and therapeutic measures.

Association of MTHFR 677C > T gene polymorphism with neonatal defects: a meta-analysis of 81444 subjects.

This meta-analysis was performed to clarify controversial associations of the MTHFR 677 C > T gene polymorphism in maternal and foetal tissue with neonatal defects. It was reported the association of MTHFR 677 C > T gene polymorphism with frequencies of neonatal defects including congenital heart disease (CHD), neural tube defects (NTD), non-syndromic cleft lip and palate (NSCL/P), and Down syndrome (DS). Depending on the neonatal defect subtypes, MTHFR 677 C > T gene polymorphism was associated with NTD, CHD (except for codominant mode of inheritance (TC/CC) and dominant mode of inheritance (TT + TC/CC); p = .167 and p = .054, respectively), DS, and NSCL/P (codominant mode of inheritance (TC/CC), p = .032) in the maternal group. However, in the neonatal group, the MTHFR 677 C > T gene polymorphism was only associated with the frequency of NTD and CHD. Maternal and neonatal MTHFR 677 C > T gene polymorphisms appear to be associated with neonatal defects but differ by defect types.IMPACT STATEMENTWhat is already known on this subject? Neonatal defects are a signifcant problem and are related to genes involved in the metabolism of homocysteine and folate.What do the results of this study add? The MTHFR 677C > T polymorphism in maternal and neonatal subjects was significantly associated with neonatal defects. When the neonatal subjects were stratified based on disease, the maternal MTHFR 677C > T polymorphism was found to be significantly correlated with all four neonatal defects. In contrast, the polymorphism in newborns was significantly associated with neural tube defects.What are the implications of these findings for clinical practice and/or further research? We believe that our study makes a significant contribution to the literature because it collectively analysed neural tube defects, congenital heart disease, cleft lip and palate, and Down syndrome in relation to the 677C > T polymorphism of MTHFR. Thus, we anticipate that this study will serve as a valuable resource for future investigations of neonatal defect prevention and maternal inheritance in newborn diseases.

Clinical and immunological characteristics in COVID-19 convalescent patients.

The humoral and cellular immunity of convalescent COVID-19 patients is involved in pathogenesis and vaccine immunity. In this study, through CoV-psV neutralization assay and IFN-γ ELISpot testing in 30 cases of COVID-19 patients after 9 months post-SARS-CoV-2 infection, it found that the ratio of memory/naive CD4+ T lymphocytes cells and levels of anti-SARS-CoV-2-IgM and RBD-IgM were slightly but significantly higher in COVID-19 severe convalescent patients than that in non-severe patients. The specific cellular and humoral immunity against SARS-CoV-2 were detectable, regardless of the severity of the disease in the acute phase. This information may help understanding the immune status after SARS-CoV-2 infection.

Meta-analysis: association of homocysteine with recurrent spontaneous abortion.

We analyzed the differences in serum homocysteine levels between patients with a history of recurrent spontaneous abortion (RSA) and those who had not experienced pregnancy-related complications. To this end, we retrieved literature and data on the association of RSA and serum homocysteine levels published before September 1st 2019 from the PubMed, EMBASE, China National Knowledge Infrastructure, and Wanfang databases. We further narrowed our literature review by focusing on peer-reviewed and full-text literature reporting on studies that used similar research methods and provided raw data or means and standard deviations while reporting results. Utilizing Stata 12.0 for a combined statistical analysis of the data, we assessed the quality of the included literature using the Newcastle Ottawa Scale. Patients who experienced RSA had higher serum homocysteine levels than the controls, with the difference being statistically significant (p < .05). High serum homocysteine levels may be an important risk factor for RSA, indicating that homocysteine may be useful as a noninvasive marker for the diagnosis of recurrent abortions.

DNAH17 is associated with asthenozoospermia and multiple morphological abnormalities of sperm flagella.

BACKGROUND: Multiple morphological abnormalities of the sperm flagella (MMAF) is one kind of severe asthenozoospermia, which is caused by dysplastic development of sperm flagella. In our study, we sought to investigate the novel gene mutations leading to severe asthenozoospermia and MMAF. METHODS AND MATERIALS: The patient's spermatozoa were tested by Papanicolaou staining and transmission electron microscopy. Whole exome sequencing was performed on the patient with severe asthenozoospermia and MMAF. Sanger sequencing verified the mutations in the family. The expression of DNAH17 was detected by immunofluorescence and Western blot. RESULTS: Spermatozoa sample from the patient showed severe asthenozoospermia and MMAF. We detected biallelic mutations (c.C4445T, p.A1482V and c.C6857T, and p.S2286L) in DNAH17 (MIM:610063). The protein expression of DNAH17 was almost undetectable in spermatozoa from the patient with the biallelic mutations. CONCLUSION: These results demonstrated that DNAH17 may be involved in severe asthenozoospermia and MMAF.

Biallelic mutations of CFAP74 may cause human primary ciliary dyskinesia and MMAF phenotype.

Primary ciliary dyskinesia (PCD) is a rare genetic disorder characterized by recurrent respiratory infections, nasosinusitis, tympanitis, and/or male infertility, all of which can severely impair the patient's quality of life. Multiple morphological abnormalities of the sperm flagella (MMAF) is one type of severe teratozoospermia and results from a variety of flagellar defects. In this study, we conducted whole-exome sequencing to identify and evaluate the genetic lesions in two patients with potential PCD and MMAF. Biallelic mutations in exon 10, c.983G>A; p.(Gly328Asp), and exon 29, c.3532G>A; p.(Asp1178Asn), of the CFAP74 (NM_001304360) gene were identified in patient 1 (P1), and biallelic mutations in exon 7, c.652C>T; p.(Arg218Trp), and exon 35, c. 4331G>C; p.(Ser1444Thr), of the same gene were identified in patient 2 (P2). Bioinformatic analysis suggested that these variants may be disease causing. Immunofluorescence confirmed that CFAP74 was absent in these patients' sperm samples. Intracytoplasmic sperm injection (ICSI) was carried out for P1, and his wife became pregnant after embryo transfer and gave birth to a healthy baby. To the best of our knowledge, this study is the first to identify the importance of CFAP74 in potential PCD and MMAF, contributing to the genetic diagnosis of these disorders and helping to predict pregnancy outcomes relevant in in vitro fertilization.

Loss-of-function mutations in centrosomal protein 112 is associated with human acephalic spermatozoa phenotype.

Acephalic spermatozoa, characterized by the headless sperm in the ejaculate, is a rare type of teratozoospermia. Here, we recruited two infertile patients with an acephalic spermatozoa phenotype to investigate the genetic pathology of acephalic spermatozoa. Whole-exome sequencing analysis was performed and found mutations in CEP112 in the two patients: homozygous mutation c.496C > T:p.(Arg166X) in exon 5 from P1; and the biallelic mutations c.2074C > T:p.(Arg692Trp) in exon 20 and c.2104C > T:p.(Arg702Cys) in exon 20 from P2. Sanger sequencing confirmed the CEP112 mutations in the two patients. In silico analysis revealed that these CEP112 mutations are deleterious and rare, and all the mutations impact the coiled-coil domain of CEP112, which may affect the protein function. The c.496C > T:p.Arg166X resulted in a truncated CEP112, which was verified by the mutation expression plasmid. The CEP112 expression was significantly reduced in the P2, suggesting the biallelic mutations c.2074C > T and c.2104C > T may affect the function and stability of CEP112. Therefore, we speculate that the loss-of-function mutations in CEP112 may be account for the human acephalic spermatozoa phenotype.

The effects and costs of laparoscopic versus abdominal myomectomy in patients with uterine fibroids: a systematic review and meta-analysis.

BACKGROUND: Abdominal myomectomy (AM) and laparoscopic myomectomy (LM) are commonly see surgery for the uterine fibroids, several randomized controlled trials (RCTs) have compared the role of AM and LM, the results remained inconsistent. Therefore, we attempted this meta-analysis to analyze the role of LM versus AM in patients with uterine fibroids. METHODS: We searched PubMed et al. databases from inception date to July 31, 2019 for RCTs that compared LM versus AM in patients with uterine fibroids. Two authors independently screened the studies and extracted data from the published articles. Summary odd ratios(OR) or mean differences(MD) with 95% confidence intervals(CI) were calculated for each outcome by means of fixed- or random-effects model. RESULTS: Twelve RCTs with a total of 1783 patients were identified, with 887 patients for and 897 patients for AM. Compared with AM, LM could significantly decrease the blood loss (OR = - 29.78, 95% CI -57.62- - 0.95), shorten the duration of postoperative ileus (OR = - 10.91, 95% CI -18.72- - 3.11), reduce the length of hospital stay (OR = - 1.57, 95% CI -2.05- - 1.08), but LM was associated with longer duration of operation (OR = 16.10, 95% CI 6.52-25.67) and higher medical cost (OR = 17.61, 95% CI 7.34-27.88). CONCLUSIONS: LM seems to be a better choice for patients with uterine fibroids, more related studies are needed to identify the role of LM and AM for the treatment of uterine fibroids.

Biallelic mutations in PMFBP1 cause acephalic spermatozoa.

The majority of men with defects in spermatogenesis remain undiagnosed. Acephalic spermatozoa is one of the diseases causing primary infertility. However, the causes underlying over half of affected cases remain unclear. Here, we report by whole-exome sequencing the identification of homozygous and compound heterozygous truncating mutations in PMFBP1 of two unrelated individuals with acephalic spermatozoa. PMFBP1 was highly and specifically expressed in human and mouse testis. Furthermore, immunofluorescence staining in sperm from a normal control showed that PMFBP1 localizes to the head-flagella junction region, and the absence of PMFBP1 was confirmed in patients harboring PMFBP1 mutations. In addition, we generated Pmfbp1 knock-out (KO) mice, which we found recapitulate the acephalic sperm phenotype. Label-free quantitative proteomic analysis of testicular sperm from Pmfbp1 KO and control mice showed 124 and 35 proteins, respectively, increased or decreased in sperm from KO mice compared to that found in control mice. Gene ontology analysis indicates that the biological process of Golgi vesicle transport was the most highly enriched in differentially expressed proteins, indicating process defects related to Golgi complex function may disturb formation of the head-neck junction. Collectively, our data indicate that PMFBP1 is necessary for sperm morphology in both humans and mice, and that biallelic truncating mutations in PMFBP1 cause acephalic spermatozoa.

Comparison between Serum HE4 and CA125 as Tumor Markers in Premenopausal Women with Benign Pelvic Mass.

BACKGROUND: The aim of the study was to evaluate the role of human epididymal secretory protein (HE4), cancer antigen 125 (CA125), and the Risk of Ovarian Malignancy Algorithm (ROMA) in diagnosing benign pelvic masses in premenopausal women. METHODS: Serum was collected from 391 premenopausal women with benign pelvic mass prior to surgery and from 45 healthy individuals. Serum HE4 and CA125 levels and ROMA scores were evaluated separately. RESULTS: Among the 391 women with benign pelvic mass, 2.3% (9/391) had elevated HE4 levels (> 70 pmol/L), while 37.1% (145/391) had elevated CA125 levels (> 35 U/mL) (p < 0001). Endometriosis provided false-positive results for CA125 levels in more than half of the cases but resulted in no significant change for HE4 level. In 13 gravid women with a mass, 30.8% (4/13) and 38.5% (5/13) had elevated HE4 and CA125 levels, respectively; however, the difference was not significant (p > 0.05). Moreover, serum levels and patient percentages for CA125 elevation significantly increased with increase in mass diameter, whereas those for HE4 did not. CONCLUSIONS: CA125 elevation showed random results for benign pelvic masses, while HE4 elevation showed a higher specificity. Thus, serum HE4 testing is a better approach than CA125 testing for diagnosing benign pelvic masses in premenopausal women.

Patients with multiple morphological abnormalities of the sperm flagella harbouring CFAP44 or CFAP43 mutations have a good pregnancy outcome following intracytoplasmic sperm injection.

Multiple morphological abnormalities of the sperm flagella (MMAF) are a rare type of male infertility. Mutations in DNAH1, CFAP43 and CFAP44 are the main aetiology of the disorder. Previously, good intracytoplasmic sperm injection (ICSI) outcomes were reported for MMAF patients with DNAH1 mutations. However, the ICSI prognosis for MMAF patients with CFAP43 or CFAP44 mutations was not known. We designed a retrospective cohort study. Molecular genetic testing identified six MMAF patients with biallelic CFAP44 (CFAP44+ group) or CFAP43 mutations and 12 patients with homozygous or compound heterozygous DNAH1 mutations (DNAH1+ group). A control group consisted of age-matched, non-MMAF men. For MMAF patients carrying CFAP44 mutations, the recorded rates of fertilisation, transferable embryos, pregnancy and delivery after ICSI were 76.47%, 88.46%, 50.0% and 50.0% respectively. The fertilisation rate was significantly higher in the CFAP44+ group than in the DNAH1+ group (76.47% vs. 54.5%, p = 0.0196). There were no statistically significant differences in the rates of transferable embryos, implantation, clinical pregnancy and miscarriage between the CFAP44+ group and either the DNAH1+ group or the age-matched control group. Our results support a good ICSI prognosis for MMAF patients carrying CFAP44 or CFAP43 mutations.

A novel electrochemical immunoassay for carcinoembryonic antigen based on glucose oxidase-encapsulated nanogold hollow spheres with a pH meter readout.

A portable electrochemical immunosensing protocol was designed for the sensitive detection of a disease-related tumor biomarker (carcinoembryonic antigen, CEA, used in this case) on a pH meter using glucose oxidase (GOx)-encapsulated gold hollow microspheres (AuHMs) for signal amplification. The assay was carried out on a monoclonal anti-CEA capture antibody-coated microplate with a sandwich-type reaction mode. The GOx-entrapped AuHM was first synthesized using the reverse micelle method and then used as the signal-generation tag for the labeling of polyclonal anti-CEA detection antibody. Accompanying the formation of the sandwiched immunocomplexes, the loaded GOx molecules in the microsphere could catalyze glucose into gluconic acid and hydrogen peroxide. The as-produced gluconic acid changed the microenvironment of the detection solution, thus resulting in the shift of the pH value, which could be quantitatively determined on a portable pH meter. The use of gold hollow microspheres was expected to enhance the loaded amount of GOx for signal amplification. Two labeling protocols including GOx-labeled secondary antibody and GOx-AuHM-labeled secondary antibody were investigated for CEA detection, and improved analytical features were acquired with GOx-AuHM labeling. With the GOx-AuHM labeling strategy, the pH meter-based immunosensing device exhibited a good analytical performance for CEA detection within the dynamic linear range of 0.1-100 ng mL-1 at a detection limit of 0.062 ng mL-1. The strong attachment of anti-CEA antibodies to GOx-AuHM brought a good repeatability and intermediate precision down to 10%. Importantly, no significant differences at the 0.05 significance level were encountered in the analysis of 12 human serum specimens between the developed immunoassay and the commercialized electrochemiluminescent method for CEA determination.

Effect of Maternal and Neonatal Factors on Neonatal Thyroid Screening Results.

BACKGROUND: Thyroid-stimulating hormone (TSH) levels are an important parameter in screening for congenital hypothyroidism (CH). This study aimed to analyze the effects of birth weight, gestational age, and delivery mode on the incidence of neonatal CH. METHODS: A retrospective cohort study of neonates born in 2015 at a maternity hospital in Xiamen, China and their mothers was conducted. Differences in TSH levels, CH positivity at baseline, and the incidence of CH according to gestational age, birth weight, and delivery mode were assessed using matched neonatal and maternal data. RESULTS: Of the 15,615 enrolled neonates, 150 had positive CH screening results at baseline and nine had confirmed CH. Premature and low-birth-weight neonates had a significantly higher incidence of CH and lower TSH levels when compared to full-term neonates and normal-to-high birth weight neonates, respectively. Neonates delivered vaginally had significantly lower TSH levels and a reduced incidence of baseline CH positivity; cesarean section delivery (odds ratio [OR] = 2.06, p = 0.006) and a maternal TSH level >2.5 mIU/L (OR = 2.37, p = 0.002) were risk factors for CH positivity at baseline. CONCLUSIONS: In this study, the incidence of CH in neonates was associated with gestational age and birth weight. Neonatal baseline CH positivity was positively associated with cesarean delivery and an early-pregnancy maternal TSH level >2.5 mIU/L.

Validation of a new kit for preeclampsia screening: A comprehensive analysis.

Objectives: Preeclampsia is a common pregnancy complication that significantly contributes to maternal mortality, perinatal mortality, and preterm delivery. The sFlt-1/PlGF (fms-like tyrosine kinase-1/placental growth factor) ratio has demonstrated robust diagnostic value for preeclampsia. This study assessed the analytical performance and diagnostic accuracy of a novel quantitative determination kit for sFlt-1 and PlGF for the diagnosis of preeclampsia. Methods: The detection performance of the test kit was validated using the Center for Medical Device Evaluation (CMDE) and Clinical and Laboratory Standards Institute (CLSI) documents. The test results were compared to those of the Elecsys immunoassay (Roche Diagnostics). Independent discovery and validation sets were used to analyze the diagnostic efficacy of the preeclampsia kit. The area under the curve (AUC) for preeclampsia at different gestational ages was calculated. Results: Correlation analysis between the test and Roche kits revealed a strong concordance (sFlt-1: r = 0.9966, P < 0.0001; PlGF: r = 0.9935, P < 0.0001). The AUCs for sFlt-1, PlGF, and the sFlt-1/PlGF ratio in diagnosing preeclampsia were 0.749, 0.795, and 0.834, respectively, in the discovery set and 0.729, 0.811, and 0.831, respectively, in the validation set. The corresponding results from the Roche kit were 0.741, 0.795, and 0.829, respectively, and 0.761, 0.864, and 0.844, respectively. Conclusions: Quantitative sFlt-1 and PlGF kits exhibited high levels of consistency with the Roche kits in terms of quantitative outcomes and diagnostic performance for preeclampsia.

Maternal and neonatal outcomes and clinical laboratory testing of pregnant women with COVID-19 during the BA.5.2/BF.7 surge.

The impact of COVID-19 on pregnant women and newborns continues to be a critical societal concern. However, the majority of research focuses on the disease resulting from the early pandemic variants, without sufficient study on the more recent BA.5.2/BF.7. We retrospectively recruited pregnant women giving birth during the surge of the BA.5.2/BF.7 and analysed the risk impact of COVID-19 on maternal and neonatal outcomes. Furthermore, subjects matched through propensity scores were used for the analysis of clinical laboratory tests. A total of 818 pregnant women were enrolled, among 276 (33.7%) were diagnosed with SARS-CoV-2 during childbirth. COVID-19 significantly increased the risk of a hospital length of stay equal to or greater than seven days and neonatal admission to the neonatal intensive care unit, with an aHR of 2.03 (95% CI, 1.22-3.38) and 1.51 (95% CI, 1.12-2.03), respectively. In the analysis of 462 matched subjects, it was found that subjects infected with SARS-CoV-2 tended slight leucopenia and coagulation abnormalities. We found that during the surge of the BA.5.2/BF.7, COVID-19 increased the risk of maternal and neonatal outcomes among Chinese pregnant women. This finding offers significant insights to guide clinical practices involving pregnant women infected with the recently emerged Omicron subvariants.

IGFBP1 inhibits the invasion, migration, and apoptosis of HTR-8/SVneo trophoblast cells in preeclampsia.

OBJECTIVE: To investigate the effects and underlying mechanisms of IGFBP1 on the biological functions of trophoblasts in simulated preeclampsia. METHODS: IGFBP1 expression in placenta was determined by immunohistochemistry. HTR-8/SVneo cells were stimulated with/without IGFBP1-overexpression and hypoxia-reoxygenation, and the proliferation, invasion, migration, and apoptosis were detected by CCK8, transwell, and flow cytometry, respectively. RESULTS: IGFBP1 expression was increased in placenta of preeclampsia. IGFBP1 overexpression inhibited proliferation, invasion, migration, and apoptosis of HTR-8/SVneo cells and induced MMP-26 expression with/without hypoxia-reoxygenation challenge. CONCLUSION: IGFBP1 affects biological functions of trophoblasts, and it may play a role in pathophysiology of preeclampsia by inducing MMP-26.

Two novel biallelic mutations in PSMC3IP in a patient affected by premature ovarian insufficiency.

Premature ovarian insufficiency (POI) is a heterogeneous condition occurring when a woman experiences a loss of ovarian activity before the age of 40. POI is one of the most common reproductive endocrine diseases in women of childbearing age. The present study investigated the clinical manifestations and genetic features of a Chinese patient affected by POI. Next­generation whole­exome capture sequencing with Sanger direct sequencing were applied to the proband and her clinically unaffected family members. Two novel compound heterozygous mutations were identified in PSMC3IP. The first was a splicing mutation (c.597+1G>T) that was inherited from her father, whereas the second mutation (c.268G>C p.D90H) was discovered in both her mother and younger sister. The two mutations were co­segregated with the disease phenotype in the family. In conclusion, the findings of the present study further support the key role of PSMC3IP in the etiology of POI and provide a novel insight into elucidating the mechanisms of female infertility.

Thyroid-stimulating hormone level is negatively associated with fertilization rate in patients with polycystic ovary syndrome undergoing in vitro fertilization.

OBJECTIVE: In this study, we investigated the effect of thyroid-stimulating hormone (TSH) level on the outcomes of in vitro fertilization (IVF) in patients with polycystic ovary syndrome (PCOS). METHODS: Data pertaining to 60 patients who underwent IVF between May 2017 and May 2018 were included in the study. Thirty-two patients were diagnosed as PCOS (PCOS group) and 28 patients had tubal infertility (control group). Serum and follicular fluid TSH levels and follicular cyclic AMP (cAMP) level were detected by ELISA. TSH receptor (TSHR) expression level in granulosa cells was quantified by RT-PCR and Western blot. RESULTS: In the PCOS group, oocyte maturation rate and fertilization rate were significantly lower than in the control group. Serum and follicular fluid TSH levels and ovarian cAMP level were higher in the PCOS group with an upregulation of ovarian TSHR. On multivariate linear regression analysis, fertilization rate showed a negative correlation with TSH levels in serum (B = -0.106, P = 0.005) and follicular fluid (B = -0.107, P = 0.001). CONCLUSION: In PCOS patients, TSH levels, both in serum and follicular fluid, were negatively correlated with IVF oocyte maturation rate and fertilization rate. The effect of TSH on controlled ovarian hyperstimulated oocyte growth was likely mediated by the TSHR/cAMP signaling pathway.