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.

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.

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.

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.

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.

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.

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.

Turner syndrome with Xp deletions and rare endometrial abnormalities: A case report.

RATIONALE: Turner syndrome (TS) is a genetic disorder associated with abnormalities of the X chromosome related to ovarian function, but whether it is associated with endometrial abnormalities is still not clear. PATIENT CONCERNS: We report the case of a 26-year-old Han Chinese woman with TS and Xp11.2 deletion, presenting with short final stature, ovarian hypofunction, unexplained cystic dilatation of the entire endometrium, and endometrial thickening. DIAGNOSES: The patient was diagnosed with chromosome Xp11.2 deletion through cytogenetic analysis and ultrasonic and endometrial pathology. INTERVENTIONS: The patient was treated with conventional in vitro fertilization preimplantation genetic testing for 1 cycle. OUTCOMES: Cytogenetic examination showed karyotype 45, X, del (X) del (p11, 2). Ultrasonic examination showed uneven endometrium thickness and a full-stage cystic dilation echo. After 1 cycle of in vitro fertilization treatment, 4 eggs were obtained without forming an available embryo. LESSONS: To our knowledge, the present case is the first report of a patient with TS with Xp deletions and ultrasound imaging endometrial abnormalities. Our findings expand the phenotypic spectrum of TS and may provide a reference for other clinicians.

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.

Overexpression of the PLK4 Gene as a Novel Strategy for the Treatment of Autosomal Recessive Microcephaly by Improving Centrosomal Dysfunction.

Autosomal recessive microcephaly and chorioretinopathy (MCCRP) is a neurodevelopmental disorder characterized by delayed psychomotor development, growth retardation with dwarfism, and ocular abnormalities, and its occurrence has been found to be closely related to variants of the gene encoding centrosomes. However, the association between centrosomal duplication defects and the etiology of microcephaly syndromes is poorly understood. It is well known that polo-like kinase 4 (PLK4) is a key regulator of centriole duplication, and the abnormalities of centrosomal function caused by its protein variation need to be further explored in the pathogenesis of microcephaly. In our study, we found that a patient with microcephaly and chorioretinopathy harbored compound heterozygous missense variants NM_014264.4: c.2221C > T (p.Gln741*) and NM_014264.4: c.2062 T > C (p.Tyr688His) in the PLK4 gene. Overexpression experiments of the variant PLK4 proteins then showed that the G741 variant rather than the T688H variant had lost centrosomal amplification ability, and the G741 variant but not the T688H variant induced centrosomal replication disorder, which further inhibited cell proliferation, cycle division and cytoskeleton morphology in HeLa cells. Moreover, the overexpression of the two variant proteins had inconsistent effects on the target protein PLK4 by western blot analysis, also indicating that T688H variant overexpression is not functionally equivalent to WT-PLK4 overexpression. Therefore, all data support the idea that the PLK4 mutation induces centriolar duplication disorder and reduces the efficiency of mitosis inducing cell death or cell proliferation in the etiology of microcephaly disorder.

The role of DNA methylation in syndromic and non-syndromic congenital heart disease.

Congenital heart disease (CHD) is a common structural birth defect worldwide, and defects typically occur in the walls and valves of the heart or enlarged blood vessels. Chromosomal abnormalities and genetic mutations only account for a small portion of the pathogenic mechanisms of CHD, and the etiology of most cases remains unknown. The role of epigenetics in various diseases, including CHD, has attracted increased attention. The contributions of DNA methylation, one of the most important epigenetic modifications, to CHD have not been illuminated. Increasing evidence suggests that aberrant DNA methylation is related to CHD. Here, we briefly introduce DNA methylation and CHD and then review the DNA methylation profiles during cardiac development and in CHD, abnormalities in maternal genome-wide DNA methylation patterns are also described. Whole genome methylation profile and important differentially methylated genes identified in recent years are summarized and clustered according to the sample type and methodologies. Finally, we discuss the novel technology for and prospects of CHD-related DNA methylation.

Upregulation of microRNA-181a-5p increases the sensitivity of HS578T breast cancer cells to cisplatin by inducing vitamin D receptor-mediated cell autophagy.

Breast cancer (BC) is the leading cause of death in females worldwide. Although cisplatin is a strong-effect and broad-spectrum chemotherapy drug, resistance to cisplatin remains a significant factor effecting clinical efficacy. The underlying mechanism of cancer cell resistance to cisplatin is not fully understood. MicroRNAs (miRs/miRNAs), as a regulator, are involved in regulating chemosensitivity to numerous chemotherapeutic drugs. The present study aimed to investigate the function of miR-181a-5p as a potential tumor suppressor in improving the efficiency of cisplatin in BC. The IC50 of cisplatin and miR-181a-5p expression were determined in five BC cell lines, and HS578T was selected as an appropriate cell line for subsequent experiments. The sensitivity of HS578T cells to cisplatin was assessed using cell proliferation, migration and apoptosis assays. Western blotting was performed to detect the expression of vitamin D receptor (VDR) and autophagy in HS578T cells. It was found that the increase in autophagy resulted in increased apoptosis and sensitivity to cisplatin in HS578T cells. miR-181a-5p transfection also inhibited the proliferation and migration ability of HS578T cells and induced apoptosis. Meanwhile, HS578T cells have increased sensitivity to cisplatin. VDR, as a target gene and autophagy regulator of miR-181a-5p, was negatively regulated by miR-181a-5p. Upon the decrease in VDR expression, the autophagy in HS578T cells was increased. These results indicate that the increase in autophagy enhanced the chemosensitivity of cisplatin by inducing apoptosis of HS578T cells and by inhibiting proliferation and migration. The present study showed that miR-181a-5p increased the chemical sensitivity of HS578T cells to cisplatin by inhibiting VDR to promote autophagy. The use of miR-181a-5p/autophagy/VDR-based treatment strategies may be a potential method to overcome cisplatin resistance in BC.

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.

Highly Sensitive Electrochemical Detection of Folic Acid by Using a Hollow Carbon Nanospheres@molybdenum Disulfide Modified Electrode.

As a nutrient in body functions, folic acid (FA) plays a very important role for human health, and thus developing a highly sensitive method for its determination is of great significance. In the present work, carbon hollow nanospheres decorated with molybdenum disulfide nanosheets (CHN@MoS2) nanomaterials were produced through a simple method and adopted to modify a glassy carbon electrode for assembling a highly sensitive electrochemical sensor of FA. After characterizing the prepared nanomaterials using scanning-/transmission-electron microscopy and Raman spectra, as well as optimizing various testing conditions, including the pH value of the buffer solution, the accumulation time and amount of nanomaterials on electrode surface, and the electrochemical determination of FA was carried out using a CHN@MoS2 electrode. Owing to the coordinative advantages from CHN and MoS2, the results show that CHN@MoS2 exhibits excellent sensing responses for FA, and it has a wide linear range from 0.08 to 10.0 µM coupled with a low detection limit of 0.02 µM. Finally, the proposed method for FA detection was successfully applied in human urine analysis. The obtained results are satisfactory, revealing that the developed method based on CHN@MoS2 nanomaterials has important applications for FA determination.

Whole-exome sequencing in patients with premature ovarian insufficiency: early detection and early intervention.

BACKGROUND: The loss of ovarian function in women, referred to as premature ovarian insufficiency (POI), is associated with a series of concomitant diseases. POI is genetically heterogeneous, and in most cases, the etiology is unknown. METHODS: Whole-exome sequencing (WES) was performed on DNA samples obtained from patients with POI, and Sanger sequencing was used to validate the detected potentially pathogenic variants. An in silico analysis was carried out to predict the pathogenicity of the variants. RESULTS: We recruited 24 patients with POI and identified variants in POI-related genes in 14 patients, including bi-allelic mutations in DNAH6, HFM1, EIF2B2, BNC, and LRPPRC and heterozygous variants in BNC1, EIF2B4, FOXL2, MCM9, FANCA, ATM, EIF2B3, and GHR. No variants in the above genes were detected in the WES data obtained from 29 women in a control group without POI. Determining a clear genetic etiology could significantly increase patient compliance with appropriate intervention strategies. CONCLUSIONS: Our study confirmed that POI is a genetically heterogeneous condition and that whole-exome sequencing is a powerful tool for determining its genetic etiology. The results of this study will aid researchers and clinicians in genetic counseling and suggests the potential of WES for the detection of POI and thus early interventions for patients with POI.

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.

LncRNAs Predicted to Interfere With the Gene Regulation Activity of miR-637 and miR-196a-5p in GBM.

Rigorous molecular characterization of biological systems has uncovered a variety of gene variations underlying normal and disease states and a remarkable complexity in the forms of RNA transcripts that exist. A recent concept, competitive endogenous RNA, suggests that some non-coding RNAs can bind to miRNAs to modulate their role in gene expression. Here, we used several platforms, integrating mRNA, non-coding RNAs and protein data to generate an RNA-protein network that may be dysregulated in human glioblastoma multiforme (GBM). Publicly available microarray data for mRNA and miRNA were used to identify differentially expressed miRNAs and mRNAs in GBM relative to non-neoplastic tissue samples. Target miRNAs were further selected based on their prognostic significance, and the intersection of their target gene set with the differentially expressed gene set in Venn diagrams. Two miRNAs, miR-637 and miR-196a-5p, were associated with poor and better prognosis, respectively, in GBM patients. Non-coding RNAs, ENSG00000203739/ENSG00000271646 and TPTEP1, were predicted to be miRNA target genes for miR-637 and miR-196a-5p and positively correlated with the selected mRNA, CYBRD1 and RUFY2. A local protein interaction network was constructed using these two mRNAs. Predictions based on the ENSG00000203739/ENSG00000271646-miR-637-CYBRD1 and TPTEP1-miR-196a-5p-RUFY2 regulation axes indicated that the two proteins may act as an oncogene and tumor suppressor, respectively, in the development of GBM. These results highlight competitive endogenous RNA networks as alternative molecular therapeutic targets in the treatment of the disease.

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.