BackgroundThe number of people living with HIV/AIDS (PLHA) in China continues to increase. Depression, a common mental disorder in this population, may confer a higher likelihood of worse health outcomes. An estimate of the prevalence of this disorder among PLHA is required to guide public health policy, but the published results vary widely and lack accuracy in China. The goal of this study was to estimate the pooled prevalence of depression or depressive symptoms among PLHA in China.MethodsA systematic literature search of several databases was conducted from inception to June 2017, focusing on studies reporting on depression or depressive symptoms among PLHA in China. The risk of bias of individual studies was assessed using a modified version of the Newcastle-Ottawa scale. The overall prevalence estimates were pooled using random-effects meta-analysis. Differences according to study-level characteristics were examined using stratified meta-analysis and meta-regression.ResultsSeventy-four observational studies including a total of 20,635 PLHA were included. The pooled prevalence of depression or depressive symptoms was 50.8% (95% CI: 46.0–55.5%) among general PLHA, 43.9% (95% CI: 36.2–51.9%) among HIV-positive men who have sex with men, 85.6% (95% CI: 64.1–95.2%) among HIV-positive former blood/plasma donors, and 51.6% (95% CI: 31.9–70.8%) among other HIV-positive populations. Significant heterogeneity was detected across studies regarding these prevalence estimates. Heterogeneity in the prevalence of depression among the general population of PLHA was partially explained by the geographic location and baseline survey year.ConclusionsBecause of the significant heterogeneity detected across studies regarding these prevalence estimates of depression or depressive symptoms, the results must be interpreted with caution. Our findings suggest that the estimates of depression or depressive symptoms among PLHA in China are considerable, which highlights the need to integrate screening and providing treatment for mental disorders in the treatment package offered to PLHA, which would ultimately lead to better health outcomes in PLHA.Electronic supplementary materialThe online version of this article (10.1186/s12888-018-1741-8) contains supplementary material, which is available to authorized users.

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This study is aimed at evaluating the diagnostic value of FIB-4 for liver fibrosis in patients with hepatitis B through a meta-analysis of diagnostic test. We conducted a comprehensive search in the Pubmed, Embase, Web of Science, and Chinese National Knowledge Infrastructure before October 31, 2016. Stata 14.0 software was used for calculation and statistical analyses. We used the sensitivity, specificity, positive and negative likelihood ratio (PLR, NLR), diagnostic odds ratio (DOR) and 95% confidence intervals (CIs) to evaluate the diagnostic value of FIB-4 for liver fibrosis in patients with hepatitis B. Twenty-six studies were included in the final analyses, with a total of 8274 individuals. The pooled parameters are calculated from all studies: sensitivity of 0.69 (95%CI:0.63-0.75), specificity of 0.81 (95%CI: 0.73-0.87), PLR of 3.63 (95%CI:2.66-4.94), NLR of 0.38 (95%CI:0.32-0.44), DOR of 9.57 (95%CI: 6.67-13.74), and area under the curve (AUC) of 0.80 (95%CI: 0.76-0.83). We also conducted subgroup based on the range of cut-off values. Results from subgroup analysis showed that cut-off was the source of heterogeneity in the present study. The sensitivity and specificity of cut-off>2 were 0.69 and 0.95 with the AUC of 0.90 (95%CI: 0.87-0.92). The overall diagnostic value of FIB-4 is not very high for liver fibrosis in patients with hepatitis B. However, the diagnostic value is affected by the cut-off value. FIB-4 has relatively high diagnostic value for detecting liver fibrosis in patients with hepatitis B when the diagnostic threshold value is more than 2.0.

Purpose To examine the associations of maternal virus infection in early pregnancy with risk of offspring congenital heart disease (CHD) and its seven common subtypes including atrial septal defect, ventricular septal defect, atrioventricular septal defect, patent ductus arteriosus, Tetralogy of Tallot, pulmonary stenosis, and transposition of the great arteries. Patients and Methods A prospective cohort study was conducted in Central China. A total of 44,048 pregnant women with singleton pregnancies at 8–14 gestational weeks were finally included and followed to 3 months postpartum. Serum was tested for virus infection including hepatitis B virus (HBV), coxsackievirus-B, human cytomegalovirus (HCMV), herpes simplex virus (HSV), and rubella virus. Multivariable modified Poisson regression models were used to estimate the relative risks (RRs) of all CHDs as well as seven common subtypes of CHD in offspring of pregnant women with different types of virus infection in early pregnancy, adjusting for confounders identified by directed acyclic graphs. Results At the end of follow-up, 564 births were diagnosed with CHD. Multivariable analyses showed that the presence of maternal viral infection in early pregnancy was independently associated with increased risks of CHD in offspring, with an adjusted relative risk of 2.21 (95% CI: 1.66–2.95) for HBV infection, 2.21 (95% CI: 1.63–3.00) for coxsackievirus-B infection, 3.12 (95% CI: 2.44–3.98) for HCMV infection, and 2.62 (95% CI: 1.95–3.51) for rubella virus infection. More specifically, the offspring of pregnant women with HCMV infection had the highest increased risk of patent ductus arteriosus (RR=10.50, 95% CI: 6.24–17.66). These findings persisted in analyses that were further adjusted for the other virus of interest in this study. Conclusion Our study proposed evidence that maternal virus infection in early pregnancy, including HBV, coxsackievirus-B, HCMV, and rubella virus, was implicated in CHD, although more studies remain needed to verify the results, especially associations in specific CHD phenotypes.

Background MTHFD1 gene may affect the embryonic development by elevated homocysteine levels, DNA synthesis and DNA methylation, but limited number of genetic variants of MTHFD1 gene was focused on the association with congenital heart disease (CHD). This study examined the role of MTHFD1 gene and maternal smoking on infant CHD risk, and investigated their interaction effects in Chinese populations. Methods A case-control study of 464 mothers of CHD infants and 504 mothers of health controls was performed. The exposures of interest were maternal tobacco exposure, single nucleotide polymorphisms (SNPs) of maternal MTHFD1 gene. The logistic regression model was used for accessing the strength of association. Results Mothers exposed to secondhand smoke during 3 months before pregnancy (adjusted odds ratio [aOR] = 1.56; 95% confidence interval [CI]: 1.13–2.15) and in the first trimester of pregnancy (aOR = 2.24; 95%CI: 1.57–3.20) were observed an increased risk of CHD. Our study also found that polymorphisms of maternal MTHFD1 gene at rs1950902 (AA vs. GG: aOR = 1.73, 95% CI: 1.01–2.97), rs2236222 (GG vs. AA: aOR = 2.38, 95% CI: 1.38–4.12), rs1256142 (GA vs.GG: aOR = 1.57, 95% CI: 1.01–2.45) and rs11849530 (GG vs. AA: aOR = 1.68, 95% CI: 1.02–2.77) were significantly associated with higher risk of CHD. However, we did not observe a significant association between maternal MTHFD1 rs2236225 and offspring CHD risk. Furthermore, we found the different degrees of interaction effects between polymorphisms of the MTHFD1 gene including rs1950902, rs2236222, rs1256142, rs11849530 and rs2236225, and maternal tobacco exposure. Conclusions Maternal polymorphisms of MTHFD1 gene, maternal tobacco exposure and their interactions are significantly associated with the risk of CHD in offspring in Han Chinese populations. However, more studies in different ethnic populations with a larger sample and prospective designs are required to confirm our findings. Trial registration Registration number: ChiCTR1800016635.