Introduction: The COVID-19 pandemic has had a devastating worldwide effect on mental health. Recent studies correlate the spreading of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with symptoms of depression, most prominent in postpartum women. Our systematic literature review scope is to identify the risk factors and predictors for postpartum depression (PPD) and describe the steps that should be taken to help postpartum women. This study will help clinicians, researchers, and policymakers to elucidate the predictors of PPD during this pandemic and prevent these adverse outcomes in future crises. Methods: We conducted a systematic search by employing databases PubMed, Google Scholar, Scopus, and Embase to identify articles published before March 2021. About 463 publications were generated during our search process and from those, 36 were reviewed, summarized, and synthesized. Studies qualified the criteria if they (1) utilized qualitative or quantitative design, (2) explored the risk factors for PPD, and (3) were written in English. Quality evaluation of each study was achieved by using criteria set by Lincoln and Guba. Results: Prevalence of depression symptoms ranged from 7% to 80.8% in postpartum women during the SARS-COV 2 pandemic. The risk factors for PPD were classified into 6 major categories: socio-demographic, psychological, pre-existing pathology, metabolic factors, previous events of miscarriage, and media misinformation. Conclusion: It is extremely vital to care for women’s mental health during pregnancy and after childbirth during these unprecedented times. This review urges the need to design adequate interventions for this vulnerable population to prevent negative consequences of PPD.

Objective: Aim of this meta-analysis is to examine the association between Hypertensive Disorder of Pregnancy and ASD. ASD is the broad current designation for a group of conditions with deficits in social interaction and communication and RRBs(restricted repetitive behaviors), common severe pervasive neurodevelopmental disorder of undetermined etiology. Environmental exposures, especially pregnancy complications, have been increasingly recognized as a potential risk factor for ASD. Design and method: We conducted a systematic literature search onPubMed, Embase and PsycINFO databases were searched. Pooled relative risks (RR) with 95% confidence intervals were calculated. Subgroup and sensitivity analyses were performed. Heterogeneity was assessed using Cochran's Q- and the I test. The presence of publication bias was evaluated by Egger's test and visual inspection of the symmetry in funnel plots. Results: A total of t welve studies meet the inclusion criteria with more than 307146 participant,including 6209 ASD. Subgroup analysis of clinical classification include: gestational hypertension, pre-eclampsia, chronic hypertension complicating pregnancy. The risk of ASD in pre-eclampsia is with OR 1.47 and CHP with OR 1.37 slightly higher than those of mothers with gestational hypertension OR 1.2. In consistence with most previous researches, higher ASD prevalence was observed in male than female,indicating a potential role for gender in the pathophysiology of ASD. The figure shows a Forest plot of the correlation between HDP and ASD Conclusions: This meta-analysis implies a possible link between Hypertensive Disorders of Pregnancy and the risk of Autism Spectrum Disorder in offspring. However, further investigation should be conducted to confirm this conclusion, and intensive prenatal surveillance and early prediction for ASD is needed.

Background: Fluvoxamine is a selective serotonin reuptake inhibitor that is known to be used as antidepressant. Repurposing of Fluvoxamine for the treatment of COVID-19 is theorized to help in the prevention of the clinical deterioration of SARS CoV-2 patients. In our systematic review and meta-analysis, we aim to assess the safety and efficacy of the drug under study in terms of its effect on the mortality and the risk of hospitalization and mechanical ventilation in non-critically ill COVID-19 patients. Methods: We performed a systematic search of seven electronic databases. The search results were screened based on the previously determined inclusion and exclusion criteria. We determined the data related to our objectives. The mortality rates, rates of hospitalization, risk of mechanical ventilation and serious side effects were extracted from the studies that successfully met our inclusion and exclusion criteria. Then, the extracted data from the included studies was included in the meta-analysis. Results: Three studies, two randomized clinical trials and one observational cohort study, with 1762 patients, were the final outcome of our search and screening processes. Among all participants, 886 patients received Fluvoxamine while 876 were controls. Follow up periods ranged from 7 days to 28 days. There was no significant difference in the intention-to-treat mortality rates between the two groups (RR = 0.66; 95% CI: 0.36 - 1.21, p-value = 0.18; I2 = 0%). However, Fluvoxamine decreased the per-protocol mortality compared to both placebo alone or placebo/standard care (RR = 0.09; 95% CI: 0.01 - 0.64, p-value = 0.02; I2 = 0% and RR = 0.09; 95% CI: 0.01 - 0.72, respectively). As compared to placebo or standard care, the all-cause hospitalization was significantly reduced in the fluvoxamine group (RR = 0.71; 95% CI: 0.54 - 0.93, p-value = 0.01; I2 = 61%). This risk reduction was not significant when compared to placebo alone (RR = 0.76; 95% CI: 0.57 - 1.00; p-value = 0.051; I2 = 48%). Furthermore, the risk of mechanical ventilation was not improved in the fluvoxamine group as compared to placebo (RR = 0.71; 95% CI: 0.43 - 1.16, p-value = 0.17; I2 = 0%). The serious adverse effects were almost the same in the treatment group and the control (13% and 12% respectively). Conclusion: Fluvoxamine does not significantly reduce the mortality rates or the risk of mechanical ventilation in SARS CoV-2 patients. Nonetheless, it was found to have a good impact on reducing all cause hospitalization among patients with COVID-19 disease. Therefore, further clinical studies are needed to determine the effectiveness of the drug and its mechanisms of action.

Aims We conducted a network meta-analysis (NMA) to determine the effects of low-dose (20 mg/day or less) conventional statin therapy (CST) and high-dose (40 mg/day or more) intensive statin therapy (IST) on the frequency of Tregs and their associated cytokines (IFN-γ, IL-10, TGF-β) compared to placebo. Methods and results PubMed, Cochrane Library, and EMBASE databases were searched for randomized clinical trials (RCTs) to identify relevant articles published until June 2021. We pooled data extracted from the included studies using the standardized mean difference (SMD). A random-effects model was used to conduct this NMA. Heterogeneity was evaluated using Cochran's Q test and the I2 test. The Grading of Recommendations, Assessment, Development and Evaluations (GRADE) was used to assess the quality of the study. Data analysis was conducted using R software. A total of 505 patients were enrolled in the 5 RCTs. NMA indicated a significant increase in Treg frequency in the CST group compared with the control group (SMD 1.77; 95% CI: 0.77–2.76; P = 0.0005) and a larger increase in the Treg frequency associated with the IST group compared with the control group (SMD 2.12; 95% CI: 1.15–3.10; P-value < 0.0001). However, there was significant heterogeneity and inconsistency among the included studies (τ2 = 0.6096; τ = 0.7808; I2 = 91.2% [80.5%; 96.0%]). When compared with placebo, both CST and IST increased the levels of secreted IL-10 (SMD 2.69; 95% CI: 2.07–3.31; P-value < 0.0001 and SMD 2.14; 95% CI: 1.76–2.52; P-value < 0.0001). Compared with the control group, CST was associated with increased levels of TGF-β (SMD 3.83; 95% CI: 0.63–7.0; P-value = 0.0189); this association was not seen in the IST group. IFN-γ levels decreased significantly in both the IST and CST groups (SMD −1.52; 95% CI: −1.94—1.10; P-value < 0.0001 and SMD −2.34; 95% CI: −2.73—1.95; P-value < 0.0001, respectively). Conclusions The findings of our study indicated that both high- and low-dose statin groups increased Treg frequency compared with the placebo group. IST demonstrated greater benefits than CST. Furthermore, statin therapy increased IL-10 and TGF-β levels and decreased IFN-γ levels. Overall, these results have significant implications for patients with ACS who would benefit from Treg-induced immunomodulatory balance.