The Coronavirus Disease 2019 (COVID-19) outbreak caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) resulted in a worldwide pandemic of a highly infectious disease. The difficulty of dealing with COVID-19 is the broad spectrum of clinical manifestations that involves various pathophysiological mechanisms, severities, duration, and complications. This study aims to help emphasize the factors related to the persistence and duration of anosmia (loss of smell) and ageusia (loss of taste) as part of post-acute COVID-19 syndrome in Saudi COVID-19 patients via a retrospective cross-sectional design. Eight hundred and eighty-one participants were recruited between March and April 2021. Those participants were 18 years or older, recovered from the COVID-19 infection, and completed 14 days after the onset of the acute phase of the disease. Among the 881 recruited participants, 808 have submitted eligible responses and were included in data analyses. The most common persistent symptoms in post-acute COVID-19 syndrome were anosmia (33.8%) and ageusia (26.4%). The data also showed a significant association between female sex and the incidence and the persistence of anosmia and ageusia. In multivariable analysis, anosmia during the acute phase was associated with BMI, asthma and shortness of breath, while anosmia during the post-acute phase was associated with sex. Ageusia during the acute phase was associated with sex, myalgia and arthralgia, while ageusia in the post-acute phase was associated with sex.

Background: Autism spectrum disorder (ASD) encompasses a group of disorders characterized by difficulties with social interaction and repetitive behavior. The condition is supposed to originate from early shifts in brain development, while the underlying processes are unknown. Moreover, a considerable number of patients with ASD experience digestive difficulties. Metalloproteases (ADAMs) are a class of enzymes capable of cleaving membrane-bound proteins. Members of this family, ADAM17 and ADAM22, have the ability to cleave proteins like the pro-inflammatory cytokine TNF-ά and glutamate synaptic molecules, which are both engaged in neuro-inflammation and glutamate excitotoxicity as crucial etiological mechanisms in ASD. ADAM17 and ADAM22 may also have a role in ASD microbiota–gut–brain axis connections by regulating immunological and inflammatory responses in the intestinal tract. Subjects and Methods: Using ELISA kits, the plasma levels of ADAM17 and ADAM22 were compared in 40 children with ASD and 40 typically developing children. All of the autistic participants’ childhood autism rating scores (CARS), social responsiveness scales (SRS), and short sensory profiles (SSP) were evaluated as indicators of ASD severity. Results: Our results showed that plasma levels of ADAM17 were significantly lower in ASD children than in control children, while ADAM22 demonstrated non-significantly lower levels. Our data also indicate that while ADAM17 correlates significantly with age, ADAM22 correlates significantly with CARS as a marker of ASD severity. Conclusions: Our interpreted data showed that alteration in ADAM17 and ADAM22 might be associated with glutamate excitotoxicity, neuroinflammation, and altered gut microbiota as etiological mechanisms of ASD and could be an indicator of the severity of the disorder.

Background: Coronary artery disease (CAD), manifested mainly as acute coronary syndrome (ACS), continues to be a major cause of mortality globally and a significant contributing factor to the global disease burden. Elevation of low-density lipoprotein cholesterol levels attributed to proprotein convertase subtilisin/Kexin type-9 (PCSK9) during and following ACS puts patients at high risk of subsequent adverse events. Evolocumab is a PCSK9 inhibitor that is associated with a significant reduction in low-density lipoprotein cholesterol (LDL-C) levels through PCSK9 inhibition in comparison to traditional statin therapy. Methods: We conducted a systematic review and meta-analysis of literature addressing the efficacy and safety of evolocumab compared to other lipid-lowering therapies or placebo. An extensive internet-based literature search using pre-determined key phrases supported by medical sub-headings and Boolean operators was performed in October 2022 to identify literature pertinent to the research topic. The search was primarily based on the National Library of Medicine (PubMed and Clinical Trials), MEDLINE, Cochrane, and the Science direct literature databases. Subsequently, the researchers devised PICOs-based screening criteria which had to be met by each identified study for inclusion in the review and meta-analysis. Two independent reviewers conducted data stratification and quality assessment of identified studies. Statistical analysis of the primary and secondary outcomes was conducted on the Cochrane REVMAN 5.4 statistical software for randomized trials. Results: Two thousand five hundred and seventy-six potential studies were identified for inclusion in the systematic review. Data stratification, screening, and quality assessment of these studies based on the eligibility criteria led to the exclusion of two thousand five hundred and sixty-seven studies as they did not meet the standards set. Nine randomized controlled trials progressed to numerical analysis for validity and reliability. Eight studies were included in the meta-analysis. Meta-analytical results showed a significant decrease in LDL-C changes from initiation of evolocumab therapy to 8 weeks following ACS compared to placebo. Similar results were derived in the sub-acute phase of ACS [SMD -1.95 (95% CI -2.29, -1.62)]. The meta-analysis revealed no statistically significant relationship between the risk of adverse effects, serious adverse effects, and major adverse cardiovascular events (MACE) from treatment using evolocumab in comparison to placebo [(relative risk, RR 1.04 (95% CI 0.99, 1.08) (Z = 1.53; p=0.12)]. Conclusion: Early evolocumab therapy initiation was associated with a significant decrease in LDL-C levels and was not associated with an increased risk of adverse effects in comparison to placebo.