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Enterovirus D68 (EV-D68) is a single-stranded positive-sense RNA virus, and it is one of the family members of Picornaviridae. Except for EV-D68, the entire family Picornaviridae has been illustrated in literature. EV-D68 was first discovered and isolated in California, USA, in 1962. EV-D68 has resulted in respiratory disorders’ outbreaks among children worldwide, and it has been detected in cases of various neurological diseases such as acute flaccid myelitis (AFM). A recent study documented a higher number of EV-D68 cases associated with AFM in Europe in 2016 compared to the 2014 outbreak. EV-D68 is mainly diagnosed by quantitative PCR, and there is an affirmative strategy for EV-D68 detection by using pan-EV PCR on the untranslated region and/or the VP1 or VP2, followed by sequencing of the PCR products. Serological tests are limited due to cross-reactivity of the antigens between the different serotypes. Many antiviral drugs for EV-D68 have been evaluated and showed promising results. In our review, we discuss the current knowledge about EV-D68 and its role in the development of AFM.

We aimed to evaluate the efficacy and safety of infliximab biosimilar, CT-P13, for patients with inflammatory bowel disease. We searched PubMed, Scopus, Ovid, and Web of Science for relevant clinical trials discussing CT-P31 administration for IBD patients either naive to biological therapy or switched from IFX therapy. Data of the rates of clinical response, clinical remission, and adverse events were extracted and pooled in a random effect model meta-analysis using CMA version 2. Thirty-two studies with a total of 3464 IBD patients treated with CT-P13 were identified. The pooled rates of clinical response among Crohn’s disease (CD) and ulcerative colitis (UC) at 8–14 weeks were 0.81 (95% CI = 0.72 to 0.87) and 0.68 (95% CI = 0.63 to 0.72), respectively, and at 48–63 weeks were 0.69 (95% CI = 0.48 to 0.85) and 0.54 (95% CI = 0.45 to 0.63) respectively. After switching from IFX to CT-P13, the pooled rates of sustained clinical response among CD and UC at 30–32 weeks were 0.84 (95% CI = 0.57 to 0.96) and 0.96 (95% CI = 0.58 to 0.99), respectively, and at 48–63 weeks were 0.51 (95% CI = 0.22 to 0.79) and 0.83 (95% CI = 0.19 to 0.99) respectively. Moreover, adverse events were reported (CD = 0.10, 95% CI 0.04 to 0.22; UC = 0.18, 95% CI 0.05 to 0.15). CT-P13 is effective and well tolerated in short and long-term periods. Switching to CT-P13 is recommended for the management of IBD.

Alpha-lipoic acid (ALA) is a naturally-occurring compound that has shown promising antioxidant and anti-inflammatory effects in experimental and human studies. The aim of this study was to assess the efficacy of ALA in the management of patients with diabetes mellitus (DM). We searched Medline (via PubMed), EBSCO, Scopus, and Web of Science for relevant randomized controlled trials. Data on glycated hemoglobin (HbA1c), blood glucose levels, lipid profile components, HOMA, and glutathione peroxidase (GPx) were extracted and pooled as the standardized mean difference (SMD) in a random effect model meta-analysis using RevMan version 5.3. Ten studies (n = 553 patients) were included. In the term of HBA1C, the overall SMD did not favor either of the two groups (SMD = 0.01, 95% CI [-0.32,0.35]; p = 0.94) in uncomplicated T2DM patients. Moreover, there was no statistically significant difference between the two groups in terms of FBG (SMD = -0.06, 95% CI [-0.44,0.33]; p = 0.78), PPBG (SMD = 0.04, 95% CI [-0.27,0.34]; p = 0.82), HDL (SMD = -0.05, 95% CI [-0.35,0.25]; p = 0.75), LDL (SMD = -0.05, 95% CI [-0.33,0.23]; p = 0.75). In terms of GPx, ALA was superior to placebo (SMD = 0.43, 95% CI [0.07,0.8]; p = 0.02). Our analysis showed that ALA was not superior to placebo in terms of HBA1C, LDL, HDL, TC, TG reduction in uncomplicated T2DM. However, in terms of GPx, ALA was significantly superior to the placebo. Further studies with larger sample sizes should investigate different doses of ALA in DM patients.

Background: Levetiracetam, a novel antiepileptic drug, has shown antidyskinetic effects in experimental animal models of Parkinson's disease (PD). The tolerability and efficacy of levetiracetam in reducing the levodopa-induced dyskinesia (LID) in PD patients have not been established. Therefore, this study aims to synthesize evidence from published prospective clinical trials about the efficacy of levetiracetam for the management of LID in PD patients. Methods: We followed the PRISMA statement guidelines during the preparation of this systematic review. A computer literature search of PubMed, EBSCO, Scopus, MEDLINE, and the web of science was carried out. We selected prospective clinical trials assessing the anti-dyskinetic efficacy of levetiracetam for treating LID in patients with PD. The Abnormal Involuntary Movement Scale (AIMS), Clinical Global Impression Score (GCI), UPDRS III, and UPDRS IV were considered as the primary outcome measures; their data were extracted and reviewed. Results: Our review included seven clinical trials with a total of 150 patients. Of them, three studies were randomized controlled trials, and the remaining were open-label single arm trials. Four studies reported poor tolerability of the levetiracetam with mild anti-dyskinetic effects. Levetiracetam slightly improved the UPDRS-IV and AIMS scores with small effect size. In the remaining three studies, levetiracetam failed to exhibit any anti-dyskinetic effects. Conclusion: Current evidence does not support the efficacy of the levetiracetam for treating LID in PD patients, however, due to the limited number of published randomized control trials (RCTs), further RCTs are required.