Background: COVID-19 is a pandemic disease caused by SARS-CoV-2, which is an RNA virus similar to HCV in the replication process. Sofosbuvir/ledipasvir is an approved drug by the FDA to treat HCV infection. This study investigates the efficacy of Sofosbuvir/ledipasvir as a treatment for patients with moderate COVID-19 infection..
Methods: This is a single-blinded parallel-randomized controlled trial. The participants were randomized equally into the intervention group received Sofosbuvir/ledipasvir (S.L. group), and the control group received Oseltamivir, Hydroxychloroquine, and Azithromycin (OCH group). The primary outcomes were the cure rate over time and the incidence of serious adverse events. The secondary outcomes included the laboratory findings.
Results: Two hundred and fifty patients were divided equally into each group. Both groups were similar regarding gender, but age was higher in the S.L. group (p=0.001). In the S.L. group, 89 (71.2%) patients were cured, while only 51 (40.8%) patients were cured in the OCH group. The cure rate was significantly higher in the S.L. group (RR=1.75, p<0.001). Kaplan-Meir plot showed a considerably higher cure over time in the S.L. group (Log-rank test, p=0.032). There were no deaths in the S.L. group, but there were six deaths (4.8%) in the OCH group (RR=0.08, p=0.013). Seven patients (5.6%) in the S.L. group and six patients (4.8%) in the OCH group were admitted to ICU (RR=1.17, P=0.776). There was no significant difference between treatment groups regarding Total Leukocyte Count, Neutrophils count, Lymph, Alanine transaminase, and Urea.
Conclusion: Sofosbuvir/ledipasvir is suggestive of being effective in treating patients with moderate COVID-19 infection. Further studies are needed to compare Sofosbuvir/ledipasvir with the new treatment protocols.
Polymorphisms in rs694539-NNMT gene (mutant AA-genotype) could be a genetic risk factor for developing NAFLD and NASH (indicating susceptibility for progression and complications). Individuals with wild type (GG-genotype) are at less risk of NAFLD development. CAP and FibroScan efficiently diagnosed steatosis and fibrosis.
Background
Several genetic polymorphisms have been proven to play a key role in the progression of non-alcoholic fatty liver disease (NAFLD) from simple steatosis to NASH with fibrosis. Our aim was to study the effect of single nucleotide polymorphisms (SNPs) in the adiponectin gene, namely rs266729 and rs3774261, on susceptibility to NAFLD and disease progression.
Results
There was a definitive association between polymorphisms of the studied SNPs and NAFLD. Among rs266729, CG was significantly higher among patients than controls showing increased risk for NAFLD (P<0.05). AA genotype of the rs3774261 variant was significantly lower in patients than in controls (P value< 0.001) while AG and GG genotypes were significantly higher in patients than in controls (P value<0.05); A allele was significantly higher among controls (P=0.019) which might have a protective effect. None of the variants correlated significantly with the degree of steatosis. Using multivariate regression analysis, there was no significant correlation with any of the independent risk factors to the degree of steatosis.
Conclusions
There was an association between polymorphisms of the studied SNPs of rs266729 and rs3774261 of the adiponectin gene and NAFLD.
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