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COVID-19 manifests with a spectrum of symptoms, varying in intensity, and can lead to fatal outcomes in certain instances. Within the human genetic makeup, the ACE2 (angiotensinconverting enzyme 2) gene governs the production of the ACE2 protein--a receptor situated on the surface of human cells. This receptor holds a pivotal role in the control of blood pressure and cardiovascular functions. This study aimed to investigate the potential impact of the ACE2 gene polymorphism (rs2285666) on serum creatinine and creatine kinase (CK) levels among COVID-19 patients and to assess its association with disease severity. The research encompassed 750 individuals diagnosed with COVID-19, all of whom were enrolled at General Hospital Tešanj. These patients were categorized into three groups based on the severity of their condition--mild, moderate, and severe. Genomic DNA was isolated from whole blood samples. The genotyping process was carried out using the Applied Biosystems QuantStudio5 RT-PCR System. Our findings revealed noteworthy associations within the group of patients exhibiting mild disease severity. Specifically, individuals carrying the CC (93.59±3.02) and TT genotypes (93.59±3.02) demonstrated significantly elevated creatinine levels in comparison to those with the CT genotype (79.32±3.27), with p-values of <0.001 and 0.011, respectively. Additionally, among patients with a mild clinical outcomes, those with the CC genotype (322.98 ± 59.04) displayed significantly higher creatine kinase levels (p=0.043) when contrasted with individuals carrying the CT genotype (151.87 ± 38.07). However, within the groups of patients with moderate and severe clinical picture, our results did not reveal statistically significant associations between different genotypes and creatinine and CK levels. ACE2 gene polymorphism (rs2285666) appears to influence creatinine and creatine kinase levels specifically in COVID-19 patients with mild disease severity, suggesting a potential genetic basis for variations in renal and muscle function within this subgroup. However, no statistically significant associations were found in patients with moderate and severe clinical outcomes. [ABSTRACT FROM AUTHOR]

Type 2 diabetes (T2D) has a continuously rising prevalence worldwide. Pharmacogenetics has been recognized as a promising concept for pharmacological treatment of T2D, as antidiabetic drugs are not equally effective and safe for all patients, and the costs of diabetes treatment are increasing. The latest published guidelines on T2D treatment firmly endorse the use of newer antidiabetic drugs, sodium-glucose cotransporter-2 inhibitors (SGLT2i), dipeptidyl peptidase-4 inhibitors (DPP-IVi), and glucagon-like peptide-1 receptor agonists (GLP-1RA), considering their satisfactory pharmacological effect and good safety profile. Furthermore, SGLT2i and GLP-1RA show protective effects in patients with established atherosclerotic cardiovascular disease and chronic kidney disease. However, there has been growing evidence that the effectiveness and safety of these drug classes could depend on genetic variability. Here, we summarized the results of the published studies on the pharmacogenetic biomarkers for the three drug classes. A number of genetic variations have been investigated so far. The explored candidate genes mostly encode drug targets, drug-metabolizing enzymes, and genes linked to T2D risk. Although many of the results are promising, it is still necessary to obtain more information from larger controlled studies to confirm their clinical significance. This approach may lead towards more personalized treatment for patients with T2D.

Aim To assess the association of single nucleotide polymorphisms (SNPs) in the ACE2 and TMPRSS2 genes with COVID-19 severity and key biomarkers. Methods The study involved 750 COVID-19 patients from Bosnia and Herzegovina, divided into three groups: mild, moderate, and severe cases. Genetic variations within the ACE2 (rs2285666) and TMPRSS2 (rs2070788) genes were examined with real-time polymerase chain reaction. Biochemical markers were determined with standard procedures. Results There was a significant difference in the rs2070788 genotype distribution between patients with mild and moderate symptoms, but not between other groups. For the rs2285666 polymorphism, no significant difference in genotype distribution was found. In patients with mild symptoms, carriers of the GG genotype of rs2070788 had significantly higher total bilirubin levels than carriers of the AA genotype. Similarly, carriers of the TT genotype of rs2285666 had significantly higher activated partial thromboplastin time and international normalized ratio, and lower lactate dehydrogenase levels compared with the CC genotype. Among patients with severe symptoms, carriers of the GG genotype showed significantly higher potassium levels than carriers of the AA genotype, while carriers of the TT genotype showed significantly higher erythrocyte count as well as hemoglobin and hematocrit levels compared with the CC genotype. Conclusion This study highlights the role of genetic factors, particularly SNPs in the ACE2 and TMPRSS2 genes, in determining COVID-19 severity, aiding patient risk assessment and prognosis. [ABSTRACT FROM AUTHOR]