Atrial fibrillation (AF) is one of the most prevalent rhythm disorders worldwide, with around 37.574 million cases around the globe (0.51 % global population). Different studies showed a high informative value of different biomarkers, including such related to the systemic inflammation, biomechanical stress and fibrosis. In this review article we aimed to study only the relation of homocysteine to the AF development. Homocysteine is a sulfur-containing amino acid, that is produced in the process of methionine metabolism. Which is a non-canonical amino acid, that is derived from the food proteins. From the scientific point of view there is a relation between hyperhomocysteinemia and myocardial fibrosis, but these mechanisms are complicated and not sufficiently studied. Homocysteine regulates activity of the ion channels through their redox state. Elevated homocysteine level can condition electrical remodeling of the cardiomyocytes through the increase of sodium current and change in the function of rapid sodium channels, increase of inwards potassium current and decrease in amount of rapid potassium channels. High homocysteine concentration also leads to the shortening of the action potential, loss of the rate adaptation of the action potential and persistent circulation of the re-entry waves. In a series of experimental studies on mice there was an association found between the homocysteine level and activity of vascular inflammation. Elevation of homocysteine level is an independent factor of the thromboembolic events and AF relapses. Population studies showed, that homocysteine is an independent risk factor for AF. So, homocysteine is an interesting target for up-stream therapy.
The ADBR2 gene has been studied for its possible relationship with the development and clinical course of chronic obstructive pulmonary disease (COPD), including response to beta-2 agonists, with existing data being contentious on the subject. So, the purpose of this study was to look into the potential impact of the arginine-16-glycine (Arg16Gly) polymorphism on the clinical course and drug utilization in COPD patients. Data show that patients with Arg16Arg have a lower number of hospital admissions for exacerbations (p=0.048), but only in the total number of exacerbations, including those treated out-patients (p=0.086). Each glycine (Gly) copy was associated with a higher number of exacerbations (OR: 0.25; 95% CI: 0.00-055; p=0.048). The number of exacerbations after LABA/LAMA treatment was similar across groups, indicating that all ADRB2 variants responded well to the treatment. Furthermore, there were no statistically significant differences in mMRC and CAT values across all study visits. Interestingly, groups differed in their use of antibiotics (AB) at all visits, with Arg16Arg being associated with the least amount of AB use. There was also a link discovered between clycine copies and increased use of glucocorticoids. As a result, Arg16Gly is involved in the clinical course of COPD as well as the utilization of drug groups. Based on the findings, we can speculate that the cross-talk between the ADRB2 gene and the corticosteroid receptor is altered in patients with the Gly16Gly genotype.
Introduction: Many recent guidelines have highlighted the importance of genetic factors in chronic obstructive pulmonary disease (COPD) development. Adrenoreceptor beta 2 (ADRB2) is believed to be linked to the response to beta 2 agonists. However, the data for this gene remains controversial. In our study we aimed to investigate the impact of the Gln27Glu gene polymorphism of ADRB2 on the clinical course of COPD. Methods: 100 patients were included into the study. We assessed GOLD group, number of exacerbations, hospitalizations, modified Medical Research Council (mMRC) dyspnea and COPD assessment test (CAT) scores, and the utilization of antibiotics, glucocorticoids, and xanthines in these patients, as well as genetic testing at inclusion. All patients had their medication changed to tiotropium/olodaterol. Results: Groups did not differ according to age, sex, smoking status, pack-years, or COPD duration. We found that patients with the Gln27Gln polymorphism had the lowest GOLD grading, D. No difference was found in the number of exacerbations, hospitalizations, and out-patient exacerbations in the year prior to inclusion and the study year. Tiotropium/olodaterol were comparable in all study groups in reducing exacerbations and hospitalizations. There was no significant difference in mMRC and CAT values between the groups. We found that Gln27Gln patients required less antibiotics at inclusion and less glucocorticoids at the end of the study. Tiotrpium/olodaterol showed variable results for different genotypes regarding the reduction in use of different drugs. Conclusion: This ADRB2 polymorphism was associated with the progression of COPD as it is linked to a more severe phenotype, requiring greater use of antibiotics and glucocorticoids. This indicates potential crosstalk at the cellular level between ADRB2 and glucocorticoid receptors and should be investigated further.
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