Background and Purpose—: This study was designed to evaluate the effectiveness and safety of rivaroxaban in real-world practice compared with effectiveness and safety of dabigatran or warfarin for stroke prevention in atrial fibrillation through meta-analyzing observational studies. Methods—: Seventeen studies were included after searching in PubMed for studies reporting the comparative effectiveness and safety of rivaroxaban versus dabigatran (n=3), rivaroxaban versus Warfarin (n=11), or both (n=3) for stroke prevention in atrial fibrillation. Results—: Overall, the risks of stroke/systematic thromboembolism with rivaroxaban were similar when compared with those with dabigatran (stroke/thromboembolism: hazard ratio, 1.02; 95% confidence interval, 0.91–1.13; I ² =70.2%, N=5), but were significantly reduced when compared with those with warfarin (hazard ratio, 0.75; 95% confidence interval, 0.64–0.85; I ² =45.1%, N=9). Major bleeding risk was significantly higher with rivaroxaban than with dabigatran (hazard ratio, 1.38; 95% confidence interval, 1.27–1.49; I ² =26.1%, N=5), but similar to that with warfarin (hazard ratio, 0.99; 95% confidence interval, 0.91–1.07; I ² =0.0%, N=6). Rivaroxaban was associated with increased all-cause mortality and gastrointestinal bleeding, but similar risk of acute myocardial infarction and intracranial hemorrhage when compared with dabigatran. When compared with warfarin, rivaroxaban was associated with similar risk of any bleeding, mortality, and acute myocardial infarction, but a higher risk of gastrointestinal bleeding and lower risk of intracranial hemorrhage. Conclusions—: In this systematic review and meta-analysis, rivaroxaban was as effective as dabigatran, but was more effective than warfarin for the prevention of stroke/thromboembolism in atrial fibrillation patients. Major bleeding risk was significantly higher with rivaroxaban than with dabigatran, as was all-cause mortality and gastrointestinal bleeding. Rivaroxaban was comparable to warfarin for major bleeding, with an increased risk in gastrointestinal bleeding and decreased risk of intracranial hemorrhage.

Vitamin D is known to have immunomodulatory properties and its deficiency is identified as an environmental risk factor for the development of autoimmune diseases, including multiple sclerosis. The aim of this study was to assess whether low-dose vitamin D supplementation could normalize the 25(OH)D serum levels in patients with relapsing-remitting multiple sclerosis (RRMS) and vitamin D deficiency (serum 25(OH)D < 75 nmol/L), and whether it may impact serum levels of selected cytokines. Among 44 patients (mean age 38.4 ± 10.1 years, 33 women and 11 men), after 12 months of low-dose vitamin D supplementation, serum levels of 25(OH)D normalized in 34 (77.3%) of the patients. Together with vitamin D increase, median levels of anti-inflammatory cytokines (IL10, TGF-β) and regulatory IFN-γ increased, while proinflammatory IL-17 remained unchanged. Moreover, an increase of inorganic phosphorus levels and decrease of PTH levels were observed, but without changes in total calcium concentration. These results may indicate that long-term supplementation with low doses of vitamin D is sufficient to compensate its deficiency in patients with RRMS and may help to maintain beneficial anti-inflammatory cytokine profile.

Background: Calcitriol, beyond its well-established role in calcium and phosphate homeostasis, contributes to immunological processes. No known vitamin D dosage regimen effectively corrects the deficiency while accounting for immunoregulatory effects. Therefore, the purpose of this assessment was to determine whether regular administration of low doses of vitamin D might correct deficiency and have immunoregulatory effects. Methods: A total of 35 healthy volunteers were asked to supplement with vitamin D daily at a dosage of 500 or 1000 IU, depending on the degree of deficiency, for 12 months. At the beginning of the study and after the end of the supplementation period, concentrations of 25(OH)D; PTH; total calcium; inorganic phosphorus; and the inflammatory cytokines IL-17, IL-10, TGF-β, and IFN-γ were determined in all participants. Results: Correction of vitamin D deficiency was achieved with accompanying decreases in PTH and pro-inflammatory cytokine concentrations, while the concentration of anti-inflammatory cytokines remained stable. Conclusions: Therefore, regular vitamin D supplementation, even in small doses, effectively corrected the deficiency and had immunomodulatory effects.

Background: This multicenter retrospective study with a control group was designed to assess the influence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on the outcomes of patients with myocardial infarction (MI). Methods: A total of 129 patients with COVID-19 who were treated for MI were included in this study. The control group comprised 129 comparable patients without SARS-CoV-2 infection. The in-hospital, out-of-hospital, and overall mortality were analyzed. Results: A total of thirty-one (24%) patients died in the study group, and two (1.6%) patients died in the control group (OR = 20.09; CI: 4.69–85.97; p < 0.001). Similar results were observed in all analyzed patient subgroups. Multivariable Cox regression analysis confirmed the significant influence of SARS-CoV-2 infection on in-hospital outcomes (HR: 8.48459; CI: 1.982–36.320; p = 0.004). Subanalysis of the groups with COVID-19 plus ST-elevation MI (STEMI) or non-ST-elevation MI (NSTEMI) revealed comparable mortality rates: 14 (21.12%) patients in the NSTEMI group and 17 (26.98%) patients in the STEMI subgroup died (OR: 1.3; CI: 0.56–3.37; p = 0.45). During out-of-hospital observation, no differences in mortality were observed (OR: 0.77; CI: 0.11–4.07; p = 0.73). Conclusions: SARS-CoV-2 infection affects the in-hospital outcomes of patients with both MI and COVID-19, regardless of MI type (STEMI vs. NSTEMI).