Context. Calcifediol has been proposed as a potential treatment for COVID-19 patients. Objective: To compare the administration or not of oral calcifediol on mortality risk of patients hospitalized because of COVID-19. Design: Retrospective, multicenter, open, non-randomized cohort study. Settings: Hospitalized care. Patients: Patients with laboratory-confirmed COVID-19 between 5 February and 5 May 2020 in five hospitals in the South of Spain. Intervention: Patients received calcifediol (25-hydroxyvitamin D3) treatment (0.266 mg/capsule, 2 capsules on entry and then one capsule on day 3, 7, 14, 21, and 28) or not. Main Outcome Measure: In-hospital mortality during the first 30 days after admission. Results: A total of 537 patients were hospitalized with COVID-19 (317 males (59%), median age, 70 years), and 79 (14.7%) received calcifediol treatment. Overall, in-hospital mortality during the first 30 days was 17.5%. The OR of death for patients receiving calcifediol (mortality rate of 5%) was 0.22 (95% CI, 0.08 to 0.61) compared to patients not receiving such treatment (mortality rate of 20%; p < 0.01). Patients who received calcifediol after admission were more likely than those not receiving treatment to have comorbidity and a lower rate of CURB-65 score for pneumonia severity ≥ 3 (one point for each of confusion, urea > 7 mmol/L, respiratory rate ≥ 30/min, systolic blood pressure < 90 mm Hg or diastolic blood pressure ≤ 60 mm Hg, and age ≥ 65 years), acute respiratory distress syndrome (moderate or severe), c-reactive protein, chronic kidney disease, and blood urea nitrogen. In a multivariable logistic regression model, adjusting for confounders, there were significant differences in mortality for patients receiving calcifediol compared with patients not receiving it (OR = 0.16 (95% CI 0.03 to 0.80). Conclusion: Among patients hospitalized with COVID-19, treatment with calcifediol, compared with those not receiving calcifediol, was significantly associated with lower in-hospital mortality during the first 30 days. The observational design and sample size may limit the interpretation of these findings.

Apart from its main function in the mitochondria as a key element in electron transport, Coenzyme Q10 (CoQ10) has been described as having multiple functions, such as oxidant action in the generation of signals and the control of membrane structure and phospholipid and cellular redox status. Among these, the most relevant and most frequently studied function is the potent antioxidant capability of its coexistent redox forms. Different clinical trials have investigated the effect of CoQ10 supplementation and its ability to reduce oxidative stress. In this review, we focused on recent advances in CoQ10 supplementation, its role as an antioxidant, and the clinical implications that this entails in the treatment of chronic diseases, in particular cardiovascular diseases, kidney disease, chronic obstructive pulmonary disease, non-alcoholic fatty liver disease, and neurodegenerative diseases. As an antioxidant, CoQ10 has proved to be of potential use as a treatment in diseases in which oxidative stress is a hallmark, and beneficial effects of CoQ10 have been reported in the treatment of chronic diseases. However, it is crucial to reach a consensus on the optimal dose and the use of different formulations, which vary from ubiquinol or ubiquinone Ubisol-Q10 or Qter®, to new analogues such as MitoQ, before we can draw a clear conclusion about its clinical use. In addition, a major effort must be made to demonstrate its beneficial effects in clinical trials, with a view to making the implementation of CoQ10 possible in clinical practice.

Several studies indicate that oxidative stress might play a central role in the initiation and maintenance of cardiovascular diseases. It remains unclear whether ceruloplasmin acts as a passive marker of inflammation or as a causal mediator. To better understand the impact of ceruloplasmin blood levels on the risk of cardiovascular disease, and paying special attention to coronary heart disease, we conducted a search on the two most commonly used electronic databases (Medline via PubMed and EMBASE) to analyze current assessment using observational studies in the general adult population. Each study was quality rated using criteria developed by the US Preventive Services Task Force. Most of 18 eligible studies reviewed support a direct relationship between ceruloplasmin elevated levels and incidence of coronary heart disease. Our results highlight the importance of promoting clinical trials that determine the functions of ceruloplasmin as a mediator in the development of coronary heart disease and evaluate whether the treatment of elevated ceruloplasmin levels has a role in the prognosis or prevention of this condition.

IntroductionAbout 25% of patients with COVID-19 develop acute respiratory distress syndrome (ARDS) associated with a high release of pro-inflammatory cytokines such as interleukin-6 (IL-6). The aim of the SARICOR study is to demonstrate that early administration of sarilumab (an IL-6 receptor inhibitor) in hospitalised patients with COVID-19, pulmonary infiltrates and a high IL-6 or D-dimer serum level could reduce the progression of ARDS requiring high-flow nasal oxygen or mechanical ventilation (non-invasive or invasive).Methods and analysisPhase II, open-label, randomised, multicentre, controlled clinical trial to study the efficacy and safety of the administration of two doses of sarilumab (200 and 400 mg) plus best available therapy (BAT) in hospitalised adults with COVID-19 presenting cytokine release syndrome. This strategy will be compared with a BAT control group. The efficacy and safety will be monitored up to 28 days postadministration. A total of 120 patients will be recruited (40 patients in each arm).Ethics and disseminationThe clinical trial has been approved by the Research Ethics Committee of the coordinating centre and authorised by the Spanish Agency of Medicines and Medical Products. If the hypothesis is verified, the dissemination of the results could change clinical practice by increasing early administration of sarilumab in adult patients with COVID-19 presenting cytokine release syndrome, thus reducing intensive care unit admissions.Trial registration numberNCT04357860.

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The significant impact of COVID-19 worldwide has made it necessary to develop tools to identify patients at high risk of severe disease and death. This work aims to validate the RIM Score-COVID in the SEMI-COVID-19 Registry. The RIM Score-COVID is a simple nomogram with high predictive capacity for in-hospital death due to COVID-19 designed using clinical and analytical parameters of patients diagnosed in the first wave of the pandemic. The nomogram uses five variables measured on arrival to the emergency department (ED): age, sex, oxygen saturation, C-reactive protein level, and neutrophil-to-platelet ratio. Validation was performed in the Spanish SEMI-COVID-19 Registry, which included consecutive patients hospitalized with confirmed COVID-19 in Spain. The cohort was divided into three time periods: T1 from February 1 to June 10, 2020 (first wave), T2 from June 11 to December 31, 2020 (second wave, pre-vaccination period), and T3 from January 1 to December 5, 2021 (vaccination period). The model’s accuracy in predicting in-hospital COVID-19 mortality was assessed using the area under the receiver operating characteristics curve (AUROC). Clinical and laboratory data from 22,566 patients were analyzed: 15,976 (70.7%) from T1, 4,233 (18.7%) from T2, and 2,357 from T3 (10.4%). AUROC of the RIM Score-COVID in the entire SEMI-COVID-19 Registry was 0.823 (95%CI 0.819–0.827) and was 0.834 (95%CI 0.830–0.839) in T1, 0.792 (95%CI 0.781–0.803) in T2, and 0.799 (95%CI 0.785–0.813) in T3. The RIM Score-COVID is a simple, easy-to-use method for predicting in-hospital COVID-19 mortality that uses parameters measured in most EDs. This tool showed good predictive ability in successive disease waves. Supplementary Information The online version contains supplementary material available at 10.1007/s11739-023-03200-3.

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