Since the appearance of the new SARS-CoV-2 coronavirus (severe acute respiratory syndrome coronavirus 2) in December 2019, in Wuhan, China; patients were admitted with symptoms of pneumonia, named coronavirus disease 2019 (COVID-19); the virus spread, affecting different provinces in China and, after a few months, it is now present in more than 150 countries around the world. World Health Organization (WHO) has declared the novel coronavirus (COVID-19) outbreak a global pandemic on March 11, 2020. 1 In Peru the first case was diagnosed on March 6th and from March 16th the government established a mandatory social isolation to prevent the COVID from further spreading in the country. COVID-19 has impacted and determined substantial changes in health systems in all countries; emergency, intensive, or intermediate care units carry the greatest burden, but several hospital wards have also been converted to COVID units, to face the growing wave of the disease. Many units of the different services, including cardiology, have redistributed their spaces and personnel dedicating them to become COVID-19 units. The resource allocation and priority setting measures, such as redirecting the personal protective equipment and hospital beds for patients with COVID-19 and the delay of elective cardiac
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cytotoxicity may involve inhibition of peroxisome proliferator-activated receptor alpha. Fenofibrate activates peroxisome proliferator-activated receptor alpha and inhibits SARS-CoV-2 replication in vitro. Whether fenofibrate can be used to treat coronavirus disease 2019 (COVID-19) infection in humans remains unknown. Here, we randomly assigned inpatients and outpatients with COVID-19 within 14 d of symptom onset to 145 mg of oral fenofibrate nanocrystal formulation versus placebo for 10 d, in a double-blinded fashion. The primary endpoint was a severity score whereby participants were ranked across hierarchical tiers incorporating time to death, mechanical ventilation duration, oxygenation, hospitalization and symptom severity and duration. In total, 701 participants were randomized to fenofibrate (n = 351) or placebo (n = 350). The mean age of participants was 49 ± 16 years, 330 (47%) were female, mean body mass index was 28 ± 6 kg/m 2 and 102 (15%) had diabetes. Death occurred in 41 participants. Compared with placebo, fenofibrate had no effect on the primary endpoint. The median (interquartile range) rank in the placebo arm was 347 (172, 453) versus 345 (175, 453) in the fenofibrate arm (P = 0.819). There was no difference in secondary and exploratory endpoints, including all-cause death, across arms. There were 61 (17%) adverse events in the placebo arm compared with 46 (13%) in the fenofibrate arm, with slightly higher incidence of gastrointestinal side effects in the fenofibrate group. Overall, among patients with COVID-19, fenofibrate has no significant effect on various clinically relevant outcomes (NCT04517396).Infection with SARS-CoV-2, the virus responsible for COVID-19, is an important public health problem. Available data suggest that COVID-19 progression is dependent on metabolic mechanisms 1 . Individuals with COVID-19 who developed acute respiratory distress syndrome and death are characterized by older age and a higher prevalence of hypertension, obesity, diabetes and cardiovascular diseases compared to individuals with milder disease [1][2][3][4][5][6] . Hyperglycaemia and hyperlipidaemia are also risk factors for acute respiratory distress in patients with COVID-19 disease 1,7 . Indeed, type 2 diabetes mellitus and the metabolic syndrome are associated with a markedly increased risk of death in the setting of 5 ).Several experimental studies suggest a mechanistic link between abnormal metabolism and the severity of SARS-CoV-2 and other coronavirus infections. Palmitoylation of the SARS-CoV-2 spike protein has been shown to be essential for virus-cell fusion and infectivity [8][9][10] . Gene expression analyses in cultured human bronchial cells infected with
Fabry disease (FD), like COVID-19, can affect multiple organs, including the lungs. Patients with FD would be expected to develop severe forms of COVID-19, not only because of lung involvement but also because of renal involvement and other comorbidities. We present two cases of patients with Fabry disease who had an infection by COVID-19. In the two cases presented, they presented mild forms of COVID-19. Although the role of the X chromosome mutation in FD on the development of severe forms of COVID-19 is unknown; in the cases presented, it is suggested that it may play a protective role in the development of COVID-19. Two cases are presented; it is suggested that FD would not be a risk factor for severe COVID-19.
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