ABSTRACT
Aim: The novel coronavirus causes acute severe respiratory syndrome (SARS COV 2), and the disease is named COVID-19. The virus spreads easily, and CO-VID-19 may be asymptomatic or cause severe pneumonia and ARDS. Hemodialysis patients are affected by COVID-19 because of the immunosuppression caused by uremia, comorbid diseases and the risk of cross-contamination during dialysis. In this study, we aimed to examine the clinical features and outcomes of 55 hemodialysis patients diagnosed with COVID-19. Material and Methods: Fifty-five hemodialysis patients who met the COVID-19 probable case definition were included in the study. Clinical and laboratory features were recorded from patient files and electronic data retrospectively. Results: The study included 55 patients, the average age was 59.6 ± 13.2 years, 49% (n = 27) were female. Hypertension, Diabetes Mellitus, coronary heart diseases were the most common comorbid diseases. Comparing survivors and non-survivors, it was seen that the non-survivors were older (p=0.010). Logistic regression analyses revealed that age, SO2, lactate, WBC, neutrophil count, CRP, LDH, CK, ALT, AST, albumin, total protein, ferritin and D-Dimer were associated with the risk of mortality Discussion: Myalgia, cough, and shortness of breath are the most common symptoms of COVID-19 infection in HD patients, with no apparent fever. Age, SO2, WBC count, neutrophil count, CRP, LDH, CK, ALT, AST, albumin, total protein, ferritin and D-Dimer were found to be associated with mortality. Close monitoring of these parameters during the follow-up and treatment of patients may provide additional benefits in terms of survival.
ABSTRACT
The coronavirus disease (COVID-19) caused by a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly worldwide. Given that this contagious viral outbreak is still unfolding, it is urgent to understand the pathogenesis of SARS-CoV-2 infection and explore effective treatments to protect patients from developing a severe illness related to COVID-19. Recently, IFN-α has been considered a potential therapeutic strategy to treat COVID-19 disease, mainly because the innate immune system rapidly produces IFN-α as the first line of defense to combat viral infections. However, IFN-α can also play a role in immunoregulatory effects, causing pathogenic damage and uncontrolled inflammatory responses. There are 13 human IFN-α subtypes that bind to the same receptor and induce different interferon-stimulated gene (ISG) expression, regulating various antiviral and immunoregulatory effects. The varying degrees of inflammatory regulations may raise concerns about the possible side effects to enlarge the inflammatory responses, exacerbating the severity of infection. Thus, the analysis of various IFN-α subtype induction during SARS-CoV-2 infection is necessary in exploring the mechanism of COVID-19 pathogenesis. This review summarizes the current understanding of IFN-α in the pathogenesis of respiratory virus diseases and IFN-α based clinical intervention used in SARS-CoV-2 infection and other respiratory virus diseases. Besides, new ideas in selecting suitable IFN-α subtypes or combinations as drug candidates for viral infection treatment will also be discussed.Key Points⢠IFN-α plays an important role in anti-viral and immunoregulatory effects in COVID-19 patients caused by SARS-CoV-2.⢠The uncontrolled inflammation and disease severity correlated to the diversity of IFN-α subtype induction.⢠Selecting suitable IFN-α subtypes or combinations as drug candidates will be beneficial for the treatment of patients with COVID-19.