Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has spread to almost 100 countries, infected over 31 M patients and resulted in 961 K deaths worldwide as of 21st September 2020. The major clinical feature of severe COVID-19 requiring ventilation is acute respiratory distress syndrome (ARDS) with multi-functional failure as a result of a cytokine storm with increased serum levels of cytokines. The pathogenesis of the respiratory failure in COVID-19 is yet unknown, but diffuse alveolar damage with interstitial thickening leading to compromised gas exchange is a plausible mechanism. Hypoxia is seen in the COVID-19 patients, however, patients present with a distinct phenotype. Intracellular levels of nitric oxide (NO) play an important role in the vasodilation of small vessels. To elucidate the intracellular levels of NO inside of RBCs in COVID-19 patients compared with that of healthy control subjects. Methods We recruited 14 COVID-19 infected cases who had pulmonary involvement of their disease, 4 non-COVID-19 healthy controls (without pulmonary involvement and were not hypoxic) and 2 hypoxic non-COVID-19 patients subjects who presented at the Masih Daneshvari Hospital of Tehran, Iran between March–May 2020. Whole blood samples were harvested from patients and intracellular NO levels in 1 × 106 red blood cells (RBC) was measured by DAF staining using flow cytometry (FACS Calibour, BD, CA, USA). Results The Mean florescent of intensity for NO was significantly enhanced in COVID-19 patients compared with healthy control subjects (P ≤ 0.05). As a further control for whether hypoxia induced this higher intracellular NO, we evaluated the levels of NO inside RBC of hypoxic patients. No significant differences in NO levels were seen between the hypoxic and non-hypoxic control group. Conclusions This pilot study demonstrates increased levels of intracellular NO in RBCs from COVID-19 patients. Future multi-centre studies should examine whether this is seen in a larger number of COVID-19 patients and whether NO therapy may be of use in these severe COVID-19 patients.

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Background/aim New treatment regimens for COVID-19, which has threatened the world recently, continue to be investigated. Although some of the treatments are promising, it is thought to be early to state that there is definitive treatment. Experiences and treatment protocol studies from treatment centers are still important. The aim of this study is to evaluate factors affecting the treatment process of the first cases followed in our clinic. Materials and methods The consecutive hospitalized patients with COVID-19 pneumonia were analyzed in this retrospective and cross-sectional study. Data were recorded from the electronic and written files of patients. Results Eighty-three patients were evaluated. The median age was 50 ± 15 years. Forty-eight (57.8%) patients had one or more comorbidities. The most common comorbidity was hypertension. The most common symptom was cough in 58 patients (70%). The overall mortality was 15%, and 85% of the patients were discharged. The time between the onset of symptoms and hospitalization was statistically significantly longer in deceased patients (P = 0.039). Age, D-Dimer, troponin, CK, CK-MB, ferritin, procalcitonin, and neutrophil to lymphocyte ratio were statistically significantly higher in deceased patients than survivor patients. In subgroup analysis, in the patients receiving azithromycin plus hydroxychloroquine and other antibiotics plus hydroxychloroquine, the duration of hospitalization was shorter in the azithromycin group (P = 0.027). Conclusion Early treatment and early admission to the hospital can be crucial for the better treatment process. Combination therapy with azithromycin may be preferred in the first treatment choice because it can shorten the length of hospital stay.