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Curr Protein Pept Sci ; 23(5): 310-320, 2022.
Article in English | MEDLINE | ID: covidwho-1892473


The pathogenesis of SARS-CoV-2 infection is related to the direct cytopathic effect and associated hyper-inflammation due to exaggerated immune response. Different experimental and clinical studies revealed that many biomarkers could be used to determine the Covid-19 severity, such as Ddimer, procalcitonin, C-reaction protein (CRP), IL-6, and ferritin. Calprotectin (CP) is associated with intestinal inflammation, intestinal injury, and different respiratory diseases such as cystic fibrosis. Thus, CP might be a possible biomarker linking intestinal injury and acute lung injury (ALI) in Covid-19. Therefore, this study aimed to find a potential role of CP regarding GITI and ALI in Covid-19. CP is a complex protein consisting of S100A8 and S100A9, belonging to the Ca+2-binding proteins S100 family abundant in the cytosol of neutrophils and expressed on the monocyte membranes, macrophages, and intestinal epithelial cells. CP is a proinflammatory protein that acts through activation of the receptor for the advanced glycation end product (RAGE) and toll-like receptor 4 (TLR4). CP is a biomarker of neutrophil activation and is released following the turnover of neutrophils. CP could be controversial; it increases airway inflammation or protects lung and airway epithelium from an exaggerated immune response. Therefore, a high level of CP in different respiratory disorders might be protective and compensate against abnormal immune responses. CP level is high in Covid-19 and correlated with Covid-19 severity and oxygen demand due to activation of proinflammatory cytokines and inflammatory signaling pathways. Therefore, CP level is elevated in both ALI and intestinal inflammation so that it could be a potential biomarker that links the respiratory and intestinal injury in Covid-19.

Acute Lung Injury , COVID-19 , Gastrointestinal Diseases , Leukocyte L1 Antigen Complex , Acute Lung Injury/virology , Biomarkers , COVID-19/complications , Cytokines/metabolism , Ferritins , Gastrointestinal Diseases/virology , Glycation End Products, Advanced/metabolism , Humans , Inflammation/metabolism , Interleukin-6/metabolism , Leukocyte L1 Antigen Complex/metabolism , Oxygen/metabolism , Procalcitonin/metabolism , SARS-CoV-2 , Toll-Like Receptor 4/metabolism
Inflammation ; 45(4): 1651-1667, 2022 Aug.
Article in English | MEDLINE | ID: covidwho-1709501


SARS-CoV-2 by the direct cytopathic effect or indirectly through the propagation of pro-inflammatory cytokines could cause endothelial dysfunction (ED) and oxidative stress (OS). It has been reported that OS is triggered by various types of viral infections, including SARS-CoV-2. Into the bargain, allopurinol is regarded as a potent antioxidant that acts through inhibition of xanthine oxidase (XO), which is an essential enzyme of purine metabolism. Herein, the present study aimed to find the potential protective effects of allopurinol on the biomarkers of OS and ED in patients with severe Covid-19. This single-center cohort study recruited 39 patients with mild-moderate Covid-19 compared with 41 patients with severe Covid-19. Nineteen patients with severe Covid-19 were on the allopurinol treatment because of underlying chronic gout 3 years ago compared with 22 Covid-19 patients not on this treatment. The recruited patients were allocated into three groups: group I, mild-moderate Covid-19 on the standard therapy (n = 39); group II, severe Covid-19 patients on the standard therapy only (n = 22); and group III, severe Covid-19 patients on the standard therapy plus allopurinol (n = 19). The duration of the study was 3 weeks from the time of hospitalization till the time of recovery. In addition, inflammatory biomarkers (D-dimer, LDH, ferritin, CRP, procalcitonin), neutrophil-lymphocyte ratio (NLR), endothelin-1 (ET-1), uric acid and oxidative stress index (OSI), CT scan score, and clinical score were evaluated at the time of admission and discharge regarding the effect of allopurinol treatment adds to the standard treatment of Covid-19. Allopurinol plus standard treatment reduced LDH, ferritin, CRP, procalcitonin, and ET-1 serum level significantly (P < 0.05) compared with Covid-19 patients on standard treatment. Besides, neutrophil (%), lymphocyte (%), and neutrophil-lymphocyte ratio (NLR) were reduced in patients with severe Covid-19 on standard treatment plus allopurinol compared with Covid-19 patients on standard treatment alone (P < 0.01). OSI was higher in patients with severe Covid-19 than mild-moderate Covid-19 patients (P = 0.00001) at admission. At the time of discharge, the oxidative status of Covid-19 patients was significantly improved compared with that at admission (P = 0.01). In conclusion, Covid-19 severity is linked with high OS and inflammatory reaction with ED development. High uric acid in patients with severe Covid-19 is correlated with high OS and inflammatory biomarkers. Allopurinol with standard treatment in patients with severe Covid-19 reduced oxidative and inflammatory disorders with significant amelioration of ED and clinical outcomes.

Allopurinol , COVID-19 , Endothelium, Vascular , Oxidative Stress , Allopurinol/therapeutic use , Biomarkers , COVID-19/drug therapy , Cohort Studies , Endothelium, Vascular/physiopathology , Ferritins , Humans , Procalcitonin , Prospective Studies , SARS-CoV-2 , Uric Acid
J Microsc Ultrastruct ; 8(4): 141-145, 2020.
Article in English | MEDLINE | ID: covidwho-1000436


COVID-19 pathology is mainly associated to a pulmonary disease which sometimes might result in an uncontrollable storm related to inflammatory diseases which could be fatal. It is well known that phosphodiesterase enzyme type 5 inhibitors (PDE5Is), such as sildenafil, have been successfully developed for the treatment of pulmonary arterial hypertension; interestingly, more recently, it was shown that PDE5Is might be also anti-inflammatory. Therefore, it would be of interest to question about the use of PDE5Is to overcome the COVID-19 storm, as much as PDE5 is mainly present in the lung tissues and vessels.