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• W3115461121 abstract "We read with interest the article by Norsa et al1Norsa L. et al.Gastroenterology. 2020; 159: 1595-1597.e1Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar on intestinal ischemia in patients with coronavirus disease 2019 (COVID-19). They further highlight the coagulopathy known to cause vascular obstructions in patients with severe COVID-19, in whom microthrombi are typically found in the lung circulation; however, also myocardial infarction and ischemic stroke were reported, particularly in the late phase of the disease. The patients reported by Norsa et al had either small or large bowel ischemia, splenic infarct, or pulmonary thromboembolism, which were fatal in 4 of the 7 cases. The mechanisms involved in COVID-19 coagulopathy were analyzed by Grobler et al,2Grobler C. et al.Int J Mol Sci. 2020; 21: 5168Crossref Scopus (101) Google Scholar who stressed the importance of early recognition of risk factors for the subsequent development of abnormal clot formation. They concluded that patients need to be treated early in the disease, when high levels of von Willebrand factor and fibrinogen are already present and may interact with activated endothelial cells.2Grobler C. et al.Int J Mol Sci. 2020; 21: 5168Crossref Scopus (101) Google Scholar Nicolai et al3Nicolai L. et al.Circulation. 2020; 142: 1176-1189Crossref PubMed Scopus (335) Google Scholar observed that platelets are activated in severe cases of COVID-19, and may be critically involved in neutrophil extracellular trap (NET) formation, a central element of immunothrombosis.3Nicolai L. et al.Circulation. 2020; 142: 1176-1189Crossref PubMed Scopus (335) Google Scholar NETs have high procoagulant potential and could therefore serve as a link to explain altered blood coagulation and microvascular thrombosis in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, elevated markers of NETosis have been found to correlate with disease severity in COVID-19.3Nicolai L. et al.Circulation. 2020; 142: 1176-1189Crossref PubMed Scopus (335) Google Scholar It remains, however, difficult to understand why only a relatively small proportion of individuals with the coronavirus-defined SARS-CoV-2 will develop a hypercoagulable state. We were puzzled by similar mechanisms occurring in a different infection known to cause binding of platelets to von Willebrand factor and the vessel wall,4Byrne M.F. et al.Gastroenterol. 2003; 124: 1846-1854Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar activate endothelial cells5Innocenti M. et al.Infect Immun. 2002; 70: 4581-4590Crossref PubMed Scopus (90) Google Scholar (which will hence release von Willebrand factor), and cause aggregation of platelets to granulocytes,6Elizalde J.I. et al.J Clin Invest. 1997; 100: 996-1005Crossref PubMed Scopus (107) Google Scholar namely infection by pathogenic strains of Helicobacter pylori.4Byrne M.F. et al.Gastroenterol. 2003; 124: 1846-1854Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar, 5Innocenti M. et al.Infect Immun. 2002; 70: 4581-4590Crossref PubMed Scopus (90) Google Scholar, 6Elizalde J.I. et al.J Clin Invest. 1997; 100: 996-1005Crossref PubMed Scopus (107) Google Scholar This pathogen secretes a protein called neutrophilic activation factor that attracts neutrophils and causes their oxidative burst. In addition, neutrophilic activation factor is a Toll-like receptor 2 agonist able to induce the expression of interleukin-12 and interleukin-23 by neutrophils and monocytes, cause a remarkable increase in the number of interferon-gamma–producing T cells and decrease of interleukin-4–secreting cells, shifting the cytokine profile of antigen-activated human T cells from Th2 to the Th1 cytotoxic phenotype.7Amedei A. et al.J Clin Invest. 2006; 116: 1092-1101Crossref PubMed Scopus (256) Google Scholar This problem was also reported to be involved in the cytokine storm aggravating COVID-19. Due to antigen mimicry, H pylori was also shown to elicit autoantibodies against several human tissues and cells, including platelets; such autoantibodies can disappear after eradication of the infection.8Gasbarrini A. et al.Lancet. 1998; 352: 878Abstract Full Text Full Text PDF PubMed Scopus (388) Google Scholar The bacterium is also able to induce autoantibodies against the vessel wall, which can in turn facilitate platelet and granulocyte aggregation and worsen vascular obstruction. Other autoantibodies known to occur in H pylori infection are those against phospholipids, leading to an antiphospholipid syndrome that subsides after eradication. As COVID-19 can result in ominous outcomes, every avenue should be pursued in an attempt to reduce its burden. Given their common mechanisms, we believe that pathogenic strains of H pylori might contribute to the severity of COVID-19, at least in some cases. Poor Outcome of Intestinal Ischemic Manifestations of COVID-19GastroenterologyVol. 159Issue 4PreviewSince the end of February, Bergamo’s province in Northern Italy has become the second epicenter worldwide after Wuhan, China of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Papa Giovanni XXIII Hospital was selected as the tertiary referral center for COVID-19, with 500 dedicated beds and more than 1500 hospitalization so far. In the first 2 months’ experience, mounting evidence was collected that coagulopathy is one of the possible predictors of poor outcomes in COVID-19 patients. Full-Text PDF ReplyGastroenterologyVol. 160Issue 6PreviewReply. We are extremely grateful for the interest of Prof Ponzetto in our article and would like to take the opportunity to answer his very interesting comments. Full-Text PDF" @default.
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