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• W3117738634 abstract "We read with great interest the letter by Dr Enrique de-Madaria et al1de-Madaria E. et al.Gastroenterology. 2021; 160: 1871Abstract Full Text Full Text PDF PubMed Scopus (43) Google Scholar and Dr Aditya Ashok.2Ashok A. et al.Gastroenterology. 2021; 160: 1872Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar de-Madaria et al1de-Madaria E. et al.Gastroenterology. 2021; 160: 1871Abstract Full Text Full Text PDF PubMed Scopus (43) Google Scholar highlighted that the definition of pancreatic injury in our study lacked specificity, because many factors could lead to increased pancreatic enzyme (PE) levels, not just pancreatic injury. Ashok et al2Ashok A. et al.Gastroenterology. 2021; 160: 1872Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar indicated that it was not recommended to use the serum PE elevations to delineate the presence or degree of pancreatic injury.2Ashok A. et al.Gastroenterology. 2021; 160: 1872Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar They all mentioned that none of our cases met the revised Atlanta classification criteria for acute pancreatitis. Indeed, our study mainly proposed and emphasized the potential pancreatic injury caused by the novel coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]).3Wang F. et al.Gastroenterology. 2020; 159: 367-370Abstract Full Text Full Text PDF PubMed Scopus (305) Google Scholar Because it was reported for the first time, the underlying mechanism confused us until now. Currently, several studies have focused on pancreatic injury in patients with Coronavirus Disease 2019 (COVID-19). Naren et al4Kumaran N.K. et al.BMJ Case Rep. 2020; 13e237903Crossref PubMed Scopus (51) Google Scholar reported the occurrence of acute necrotizing pancreatitis in a patients with COVID-19 in the absence of any known risk factors. Severe acute pancreatitis was also found in 2 family clusters with SARS-CoV-2 infection.5Hadi A. et al.Pancreatology. 2020; 20: 665-667Crossref PubMed Scopus (153) Google Scholar Furthermore, SARS-CoV-2 RNA was detected in the pancreatic pseudocysts of a patients with COVID-19.6Schepis T. et al.Pancreatology. 2020; 20: 1011-1012Crossref PubMed Scopus (46) Google Scholar In the Giuseppe et al7Giuseppe B. et al.J Med Virol. 2021; 93: 74-75Crossref PubMed Scopus (30) Google Scholar study of 70 COVID-19 cases, 6 (8.5%) demonstrated pancreatic abnormalities with significant evaluations of serum PE activity. Mechanistically, it had been found that angiotensin-converting enzyme 2 (ACE2), receptor of SARS-CoV-2, was more highly expressed in the pancreas than the lungs.8Liu F. et al.Clin Gastroenterol Hepatol. 2020; 18: 2128-2130Abstract Full Text Full Text PDF PubMed Scopus (388) Google Scholar Studies further demonstrated that ACE2 and transmembrane serine protease 2 were prominently expressed in pancreatic ductal epithelium and microvasculature.9Kusmartseva I. et al.Cell Metab. 2020; 32: 1041-1051Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar,10Coate K.C. et al.Cell Metab. 2020; 32: 1028-1040Abstract Full Text Full Text PDF PubMed Scopus (120) Google Scholar Moreover, the autopsies of 3 COVID-19 cases showed degeneration of islet cells.11Yao X. et al.Zhonghua Bing Li Xue Za Zhi. 2020; 49: 411-417PubMed Google Scholar In addition, ACE2 and transmembrane serine protease 2 were found to be highly expressed in gastrointestinal epithelial cells, and the virus could be detected in stools. Thus, SARS-CoV-2 might infect the pancreas by spreading from duodenal epithelium to pancreatic ductal epithelium. Most importantly, during the outbreak of another coronavirus (SARS-CoV) in 2003, its antigen and RNA were detected in pancreatic cells.12Ding Y. et al.J Pathol. 2004; 203: 622-630Crossref PubMed Scopus (812) Google Scholar Collectively, these results indicated the pancreas as a potential target of SARS-CoV-2. In addition, viral sepsis was hypothesized in the COVID-19 progression.13Li H. et al.Lancet. 2020; 395: 1517-1520Abstract Full Text Full Text PDF PubMed Scopus (793) Google Scholar Severe SARS-CoV-2 infection could cause alveolar macrophages or epithelial cells to produce various proinflammatory cytokines and chemokines and led to uncontrolled inflammation cascade and cytokine storm. Meanwhile, severe endotheliitis directly induced by SARS-CoV-2 could further cause diffuse microischemic disease in the pancreas.14de-Madaria E. et al.Nat Rev Gastroenterol Hepatol. 2021; 18: 3-4Crossref PubMed Scopus (85) Google Scholar Thus, the disseminated SARS-CoV-2 could also directly attack multiple other organs, including the pancreas. Eventually, viral sepsis, ischemic damage, and multiple organ failure occurred. Furthermore, up to 16% of patients with severe COVID-19 had elevated PE levels and 7% showed significant changes in the pancreas on computed tomography, but fewer than 2% in patients with non-severe COVID-19.8Liu F. et al.Clin Gastroenterol Hepatol. 2020; 18: 2128-2130Abstract Full Text Full Text PDF PubMed Scopus (388) Google Scholar Taken together, we must pay attention to potential pancreatic injuries during the management of COVID-19. Increased Amylase and Lipase in Patients With COVID-19 Pneumonia: Don't Blame the Pancreas Just Yet!GastroenterologyVol. 160Issue 5PreviewWe have read with interest the article entitled Pancreatic injury patterns in patients with COVID-19 pneumonia by Dr Wang and colleagues.1 This was a retrospective study involving 52 patients with Coronavirus Disease 2019 (COVID-19) admitted to the Zhongnan Hospital of Wuhan University, China. It aimed to describe the incidence of pancreatic injury in patients with COVID-19, defined as any abnormality in amylase or lipase. Based on this, 17% of patients with COVID-19 met criteria for pancreatic injury. Full-Text PDF" @default.
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