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This month’s round up of clinical studies is a fitting end to 2021 – they provide a close look at the intersection between pancreatic pathology and SARS CoV-2 infection. The first study, out of the UK, speculated that SARS CoV-2 virus may be associated with development of idiopathic pancreatitis.1 They followed 1,476 patients with acute pancreatitis for 12 months (118 of whom were positive for SARS CoV-2, and 1,358 of whom were negative for the virus). The patients underwent magnetic resonance cholangiopancreatography, endoscopic ultrasound, or biochemical investigations to exclude other causes of pancreatitis. Remarkably, as the paper states, “Patients who were SARS-CoV-2 positive were more likely to have idiopathic acute pancreatitis (AP, 34.7% vs 13.9%, P < .001) with over five times increased risk after adjusting for age, smoking status, body mass index and ethnicity (odds ration [OR] 5.34, P < .001).”
Secondarily, the authors aimed to determine if SARS CoV-2 infection would increase risk for diabetes mellitus (DM) and pancreatic exocrine insufficiency (PEI). Notably, SARS-CoV-2 did not increase the risk of DM (2.3% vs 2.5%, OR 0.61, P = .541) or PEI (OR 1.11, P = .828) (P > .05). The relationship between pancreatitis and SARS CoV-2 infection is indeed an important one – the authors point out that autopsy studies have demonstrated the presence of virus in pancreatic tissue. There is clear mechanistic reason for trophism as ACE 2 receptors are found on exocrine and endocrine cells of the pancreas.
Another study, out of Hubei Province, China, looked at the association of elevated serum amylase (ESA) with mortality and other adverse outcomes in hospitalized patients with COVID-19.2 Their retrospective study included 1,515 inpatients with COVID-19. Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 times the upper limit of normal (ULN). Somewhat not unexpectedly, hyperamylasemia was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes, such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79). The authors conclude that, “Since early intervention might change the outcome, serum amylase should be monitored dynamically during hospitalization.” It appears to be unclear what would be practice changing, assuming patients would already be receiving appropriate resuscitation.
More interesting, perhaps, is the question of whether or not the pancreas is merely a bystander casualty or an active protagonist in the role of sepsis and disease severity in highly morbid diseases, such as COVID-19.
References
1. Nayar M et al. SARS-CoV-2 infection is associated with an increased risk of idiopathic acute pancreatitis but not pancreatic exocrine insufficiency or diabetes: long-term results of the COVIDPAN study. Gut 2021(Nov 11).
2. Li G et al. Serum amylase elevation is associated with adverse clinical outcomes in patients with coronavirus disease 2019. Aging (Albany NY) 2021;13(20):23442–58 (Oct 2021).
This month’s round up of clinical studies is a fitting end to 2021 – they provide a close look at the intersection between pancreatic pathology and SARS CoV-2 infection. The first study, out of the UK, speculated that SARS CoV-2 virus may be associated with development of idiopathic pancreatitis.1 They followed 1,476 patients with acute pancreatitis for 12 months (118 of whom were positive for SARS CoV-2, and 1,358 of whom were negative for the virus). The patients underwent magnetic resonance cholangiopancreatography, endoscopic ultrasound, or biochemical investigations to exclude other causes of pancreatitis. Remarkably, as the paper states, “Patients who were SARS-CoV-2 positive were more likely to have idiopathic acute pancreatitis (AP, 34.7% vs 13.9%, P < .001) with over five times increased risk after adjusting for age, smoking status, body mass index and ethnicity (odds ration [OR] 5.34, P < .001).”
Secondarily, the authors aimed to determine if SARS CoV-2 infection would increase risk for diabetes mellitus (DM) and pancreatic exocrine insufficiency (PEI). Notably, SARS-CoV-2 did not increase the risk of DM (2.3% vs 2.5%, OR 0.61, P = .541) or PEI (OR 1.11, P = .828) (P > .05). The relationship between pancreatitis and SARS CoV-2 infection is indeed an important one – the authors point out that autopsy studies have demonstrated the presence of virus in pancreatic tissue. There is clear mechanistic reason for trophism as ACE 2 receptors are found on exocrine and endocrine cells of the pancreas.
Another study, out of Hubei Province, China, looked at the association of elevated serum amylase (ESA) with mortality and other adverse outcomes in hospitalized patients with COVID-19.2 Their retrospective study included 1,515 inpatients with COVID-19. Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 times the upper limit of normal (ULN). Somewhat not unexpectedly, hyperamylasemia was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes, such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79). The authors conclude that, “Since early intervention might change the outcome, serum amylase should be monitored dynamically during hospitalization.” It appears to be unclear what would be practice changing, assuming patients would already be receiving appropriate resuscitation.
More interesting, perhaps, is the question of whether or not the pancreas is merely a bystander casualty or an active protagonist in the role of sepsis and disease severity in highly morbid diseases, such as COVID-19.
References
1. Nayar M et al. SARS-CoV-2 infection is associated with an increased risk of idiopathic acute pancreatitis but not pancreatic exocrine insufficiency or diabetes: long-term results of the COVIDPAN study. Gut 2021(Nov 11).
2. Li G et al. Serum amylase elevation is associated with adverse clinical outcomes in patients with coronavirus disease 2019. Aging (Albany NY) 2021;13(20):23442–58 (Oct 2021).
This month’s round up of clinical studies is a fitting end to 2021 – they provide a close look at the intersection between pancreatic pathology and SARS CoV-2 infection. The first study, out of the UK, speculated that SARS CoV-2 virus may be associated with development of idiopathic pancreatitis.1 They followed 1,476 patients with acute pancreatitis for 12 months (118 of whom were positive for SARS CoV-2, and 1,358 of whom were negative for the virus). The patients underwent magnetic resonance cholangiopancreatography, endoscopic ultrasound, or biochemical investigations to exclude other causes of pancreatitis. Remarkably, as the paper states, “Patients who were SARS-CoV-2 positive were more likely to have idiopathic acute pancreatitis (AP, 34.7% vs 13.9%, P < .001) with over five times increased risk after adjusting for age, smoking status, body mass index and ethnicity (odds ration [OR] 5.34, P < .001).”
Secondarily, the authors aimed to determine if SARS CoV-2 infection would increase risk for diabetes mellitus (DM) and pancreatic exocrine insufficiency (PEI). Notably, SARS-CoV-2 did not increase the risk of DM (2.3% vs 2.5%, OR 0.61, P = .541) or PEI (OR 1.11, P = .828) (P > .05). The relationship between pancreatitis and SARS CoV-2 infection is indeed an important one – the authors point out that autopsy studies have demonstrated the presence of virus in pancreatic tissue. There is clear mechanistic reason for trophism as ACE 2 receptors are found on exocrine and endocrine cells of the pancreas.
Another study, out of Hubei Province, China, looked at the association of elevated serum amylase (ESA) with mortality and other adverse outcomes in hospitalized patients with COVID-19.2 Their retrospective study included 1,515 inpatients with COVID-19. Overall, 196 patients had ESA, of which 9.7% had an ESA of >3 times the upper limit of normal (ULN). Somewhat not unexpectedly, hyperamylasemia was independently associated with mortality (1-3-times ULN [1-3 ULN]: hazard ratio [HR] 1.63; P = .034; >3-fold ULN [>3 ULN]: HR 8.90; P < .001) and adverse outcomes, such as sepsis (1-3 ULN: odds ratio [OR] 1.15; >3 ULN: OR 1.87), disseminated intravascular coagulation (1-3 ULN: OR 1.13; >3 ULN: OR 1.65), cardiac injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.71), acute respiratory distress syndrome (1-3 ULN: OR 1.21; >3 ULN: OR 1.62), and acute kidney injury (1-3 ULN: OR 1.24; >3 ULN: OR 1.79). The authors conclude that, “Since early intervention might change the outcome, serum amylase should be monitored dynamically during hospitalization.” It appears to be unclear what would be practice changing, assuming patients would already be receiving appropriate resuscitation.
More interesting, perhaps, is the question of whether or not the pancreas is merely a bystander casualty or an active protagonist in the role of sepsis and disease severity in highly morbid diseases, such as COVID-19.
References
1. Nayar M et al. SARS-CoV-2 infection is associated with an increased risk of idiopathic acute pancreatitis but not pancreatic exocrine insufficiency or diabetes: long-term results of the COVIDPAN study. Gut 2021(Nov 11).
2. Li G et al. Serum amylase elevation is associated with adverse clinical outcomes in patients with coronavirus disease 2019. Aging (Albany NY) 2021;13(20):23442–58 (Oct 2021).