Pancreatic damage in COVID‐19: Why? How?

Diabetes and COVID19: a bidirectional relationship

European Journal of Clinical Nutrition ◽

10.1038/s41430-021-00961-y ◽

2021 ◽

Author(s):

Ranjit Unnikrishnan ◽

Anoop Misra

Keyword(s):

Clinical Care ◽

Severe Disease ◽

Respiratory Involvement ◽

Pancreatic Damage ◽

Increased Risk ◽

Bidirectional Relationship ◽

Rapid Spread ◽

Relationship Of ◽

The Relationship ◽

New Onset

AbstractThe advent and rapid spread of the coronavirus disease-2019 (COVID19) pandemic across the world has focused attention on the relationship of commonly occurring comorbidities such as diabetes on the course and outcomes of this infection. While diabetes does not seem to be associated with an increased risk of COVID19 infection per se, it has been clearly demonstrated that the presence of hyperglycemia of any degree predisposes to worse outcomes, such as more severe respiratory involvement, ICU admissions, need for mechanical ventilation and mortality. Further, COVID19 infection has been associated with the development of new-onset hyperglycemia and diabetes, and worsening of glycemic control in pre-existing diabetes, due to direct pancreatic damage by the virus, body’s stress response to infection (including cytokine storm) and use of diabetogenic drugs such as corticosteroids in the treatment of severe COVID19. In addition, public health measures taken to flatten the pandemic curve (such as lockdowns) can also adversely impact persons with diabetes by limiting their access to clinical care, healthy diet, and opportunities to exercise. Most antidiabetic medications can continue to be used in patients with mild COVID19 but switching over to insulin is preferred in severe disease.

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Diabetes and COVID19: a bidirectional relationship

Nutrition and Diabetes ◽

10.1038/s41387-021-00163-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Ranjit Unnikrishnan ◽

Anoop Misra

Keyword(s):

Clinical Care ◽

Severe Disease ◽

Respiratory Involvement ◽

Pancreatic Damage ◽

Increased Risk ◽

Bidirectional Relationship ◽

Rapid Spread ◽

Relationship Of ◽

The Relationship ◽

New Onset

AbstractThe advent and rapid spread of the coronavirus disease-2019 (COVID19) pandemic across the world has focused attention on the relationship of commonly occurring comorbidities such as diabetes on the course and outcomes of this infection. While diabetes does not seem to be associated with an increased risk of COVID19 infection per se, it has been clearly demonstrated that the presence of hyperglycemia of any degree predisposes to worse outcomes, such as more severe respiratory involvement, ICU admissions, need for mechanical ventilation and mortality. Further, COVID19 infection has been associated with the development of new-onset hyperglycemia and diabetes, and worsening of glycemic control in pre-existing diabetes, due to direct pancreatic damage by the virus, body’s stress response to infection (including cytokine storm) and use of diabetogenic drugs such as corticosteroids in the treatment of severe COVID19. In addition, public health measures taken to flatten the pandemic curve (such as lockdowns) can also adversely impact persons with diabetes by limiting their access to clinical care, healthy diet, and opportunities to exercise. Most antidiabetic medications can continue to be used in patients with mild COVID19 but switching over to insulin is preferred in severe disease.

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Pancreatic Duct Stents in the Prophylaxis of Pancreatic Damage after Endoscopic Retrograde Cholangiopancreatography: A Systematic Analysis of Benefits and Associated Risks

Digestion ◽

10.1159/000106774 ◽

2007 ◽

Vol 75 (2-3) ◽

pp. 156-163 ◽

Cited By ~ 54

Author(s):

Angelo Andriulli ◽

Rosario Forlano ◽

Grazia Napolitano ◽

Pasquale Conoscitore ◽

Nazario Caruso ◽

...

Keyword(s):

Pancreatic Duct ◽

Endoscopic Retrograde Cholangiopancreatography ◽

Endoscopic Retrograde ◽

Systematic Analysis ◽

Pancreatic Damage

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Hyperbilirubinemia Reduces the Streptozotocin-Induced Pancreatic Damage through Attenuating the Oxidative Stress in the Gunn Rat

The Tohoku Journal of Experimental Medicine ◽

10.1620/tjem.222.265 ◽

2010 ◽

Vol 222 (4) ◽

pp. 265-273 ◽

Cited By ~ 19

Author(s):

Yan Yan Fu ◽

Kyung Ja Kang ◽

Jung Myung Ahn ◽

Hae-Ryoung Kim ◽

Ki Young Na ◽

...

Keyword(s):

Oxidative Stress ◽

Gunn Rat ◽

Pancreatic Damage

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Decreased calmodulin recruitment triggers PMCA4 dysfunction and pancreatic injury in cystic fibrosis

10.1101/2020.09.10.290940 ◽

2020 ◽

Author(s):

Tamara Madácsy ◽

Árpad Varga ◽

Noémi Papp ◽

Barnabás Deák ◽

Bálint Tél ◽

...

Keyword(s):

Cystic Fibrosis ◽

Intracellular Signaling ◽

Pancreatic Injury ◽

Exocrine Pancreatic Function ◽

Model Systems ◽

Multiple Model ◽

Calmodulin Binding ◽

Ductal Cells ◽

Pancreatic Damage ◽

Intracellular Ca

ABSTRACTExocrine pancreatic damage is a common complication of cystic fibrosis (CF), which can significantly debilitate the quality of life and life expectancy of CF patients. The cystic fibrosis transmembrane conductance regulator (CFTR) has a major role in pancreatic ductal ion secretion, however, it presumably has an influence on intracellular signaling as well. Here we describe in multiple model systems, including iPSC-derived human pancreatic organoids from CF patients, that the activity of PMCA4 is impaired by the decreased expression of CFTR in ductal cells. The regulation of PMCA4, which colocalizes and physically interacts with CFTR on the apical membrane of the ductal cells, is dependent on the calmodulin binding ability of CFTR. Moreover, CFTR seems to be involved in the process of the apical recruitment of calmodulin, which enhances its role in calcium signaling and homeostasis. Sustained intracellular Ca2+ elevation in CFTR KO cells undermined the mitochondrial function and increased apoptosis. Based on these, the prevention of sustained intracellular Ca2+ overload may improve the exocrine pancreatic function and may have a potential therapeutic aspect in CF.

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Normal levels of serum pancreatic enzymes in patients with progressive familial intrahepatic cholestasis type 2.

Acta Biochimica Polonica ◽

10.18388/abp.2010_2446 ◽

2010 ◽

Vol 57 (4) ◽

Author(s):

Jaroslaw Walkowiak ◽

Irena Jankowska ◽

Aleksandra Lisowska ◽

Maciej Biczysko ◽

Aldona Wierzbicka ◽

...

Keyword(s):

Intrahepatic Cholestasis ◽

Elevated Serum ◽

Normal Serum ◽

Pancreatic Enzymes ◽

Serum Lipase ◽

Progressive Familial Intrahepatic Cholestasis ◽

Elastase 1 ◽

Pancreatic Damage ◽

High Prevalence

High prevalence of elevated serum pancreatic enzymes in children with cholestasis with normal fecal elastase-1 concentrations has been documented. However, this state is related predominantly to biliary atresia. Therefore, we aimed to assess pancreatic damage by measuring serum pancreatic enzymes in patients with progressive familial intrahepatic cholestasis type 2 (PFIC type 2). Twenty PFIC type 2 patients with normal serum bilirubin and bile acid concentrations were included in the study. Thirty pancreatic insufficient cystic fibrosis (PI-CF) patients, thirty patients with acute pancreatitis (AP) and thirty healthy subjects (HS) served for the purpose of comparison. In all subjects, serum lipase and elastase-1 levels were measured. In all but one PFIC type 2 patients and all HS normal lipase activities were found. Serum elastase-1 concentrations were normal in all PFIC type 2 patients and HS. The enzyme levels were very similar in both groups studied. Lipase activities in PFIC type 2 patients were significantly higher than in PI-CF patients (p < 0.00001) and lower than in patients with AP (p < 0.00001). Serum elastase-1 levels in PFIC type 2 patients were significantly lower than in patients with AP (p < 0.00001) and not different from those in PI-CF patients. In conclusion. serum pancreatic enzymes in patients with PFIC type 2 are normal. No pancreatic damage in these patients could be detected.

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α-Methylspermidine protects against carbon tetrachloride-induced hepatic and pancreatic damage

Amino Acids ◽

10.1007/s00726-009-0418-5 ◽

2009 ◽

Vol 38 (2) ◽

pp. 575-581 ◽

Cited By ~ 9

Author(s):

Mervi T. Hyvönen ◽

Riitta Sinervirta ◽

Nikolay Grigorenko ◽

Alex R. Khomutov ◽

Jouko Vepsäläinen ◽

...

Keyword(s):

Carbon Tetrachloride ◽

Pancreatic Damage

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Pancreatitis following spinal cord injury

Journal of Neurosurgery ◽

10.3171/jns.1977.47.6.0917 ◽

1977 ◽

Vol 47 (6) ◽

pp. 917-922 ◽

Cited By ~ 17

Author(s):

Michael E. Carey ◽

Francis C. Nance ◽

Homer D. Kirgis ◽

Harold F. Young ◽

Lloyd C. Megison ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Parasympathetic Nervous System ◽

Sphincter Of Oddi ◽

Systemic Circulation ◽

Content Type ◽

Pancreatic Damage ◽

Cord Injury ◽

Tract Infections ◽

Stimulation Of

✓ Six cases of pancreatitis following spinal cord injury are presented. No single, etiologically accepted mechanism already postulated to cause pancreatitis can account for all the cases reported. The authors hypothesize that spinal cord disruption may produce pancreatitis by sympathetic-parasympathetic nervous system imbalance resulting in over-stimulation of the sphincter of Oddi. This may lead to stasis of secretions with absorption of amylase into the systemic circulation, and structural pancreatic damage. Pancreatitis in those with cord injuries is easily overlooked because abdominal pain is usually absent and fever is usually attributed to more frequently occurring pulmonary or urinary tract infections. Recognition of this complication is important in order to decrease the morbidity and mortality that follows spinal cord damage.

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