scholarly journals Pancreatic Injury and Coronavirus Disease-2019

2021 ◽  
Vol 9 (F) ◽  
pp. 405-409
Author(s):  
Masrul Lubis ◽  
Gontar Alamsyah Siregar ◽  
Lukman Hakim Zain ◽  
Ilhamd Ilhamd ◽  
Taufik Sungkar ◽  
...  

BACKGROUND: Coronavirus disease 2019 can induce dysfunction in a couple of organs, including kidney, heart, liver, gut, and pancreas. Pancreatic injury is an inflammatory situation of the exocrine pancreas, precipitated mostly by gallstones and alcohol intake. We found the fact that lack of research about the influence of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in pancreatic injury. METHODS: A literature searching was conducted through the PubMed, Science Direct, Medline, and Google Scholar searching engines using the following keywords: (“severe acute respiratory tract syndrome-coronavirus 2019” OR “COVID-19” OR “coronavirus 2019” OR “SARS-CoV-2”) AND (“pancreas” OR “pancreatitis” OR “hyperamylasemia” OR “pancreatic injury” OR “pancreatic damage” OR “pancreatic disturbance”). All articles and abstracts in English from literature review, case report, original article, systematic review, and meta-analysis were involved. RESULTS: A total of 17 literatures were gathered. Through the studies, we found that several pathways may damage pancreas in coronavirus disease 2019 (COVID-19) patients, either due to direct virus-mediated damage of the exocrine pancreas via the angiotensin converting enzyme 2 receptors, the severe COVID-19 contamination which can lead to systemic inflammation and pancreatic injury, or the virus-mediated injury to the islet cells. The prevalence of pancreatitis in patients with COVID-19 was low. Elevated pancreatic enzyme level was one of the sign of pancreatic involvement. CONCLUSION: Pancreatic injury may occur in patients with severe COVID-19 due to several pathways. Assessment of pancreatitis severity may aid in managing pancreatitis in this particular population.

2016 ◽  
Vol 45 (2) ◽  
pp. 321-334 ◽  
Author(s):  
Jianying Wang ◽  
Wenhu Huang ◽  
Stephane Thibault ◽  
Thomas P. Brown ◽  
Walter Bobrowski ◽  
...  

Detecting and monitoring exocrine pancreatic damage during nonclinical and clinical testing is challenging because classical biomarkers amylase and lipase have limited sensitivity and specificity. Novel biomarkers for drug-induced pancreatic injury are needed to improve safety assessment and reduce late-stage attrition rates. In a series of studies, miR-216a and miR-217 were evaluated as potential biomarkers of acute exocrine pancreatic toxicity in rats. Our results revealed that miR-216a and miR-217 were almost exclusively expressed in rat pancreas and that circulating miR-216a and miR-217 were significantly increased in rats following administration of established exocrine pancreatic toxicants caerulein (CL) and 1-cyano-2-hydroxy-3-butene (CHB) as well as in rats administered a proprietary molecule known to primarily affect the exocrine pancreas. Conversely, neither microRNA was increased in rats administered a proprietary molecule known to cause a lesion at the pancreatic endocrine–exocrine interface (EEI) or in rats administered an established renal toxicant. Compared with amylase and lipase, increases in miR-216a and miR-217 were of greater magnitude, persisted longer, and/or correlated better with microscopic findings within the exocrine pancreas. Our findings demonstrate that in rats, miR-216a and miR-217 are sensitive and specific biomarkers of acute exocrine pancreatic toxicity that may add value to the measurement of classical pancreatic biomarkers.


2010 ◽  
Vol 21 (11) ◽  
pp. 1843-1850 ◽  
Author(s):  
Qiqi Mao ◽  
Yiwei Lin ◽  
Xiangyi Zheng ◽  
Jie Qin ◽  
Kai Yang ◽  
...  

2000 ◽  
Vol 51 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Angelo Andriulli ◽  
Gioacchino Leandro ◽  
Grazia Niro ◽  
Alessandra Mangia ◽  
Virginia Festa ◽  
...  

Circulation ◽  
2016 ◽  
Vol 133 (suppl_1) ◽  
Author(s):  
Elizabeth Mostofsky ◽  
Harpreet S Chahal ◽  
Kenneth J Mukamal ◽  
Eric B Rimm ◽  
Murray A Mittleman

Introduction: Although considerable research describes the cardiovascular effects of habitual moderate and heavy alcohol consumption, the acute risks following alcohol intake have not been well characterized. Based on its physiological effects, alcohol may have markedly different effects on acute and long-term risk. We assessed the hypothesis that moderate alcohol consumption is associated with an immediately higher risk of cardiovascular events that becomes protective after 24 hours, whereas heavy alcohol drinking is associated with higher cardiovascular risk both immediately and in the following days. Methods: We searched CINAHL, Embase, PubMed and PsycINFO from inception to March 12 2015, supplemented with manual screening for observational studies assessing the association between alcohol intake and cardiovascular events in the following hours and days. We calculated pooled relative risks (RRs) and 95% confidence intervals (CIs) for the association between alcohol intake and myocardial infarction (MI), ischemic stroke (IS) and hemorrhagic stroke (HS) using DerSimonian and Laird random-effects models to model any alcohol intake or dose-response relationships of alcohol intake and cardiovascular events. Results: Among 1056 citations and 37 full-text articles reviewed, 23 studies (29457 participants) were included. Moderate alcohol consumption was associated with an acutely higher cardiovascular risk that was attenuated after 24 hours and even protective for MI and HS (≈2-4 drinks: RR=30% lower risk), and protective against IS within one week (≈6 drinks: RR=19% lower risk). In contrast, heavy alcohol drinking was associated with higher cardiovascular risk in the following day (≈6-9 drinks: RR=1.3-2.3) and week (≈19-30 drinks: RR=2.25-6.2). Conclusions: In conclusion, there appears to be a consistent finding of an acutely higher cardiovascular risk following any alcohol consumption but by 24 hours, only heavy alcohol intake conferred continued risk.


2017 ◽  
Vol 177 (3) ◽  
pp. 696-707 ◽  
Author(s):  
H. Yen ◽  
A. Dhana ◽  
J.‐P. Okhovat ◽  
A. Qureshi ◽  
N. Keum ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Peili Ding ◽  
Bin Song ◽  
Xuelin Liu ◽  
Xing Fang ◽  
Hongliu Cai ◽  
...  

Background: Pancreatic enzyme elevation has been reported in patients with COVID-19 during the pandemic. However, with the shortage of medical resources and information, several challenges are faced in the examination and treatment of this condition in COVID-19 patients. There is little information on whether such condition is caused by pancreatic injury, and if this is a warning sign of life threatening complications like multiple organ failure in patients. The objective of this study is to explore the relationship between elevated pancreatic enzymes and the underlying risk factors during the management of COVID-19 patients.Method: A total of 55 COVID-19 patients admitted to the intensive care unit (ICU) of Wuhan Jinyintan hospital from January 1 to March 30, 2020 were enrolled in this study. All participants underwent transabdominal ultrasound imaging to assess their pancreas.Results: Out of the 55 patients, three patients had pancreatitis, 29 (52.7%) with elevated pancreatic enzymes, and 23 (41.8%) without. The most common symptoms of patients with COVID-19 were fever and cough. There was no statistical difference in most baseline characteristics except myalgia on admission. Compared with those having normal enzyme levels, patients with elevated pancreatic enzymes had higher rates of mortality (79.3 vs. 52.2%; P = 0.038), and lower rates of discharge (20.7 vs. 47.8%; P = 0.038). Patients with elevated enzymes had higher incidence of mechanical ventilation (P = 0.004) and kidney injury (P = 0.042) than patients without elevated pancreatic enzymes. The results of multivariable logistic analysis showed that the odds ratio were 10.202 (P = 0.002) for mechanical ventilation and 7.673 (P = 0.014) for kidney injury with the elevated enzymes vs. the normal conditions.Conclusions: The findings show that the incidences of pancreatic enzymes elevation are not low in critical COVID-19 patients and only a few of them progressed to acute pancreatitis (AP). Increased pancreatic enzymes levels is associated with poor prognosis in COVID-19 patients. In addition, the kidney injury and oxygenation degradation are associated with the pancreatic enzymes elevation in COVID-19 patients.


2020 ◽  
Author(s):  
Tamara Madácsy ◽  
Árpad Varga ◽  
Noémi Papp ◽  
Barnabás Deák ◽  
Bálint Tél ◽  
...  

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.


2020 ◽  
Author(s):  
Franc Casanova Ferrer ◽  
María Pascual ◽  
Marta R. Hidalgo ◽  
Pablo Malmierca-Merlo ◽  
Consuelo Guerri ◽  
...  

AbstractThe abuse of alcohol, one of the most popular psychoactive substances, can cause several pathological and psychological consequences, including alcohol use disorder (AUD). An impaired ability to stop or control alcohol intake despite adverse health or social consequences characterize AUD. While AUDs predominantly occur in men, growing evidence suggests the existence of distinct cognitive and biological consequences of alcohol dependence in women. The molecular and physiological mechanisms participating in these differential effects remain unknown. Transcriptomic technology permits the detection of the biological mechanisms responsible for such sex-based differences, which supports the subsequent development of novel personalized therapeutics to treat AUD. We conducted a systematic review and meta-analysis of transcriptomics studies regarding alcohol dependence in humans with representation from both sexes. For each study, we processed and analyzed transcriptomic data to obtain a functional profile of pathways and biological functions and then integrated the resulting data by meta-analysis to characterize any sex-based transcriptomic differences associated with AUD. Global results of the transcriptomic analysis revealed the association of decreased tissue regeneration, embryo malformations, altered intracellular transport, and increased rate of RNA and protein replacement with female AUD patients. Meanwhile, our analysis indicated that increased inflammatory response and blood pressure and a reduction in DNA repair capabilities associated with male AUD patients. In summary, our functional meta-analysis of transcriptomic studies provides evidence for differential biological mechanisms that AUD patients of differing sex.Abstract Figure


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