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International Journal of Clinical... Oct 2021We aimed to evaluate the elevation of amylase and lipase enzymes in coronavirus disease 2019 (COVID-19) patients and their relationship with the severity of COVID-19.
OBJECT
We aimed to evaluate the elevation of amylase and lipase enzymes in coronavirus disease 2019 (COVID-19) patients and their relationship with the severity of COVID-19.
METHOD
In this study, 1378 patients with COVID-19 infection were included. Relation of elevated amylase and lipase levels and comorbidities with the severity of COVID-19 was analysed. The effects of haemodynamic parameters and organ failure on pancreatic enzymes and their relations with prognosis were statistically analysed.
RESULTS
The 1378 patients comprised of 700 (51.8%) men and 678 (%49.2) women. Of all patients, 687 (49.9%) had mild and 691 (50.1%) patients had severe COVID-19 infection. Amylase elevation at different levels occurred in 316 (%23) out of 1378 patients. In these patients, the amylase levels increased one to three times in 261 and three times in 55 patients. Pancreatitis was detected in only six (%1.89) of these patients according to the Atlanta criteria. According to univariate and multivariate analyses, elevated amylase levels were significantly associated with the severity of COVID-19 (odds ratio [OR]: 4.37; P < .001). Moreover, diabetes mellitus (DM; OR: 1.82; P = .001), kidney failure (OR: 5.18; P < .001), liver damage (OR: 6.63; P < .001), hypotension (OR: 6.86; P < .001) and sepsis (OR: 6.20; P = .008) were found to be associated with mortality from COVID-19.
CONCLUSION
Elevated pancreatic enzyme levels in COVID-19 infections are related to the severity of COVID-19 infection and haemodynamic instability. In a similar way to other organs, the pancreas can be affected by severe COVID-19 infection.
Topics: Acute Disease; Amylases; COVID-19; Female; Humans; Male; Pancreas; Pancreatitis
PubMed: 34331821
DOI: 10.1111/ijcp.14692 -
International Journal of Nanomedicine 2022Pancreatitis is an inflammatory reaction of pancreatic tissue digestion, edema, bleeding and even necrosis caused by activation of pancreatin due to various causes. In... (Review)
Review
Pancreatitis is an inflammatory reaction of pancreatic tissue digestion, edema, bleeding and even necrosis caused by activation of pancreatin due to various causes. In particular, patients with severe acute pancreatitis (SAP) often suffer from secondary infection, peritonitis and shock, and have a high mortality rate. Chronic pancreatitis (CP) can cause permanent damage to the pancreas. Due to the innate characteristics, structure and location of the pancreas, there is no effective treatment, only relief of symptoms. Especially, AP is an unpredictable and potentially fatal disease, and the timely diagnosis and treatment remains a major challenge. With the rapid development of nanomedicine technology, many potential tools can be used to address this problem. In this review, we have introduced the pathophysiological processes of pancreatitis to understanding its etiology and severity. Most importantly, the current progress in the diagnosis and treatment tools of pancreatitis based on nanomedicine is summarized and prospected.
Topics: Acute Disease; Humans; Necrosis; Pancreas; Pancreatin; Pancreatitis
PubMed: 36160469
DOI: 10.2147/IJN.S385590 -
SARS-CoV-2 and the pancreas: What do we know about acute pancreatitis in COVID-19 positive patients?World Journal of Gastroenterology Sep 2022Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause pancreatic damage, both directly to the pancreas angiotensin-converting enzyme 2 receptors (the...
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause pancreatic damage, both directly to the pancreas angiotensin-converting enzyme 2 receptors (the transmembrane proteins required for SARS-CoV-2 entry, which are highly expressed by pancreatic cells) and indirectly through locoregional vasculitis and thrombosis. Despite that, there is no clear evidence that SARS-CoV-2 is an etiological agent of acute pancreatitis. Acute pancreatitis in coronavirus disease 2019 (COVID-19) positive patients often recognizes biliary or alcoholic etiology. The prevalence of acute pancreatitis in COVID-19 positive patients is not exactly known. However, COVID-19 positive patients with acute pancreatitis have a higher mortality and an increased risk of intensive care unit admission and necrosis compared to COVID-19 negative patients. Acute respiratory distress syndrome is the most frequent cause of death in COVID-19 positive patients and concomitant acute pancreatitis. In this article, we reported recent evidence on the correlation between COVID-19 infection and acute pancreatitis.
Topics: Acute Disease; Angiotensin-Converting Enzyme 2; COVID-19; Humans; Pancreas; Pancreatitis; SARS-CoV-2
PubMed: 36185634
DOI: 10.3748/wjg.v28.i36.5240 -
Advanced Biology Aug 2023COVID-19 disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to enormous morbidity and mortality worldwide. After gaining entry into... (Review)
Review
COVID-19 disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to enormous morbidity and mortality worldwide. After gaining entry into the human host, the virus initially infects the upper and lower respiratory tract, subsequently invading multiple organs, including the pancreas. While on one hand, diabetes mellitus (DM) is a significant risk factor for severe COVID-19 infection and associated death, recent reports have shown the onset of DM in COVID-19-recovered patients. SARS-CoV-2 infiltrates the pancreatic islets and activates stress response and inflammatory signaling pathways, impairs glucose metabolism, and consequently leads to their death. Indeed, the pancreatic autopsy samples of COVID-19 patients reveal the presence of SARS-CoV-2 particles in β-cells. The current review describes how the virus enters the host cells and activates an immunological response. Further, it takes a closer look into the interrelationship between COVID-19 and DM with the aim to provide mechanistic insights into the process by which SARS-CoV-2 infects the pancreas and mediates dysfunction and death of endocrine islets. The effects of known anti-diabetic interventions for COVID-19 management are also discussed. The application of mesenchymal stem cells (MSCs) as a future therapy for pancreatic β-cells damage to reverse COVID-19-induced DM is also emphasized.
Topics: Humans; COVID-19; SARS-CoV-2; Diabetes Mellitus; Risk Factors; Pancreas
PubMed: 37246237
DOI: 10.1002/adbi.202300107 -
Hong Kong Medical Journal = Xianggang... Apr 2021
Topics: COVID-19; Exocrine Pancreatic Insufficiency; Humans; Pancreas; Pancreatic Function Tests; SARS-CoV-2
PubMed: 33843611
DOI: 10.12809/hkmj209056 -
Cardiovascular Research Aug 2020
Topics: Animals; Autoimmune Diseases; Coxsackievirus Infections; Mice; Myocarditis; Pancreas; Virulence
PubMed: 32167527
DOI: 10.1093/cvr/cvaa057 -
Cells Jan 2023The novel coronavirus, SARS-CoV-2, rapidly spread worldwide, causing an ongoing global pandemic. While the respiratory system is the most common site of infection, a... (Review)
Review
The novel coronavirus, SARS-CoV-2, rapidly spread worldwide, causing an ongoing global pandemic. While the respiratory system is the most common site of infection, a significant number of reported cases indicate gastrointestinal (GI) involvement. GI symptoms include anorexia, abdominal pain, nausea, vomiting, and diarrhea. Although the mechanisms of GI pathogenesis are still being examined, viral components isolated from stool samples of infected patients suggest a potential fecal-oral transmission route. In addition, viral RNA has been detected in blood samples of infected patients, making hematologic dissemination of the virus a proposed route for GI involvement. Angiotensin-converting enzyme 2 (ACE2) receptors serve as the cellular entry mechanism for the virus, and these receptors are particularly abundant throughout the GI tract, making the intestine, liver, and pancreas potential extrapulmonary sites for infection and reservoirs sites for developing mutations and new variants that contribute to the uncontrolled spread of the disease and resistance to treatments. This transmission mechanism and the dysregulation of the immune system play a significant role in the profound inflammatory and coagulative cascades that contribute to the increased severity and risk of death in several COVID-19 patients. This article reviews various potential mechanisms of gastrointestinal, liver, and pancreatic injury.
Topics: Humans; COVID-19; SARS-CoV-2; Liver; Intestines; Pancreas
PubMed: 36672197
DOI: 10.3390/cells12020262 -
Cell Metabolism Aug 2021Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen...
Recent clinical data have suggested a correlation between coronavirus disease 2019 (COVID-19) and diabetes. Here, we describe the detection of SARS-CoV-2 viral antigen in pancreatic beta cells in autopsy samples from individuals with COVID-19. Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19.
Topics: Acetamides; Adolescent; Adult; Aged; Aged, 80 and over; Animals; COVID-19; Cell Transdifferentiation; Chlorocebus aethiops; Cyclohexylamines; Cytokines; Eukaryotic Initiation Factor-2; Female; Glucagon; Host-Pathogen Interactions; Humans; Insulin; Insulin-Secreting Cells; Male; Middle Aged; Phenotype; SARS-CoV-2; Signal Transduction; Tissue Culture Techniques; Trypsin; Vero Cells; Young Adult
PubMed: 34081913
DOI: 10.1016/j.cmet.2021.05.015 -
Archives of Microbiology Jul 2023According to previous studies, Helicobacter pylori infection is associated with liver disease. In order to better understand the risk of acquiring various liver... (Review)
Review
According to previous studies, Helicobacter pylori infection is associated with liver disease. In order to better understand the risk of acquiring various liver diseases, we reviewed current knowledge on the impact of H. pylori on the onset, intensification, and progression of various liver diseases caused by the infection of H. pylori. It has been estimated that between 50 and 90% of people worldwide have been infected with H. pylori. The bacterium is mostly responsible for inflamed gastric mucosa, ulcers, and cancers associated with the gastric mucosa. Through the active antioxidant system in H. pylori, the bacteria can neutralize free radicals by synthesizing VacA, a toxin that causes cell damage and apoptosis. Furthermore, there is a possibility that CagA genes may play a role in cancer development. People who have been infected with H. pylori are likely to develop lesions in the skin, the circulation system, and the pancreas. Moreover, transferring blood from the stomach may allow H. pylori to colonize the liver. The bacterium worsened liver function during autoimmune inflammation, toxic injury, chronic HCV infection, chronic HBV infection, and liver cirrhosis. Increasing portal pressure, hyperammonemia, and esophageal varices may be associated with H pylori infection. As a result, it is crucial to diagnose and treat this infection in patients with H. pylori.
Topics: Humans; Helicobacter pylori; Helicobacter Infections; Liver Diseases; Hepatitis C; Antioxidants
PubMed: 37430019
DOI: 10.1007/s00203-023-03602-z -
Platelets Feb 2022Hepatitis B virus (HBV) is a kind of hepatotropic DNA virus. The main target organ is liver, except for liver, HBV has been found in a variety of extrahepatic tissues,... (Review)
Review
Hepatitis B virus (HBV) is a kind of hepatotropic DNA virus. The main target organ is liver, except for liver, HBV has been found in a variety of extrahepatic tissues, such as kidney, thyroid, pancreas, bone marrow, etc. HBV can cause severe complications by invading these tissues. Among them, pancytopenia is one of the common complications, especially thrombocytopenia that causes life-threatening bleeding. However, the mechanism of thrombocytopenia is unclear and the treatment is extremely difficult. It has been confirmed that HBV has a close relationship with platelets. HBV can directly infect bone marrow, inhibit platelet production, and accelerate platelet destruction by activating monocyte-macrophage system and immune system. While platelets act as a double-edged sword to HBV. On one hand, the activated platelets can degranulate and release inflammatory mediators to help clear the viruses. Furthermore, platelets can provide anti-fibrotic molecules to improve liver functions and reduce hepatic fibrosis. On the other hand, platelets can also cause negative effects. The infected platelets collect HBV-specific CD8 T cells and nonspecific inflammatory cells into liver parenchyma, inducing chronic inflammation, liver fibrosis and hepatic carcinoma. This article explores the interaction between HBV infection and platelets, providing a theoretical basis for clinical treatment of thrombocytopenia and severe hemorrhage caused by HBV infection.
Topics: Blood Platelets; Hepatitis B; Hepatitis B virus; Humans
PubMed: 34806523
DOI: 10.1080/09537104.2021.2002836