COVID-19 and the Gastrointestinal Tract
Abstract
:1. Introduction
- In a report from the Chinese Center for Disease Control and Prevention (CDC) including about 44,500 confirmed infections, mild disease was reported in 81% of patients. Severe disease (e.g., dyspnea, hypoxia, or >50 percent lung involvement) was reported in 14%. Critical disease was reported in 5%, and the overall case fatality rate was 2.3%, with no deaths among noncritical patients [12].
- Out of 1.3 million cases reported to the United States Centers for Disease Control and Prevention (CDC) through the end of May 2020, 14% of patients were hospitalized, 2% were admitted to the intensive care unit, and 5% died [13].
2. Upper Gastrointestinal Tract
3. Pancreatic Involvement
4. Gallbladder and Biliary
5. Liver Involvement
- Moderate microvesicular steatosis.
- Mild inflammatory infiltrates in the hepatic lobule and portal tract.
- Mild sinusoidal dilatation.
- Focal macrovesicular steatosis.
- Mild lobular lymphocytic infiltration, which was not significant in portal areas.
- A significant increasing trend in COVID-19 mortality rates by HAV susceptibility has been described. The immunity of children against HAV (a virus with similar taxonomy to coronaviruses), acquired either by vaccination in developed countries or by infection in underdeveloped countries, may have contributed to this protection. The loss of immunity to HAV as the result of aging may have led to an increased COVID-19 morbidity in the elderly [38].HAV replication occurs in hepatocyte cytoplasm, thus hepatocellular damage is mediated by direct cytotoxicity. Interferon-gamma (IFN-γ) has a key role in the clearance of HAV of infected hepatocytes. On the other hand, the HAV vaccine is highly immunogenic, inducing seropositivity in 97% of adults after the second dose. The HAV vaccine causes specific proliferation of mononuclear cells in peripheral blood and the release of IFN-γ, thus making it possible that the immune response caused by the HAV vaccine might be protective against COVID-19 infection by an adaptive immunity cross-reaction [39].
- As HBV infection can alter innate immune responses, and uncontrolled innate responses and impaired adaptive immune responses caused by the COVID-19 disease may generate tissue damage, it is plausible that co-infection of SARS-CoV-2 and HBV may synergistically cause disturbances of the immune function and that of the liver.In a retrospective study, Lin et al. reported higher rates of abnormal liver function test in tCOVID-19 positive- HBV inactive carriers compared to their non-HBV carriers counterparts [40]. Similarly, Zou reported higher incidences of liver function test abnormalities among chronic HBV carriers with COVID-19 disease. Among HBV- COVID19 coinfected hospitalized patients, 13.33% developed liver injury; 71.43% recovered after eight days and 28.57% rapidly progressed to acute-on-chronic liver failure; patients with liver injury are more likely to have severe illness, higher incidence of complications and mortality [41].On the other hand, among patients with chronic HBV infection, Liu et al. reported no statistically significant differences in the median time to SARS-CoV2 clearance or progression to severe COVID-19 disease, but three out of 19 patients presented HBV reactivation. Diffuse ballooning degeneration, necrosis of isolated hepatocytes, periportal fibrosis, few inflammatory cells infiltrating the portal tract, positive HBsA and negative hepatitis B core antigen immunohistochemistry were the main histopathological findings [42].
- In a retrospective analysis of the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES), testing rates for SARS-CoV-2 among HCV positive patients was found to be only 8.3%, with 6.2% of tests being positive.HCV positive persons with SARS-CoV-2 coinfection were more likely to be black, have a higher body mass index, diabetes or stroke, with no apparent association between liver fibrosis and infection rate [43].
6. Gut Involvement
- Ileal epithelial cells have high ACE2 expression rates (~30% ACE2-positive cells). [17] COVID-19 leads to the infection of ileal cells followed by expression of the viral nucleocapsid protein, meaning SARS-CoV-2 may spread from infected to uninfected cells in the GI tract, generating mucosal immune cell activation.
- Viraemia following lung infection may occur in approximately 1% of cases, leading to a secondary attack of SARS-CoV2 on ACE2 target organs, including the gut and kidney [46].
- Crosstalk between gut microbiota and the lungs contribute to maintain host homeostasis and disease development in association with the immune system, where the distal (gut) immune modulation during respiratory illness is mediated by gut microbiota. Similarly, lung microbiota influences both respiratory and gastrointestinal health [47]. This gut-lung interaction (gut-lung axis) may influence COVID-19 severity [48,49].On the luminal surface of intestinal epithelial cells, ACE2 associates with the neutral amino acid transporter B0AT1 and regulates intestinal microflora. SARS-CoV-2 infection of the GI tract itself alters the levels of ACE2 at the brush border, leading to dysbiosis and inflammation [50].
7. Vaccine-Related Gastrointestinal Symptoms
- Among patients who received COVID-19 mRNA vaccines, gastrointestinal adverse events were the third most common type of adverse events after immunization, being reported in 25.54% of patients. Among the gastrointestinal symptoms, nausea represented 56.41% of symptoms, followed by vomiting (14.7%) and diarrhea (14.13%) [70].
- Regarding the Ad26.COV2.S vaccine, nausea was the third most common systemic adverse effect, being present in 14.2% of patients [71].
8. Conclusions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
Abbreviations
COVID-19 | Coronavirus disease 2019. |
SARS-CoV-2 | severe acute respiratory syndrome coronavirus 2. |
SARS | Severe Acute Respiratory Syndrome. |
ACE2 | Angiotensin-converting enzyme 2. |
TMPRSS2 | Transmembrane protease, serine 2. |
KIM1 | kidney injury molecule-1. |
RBD | Receptor-binding domain. |
CDC | Center for Disease Control and Prevention. |
Ig | Immunoglobulin. |
IgV | Immunoglobulin variable. |
ALT | Alanine Aminotransferase. |
AST | Aspartate Aminotransferase. |
GI | Gastrointestinal. |
PPIs | proton pump inhibitors. |
H2Ras | H2 receptor antagonists. |
AIH | autoimmune hepatitis. |
CLD | chronic liver disease. |
ICU | intensive care unit. |
HAV | Hepatitis A virus. |
HBV | Hepatitis B virus. |
HCV | Hepatitis C virus. |
IFN-γ | Interferon-gamma |
IBD | Inflammatory Bowel Disease. |
ARDS | Acute respiratory distress syndrome. |
TNF | Tumoral necrosis factor. |
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Epidemiological risk. | Questions remain regarding fecal-oral transmission. SARS-CoV-2 RNA can be detected in the endoscopic specimens from the oesophagus, stomach, duodenum and rectum [72]. Substantial amounts of SARS-CoV-2 RNA can be detected in stool specimens from COVID-19 patients [73]. SARS-CoV-2 RNA has been detected in the sewage of hospitals treating patients with SACOVID-19 disease and the virus remained infectious up to 2 weeks in sewage water [74]. |
Diagnostic procedures | COVID-19 could possibly be transmitted by endoscopes; theoretically due to contact with mucous membranes and body fluids. GI societies have advocate for rescheduling non-urgent procedures and perform only emergent or urgent ones. Pre-endoscopy screening was initially recommended; upgraded guidelines state that, with widespread vaccination of health care workers and the general population, pre-endoscopy screening may not always be necessary, and placed a high value on minimizing additional delays in patient care [74,75]. |
Current medication history | Plausible clinical benefit with famotidine in COVID-19 cases [19]. Impact of acid suppression on risk for COVID-19 is unknown so far [20]. Immunosupression schedule in patients with IBD must be reassessed on a personalized basis [55]. |
Expected clinical course among patients with known comorbidities. | Among patients with bariatric surgery history and COVID-19 disease 1.6% fatality rate. Persistent type 2 diabetes and higher percent weight loss since bariatric surgery are associated with severe COVID-19 [22]. Mortality among patients with COVID-19 and cirrhosis has been reported to be 32%, being older age, higher Child-Pugh and alcohol related liver disease the main factors associated with death [35]/ Similar hospitalization rates, ICU admission and death between patients with AIH and non-AIH CLD [36]. Among persons living with chronic HBV infection, it has been reported that there is no statistically significant differences in the median time to SARS-CoV2 clearance or progression to severe COVID-19 disease [42]. COVID-19-HCV coinfected patients have been reported to have higher hospitalization rates, but ICU admission and mortality are similar between those with and without HCV infection [45]. No current evidence of increased infection rates or worse disease severity of COVID-19 in IBD patients [54]. |
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Mucino-Bermejo, M.-J. COVID-19 and the Gastrointestinal Tract. Gastroenterol. Insights 2021, 12, 394-404. https://doi.org/10.3390/gastroent12040038
Mucino-Bermejo M-J. COVID-19 and the Gastrointestinal Tract. Gastroenterology Insights. 2021; 12(4):394-404. https://doi.org/10.3390/gastroent12040038
Chicago/Turabian StyleMucino-Bermejo, María-Jimena. 2021. "COVID-19 and the Gastrointestinal Tract" Gastroenterology Insights 12, no. 4: 394-404. https://doi.org/10.3390/gastroent12040038