Evidence map›Paper›PMID 34040326›Full record

ReviewWorld journal of gastroenterology2021

Pathophysiological mechanisms underlying gastrointestinal symptoms in patients with COVID-19.

Byungchang Jin, Rajan Singh, Se Eun Ha, Hannah Zogg, Paul J Park, Seungil Ro

Abstract readReview
In one paragraph

Review in World journal of gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 3 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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  19. Contribution of CD4+ T cell-mediated inflammation to diarrhea in patients with COVID-19.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Byungchang JinDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, United States.
Rajan SinghDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, United States.
Se Eun HaDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, United States.
Hannah ZoggDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, United States.
Paul J ParkDepartment of Medicine, Renown Health, Reno, NV 89557, United States.
Seungil RoDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, United States. sro@med.unr.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal (GI) symptoms, such as diarrhea, abdominal pain, vomiting, and anorexia, are frequently observed in patients with coronavirus disease 2019 (COVID-19). However, the pathophysiological mechanisms connecting these GI symptoms to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections remain elusive. Previous studies indicate that the entry of SARS-CoV-2 into intestinal cells leads to downregulation of angiotensin converting enzyme 2 (ACE2) receptors resulting in impaired barrier function. While intestinal ACE2 functions as a chaperone for the amino acid transporter B0AT1, the B0AT1/ACE2 complex within the intestinal epithelium acts as a regulator of gut microbiota composition and function. Alternations to the B0AT1/ACE2 complex lead to microbial dysbiosis through increased local and systemic immune responses. Previous studies have also suggested that altered serotonin metabolism may be the underlying cause of GI disorders involving diarrhea. The findings of elevated plasma serotonin levels and high fecal calprotectin in COVID-19 patients with diarrhea indicate that the viral infection evokes a systemic inflammatory response that specifically involves the GI. Interestingly, the elevated proinflammatory cytokines correlate with elevated serotonin and fecal calprotectin levels further supporting the evidence of GI inflammation, a hallmark of functional GI disorders. Moreover, the finding that rectal swabs of COVID-19 patients remain positive for SARS-CoV-2 even after the nasopharynx clears the virus, suggests that viral replication and shedding from the GI tract may be more robust than that of the respiratory tract, further indicating fecal-oral transmission as another important route of viral spread. This review summarized the evidence for pathophysiological mechanisms (impaired barrier function, gut inflammation, altered serotonin metabolism and gut microbiota dysbiosis) underlying the GI symptoms in patients with COVID-19.

Indexed as

COVID-19Gastrointestinal DiseasesDysbiosisGastrointestinal TractHumansSARS-CoV-2Angiotensin converting enzyme 2 receptorCOVID-19Gastrointestinal symptomsGut microbiota dysbiosisImpaired barrier functionSerotonin

Identifiers

PMID34040326
PMCPMC8130047

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.