COVID-19 and celiac disease: A pathogenetic hypothesis for a celiac outbreak

Chiara Maria Trovato; Monica Montuori; Nicoletta Pietropaoli; Salvatore Oliva

doi:10.1111/ijcp.14452

COVID-19 and celiac disease: A pathogenetic hypothesis for a celiac outbreak

Chiara Maria Trovato, Monica Montuori, Nicoletta Pietropaoli, Salvatore Oliva

Ospedale Pediatrico Bambino Gesu

Research output: Contribution to journal › Article › peer-review

Abstract

BACKGROUND: A growing body of evidence supports the intestinal trophism of SARS-CoV-2, with ciliated cells and intestinal enterocytes being target cells because of the high expression of ACE2 and TMPRSS2. Indeed, COVID-19 promotes a "cytokine storm" in the intestinal mucosa: the resulting epithelial damage leads to increased barrier permeability, allowing the passage of gliadin in the intestinal lamina.

METHODS: Based on current literature, we hypothesize the role of COVID-19 as a potential trigger factor for celiac disease in predisposed patients.

CONCLUSIONS: Genetically predisposed patients could be more likely to develop celiac disease following SARS-CoV-2 infection, making COVID-19 a candidate culprit for a potential outbreak of celiac disease in the forthcoming future.

Original language	English
Pages (from-to)	e14452
Journal	International Journal of Clinical Practice
Volume	75
Issue number	9
DOIs	https://doi.org/10.1111/ijcp.14452
Publication status	Published - Sept 2021

Keywords

COVID-19
Celiac Disease/epidemiology
Disease Outbreaks
Gliadin
Humans
SARS-CoV-2

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10.1111/ijcp.14452

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title = "COVID-19 and celiac disease: A pathogenetic hypothesis for a celiac outbreak",

abstract = "BACKGROUND: A growing body of evidence supports the intestinal trophism of SARS-CoV-2, with ciliated cells and intestinal enterocytes being target cells because of the high expression of ACE2 and TMPRSS2. Indeed, COVID-19 promotes a {"}cytokine storm{"} in the intestinal mucosa: the resulting epithelial damage leads to increased barrier permeability, allowing the passage of gliadin in the intestinal lamina.METHODS: Based on current literature, we hypothesize the role of COVID-19 as a potential trigger factor for celiac disease in predisposed patients.CONCLUSIONS: Genetically predisposed patients could be more likely to develop celiac disease following SARS-CoV-2 infection, making COVID-19 a candidate culprit for a potential outbreak of celiac disease in the forthcoming future.",

keywords = "COVID-19, Celiac Disease/epidemiology, Disease Outbreaks, Gliadin, Humans, SARS-CoV-2",

author = "Trovato, {Chiara Maria} and Monica Montuori and Nicoletta Pietropaoli and Salvatore Oliva",

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year = "2021",

month = sep,

doi = "10.1111/ijcp.14452",

language = "English",

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journal = "Medicine illustrated",

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TY - JOUR

T1 - COVID-19 and celiac disease

T2 - A pathogenetic hypothesis for a celiac outbreak

AU - Trovato, Chiara Maria

AU - Montuori, Monica

AU - Pietropaoli, Nicoletta

AU - Oliva, Salvatore

PY - 2021/9

Y1 - 2021/9

N2 - BACKGROUND: A growing body of evidence supports the intestinal trophism of SARS-CoV-2, with ciliated cells and intestinal enterocytes being target cells because of the high expression of ACE2 and TMPRSS2. Indeed, COVID-19 promotes a "cytokine storm" in the intestinal mucosa: the resulting epithelial damage leads to increased barrier permeability, allowing the passage of gliadin in the intestinal lamina.METHODS: Based on current literature, we hypothesize the role of COVID-19 as a potential trigger factor for celiac disease in predisposed patients.CONCLUSIONS: Genetically predisposed patients could be more likely to develop celiac disease following SARS-CoV-2 infection, making COVID-19 a candidate culprit for a potential outbreak of celiac disease in the forthcoming future.

AB - BACKGROUND: A growing body of evidence supports the intestinal trophism of SARS-CoV-2, with ciliated cells and intestinal enterocytes being target cells because of the high expression of ACE2 and TMPRSS2. Indeed, COVID-19 promotes a "cytokine storm" in the intestinal mucosa: the resulting epithelial damage leads to increased barrier permeability, allowing the passage of gliadin in the intestinal lamina.METHODS: Based on current literature, we hypothesize the role of COVID-19 as a potential trigger factor for celiac disease in predisposed patients.CONCLUSIONS: Genetically predisposed patients could be more likely to develop celiac disease following SARS-CoV-2 infection, making COVID-19 a candidate culprit for a potential outbreak of celiac disease in the forthcoming future.

KW - COVID-19

KW - Celiac Disease/epidemiology

KW - Disease Outbreaks

KW - Gliadin

KW - Humans

KW - SARS-CoV-2

U2 - 10.1111/ijcp.14452

DO - 10.1111/ijcp.14452

M3 - Article

C2 - 34145702

SN - 1368-5031

VL - 75

SP - e14452

JO - Medicine illustrated

JF - Medicine illustrated

IS - 9

ER -

COVID-19 and celiac disease: A pathogenetic hypothesis for a celiac outbreak

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