Carlo Romano Settanni, Gianluca Ianiro, Francesca Romana Ponziani, Stefano Bibbò, Jonathan Philip Segal, Giovanni Cammarota, and Antonio Gasbarrini
Abstract
In December 2019 a novel coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), started spreading from Wuhan city of Chinese Hubei province and rapidly became a global pandemic. Clinical symptoms of the disease range from paucisymptomatic disease to a much more severe disease. Typical symptoms of the initial phase include fever and cough, with possible progression to acute respiratory distress syndrome. Gastrointestinal manifestations such as diarrhoea, vomiting and abdominal pain are reported in a considerable number of affected individuals and may be due to the SARS-CoV-2 tropism for the peptidase angiotensin receptor 2. The intestinal homeostasis and microenvironment appear to play a major role in the pathogenesis of COVID-19 and in the enhancement of the systemic inflammatory responses. Long-term consequences of COVID-19 include respiratory disturbances and other disabling manifestations, such as fatigue and psychological impairment. To date, there is a paucity of data on the gastrointestinal sequelae of SARS-CoV-2 infection. Since COVID-19 can directly or indirectly affect the gut physiology in different ways, it is plausible that functional bowel diseases may occur after the recovery because of potential pathophysiological alterations (dysbiosis, disruption of the intestinal barrier, mucosal microinflammation, post-infectious states, immune dysregulation and psychological stress). In this review we speculate that COVID-19 can trigger irritable bowel syndrome and we discuss the potential mechanisms.
CONCLUSION
The COVID-19 pandemic is a threat to global public health. A wide spectrum of respiratory and systemic symptoms can occur during the acute disease with different degrees of severity, and some of them can persist over time after the recovery. A large body of evidence supports the gastrointestinal involvement of SARS-CoV-2 infection during the acute phase, possibly because the intestinal ACE2 is an additional target of viral infection. Importantly, little is known about the gastrointestinal sequelae; at present, there is no study reporting the occurrence of IBS in individuals recovered from COVID-19. However, a number of considerations may be made regarding the plausible role of COVID-19, its management and global setting in the enhancement of IBS. Specifically, it can be assumed that many factors contributing to promote a dysbiotic state, epithelial barrier impairment, intestinal inflammation and gut dysfunction (like antibiotics and other treatments of the acute phase, gut-lung axis impairment, disease-related psychological stress, as well as the virus itself) can be involved in this process. Prospective cohort studies are necessary to confirm these hypotheses before clinical significance can be concluded.