Clinical Problem
An increasingly recognized subset of patients develops post-infection sequelae also described as long COVID or postacute COVID-19 syndrome (PACS). These patients experience a myriad of neurologic, respiratory, cardiac, psychiatric, and/or GI symptoms that persist for 4 weeks or more from the initial diagnosis of SARS-CoV-2.
Epidemiology
In a survey study of 749 survivors, 29% reported at least 1 new chronic GI symptom 6 months after their COVID-19 infection, with heartburn, constipation, diarrhea, and abdominal pain being the most common.2 Of the patients with abdominal pain, 39% met Rome IV criteria for irritable bowel syndrome (IBS). Other studies also reported a 30%–40% prevalence of GI PACS. Additionally, COVID-19 infection was associated with worsening severity of preexisting IBS symptoms. Some risk factors for GI PACS include the presence of GI symptoms during acute infection, psychiatric diagnoses (depression, anxiety) both pre- and post-COVID-19, need for hospitalization during acute illness, and loss of smell and taste. Infectious gastroenteritis is an established risk-factor for development of disorders of gut-brain interaction (DGBI), particularly post-infection IBS (PI-IBS). Many of the risk factors for GI PACS described are also known predisposing factors for PI-IBS, with some exceptions, such as female gender, a risk factor for PI-IBS but not consistently associated with GI PACS. In addition to IBS, other de novo DGBIs, such as functional dyspepsia, heartburn, chest pain, and dysphagia, can be experienced in the spectrum of GI PACS.
Disease Mechanisms
The pathophysiology of PACS including that of the GI manifestations is incompletely understood; however, it is likely multifactorial (Figure 1). Epithelial invasion by SARS-CoV-2 is substantiated by the high expression levels of angiotensin-converting enzyme-2 on the enterocytes and colonocytes. The angiotensin-converting enzyme-2 is a negative regulator of the renin-angiotensin system and has a protective cellular role, including in the intestinal tract. Following the entry of SARS-CoV-2 in the cell, angiotensin-converting enzyme-2 protein is downregulated, resulting in an increase in angiotensin-II, the likely molecular mechanism of severe acute respiratory syndrome and systemic inflammatory response development with this coronavirus. Intestinal microbial dysbiosis has also been associated with acute SARS-CoV-2 infection and PACS. Long-term respiratory dysfunction after COVID-19 is associated with altered gut microbiota and persistently elevated lipopolysaccharide-binding protein levels. One study showed that dysbiosis in COVID-19 patients continued throughout their hospitalizations and up to 21 days from disease onset, with a decrease in health-promoting, short-chain fatty acid–forming bacteria.3 Gut microbiome of patients with PACS was characterized by higher levels of Ruminococcus gnavus and Bacteroides vulgatus, and lower levels of Faecalibacterium prausnitzii. Interestingly, presence of butyrate-producing bacteria showed an inverse correlation with development of PACS at 6 months.4 A recent study also suggested that salivary microbiome during acute infection may predict the development of GI PACS.5
Read the rest of this article HERE.
Source: Walter W. Chan and Madhusudan Grover. The COVID-19 Pandemic and Post-Infection Irritable Bowel Syndrome: What Lies Ahead for Gastroenterologists. Published: August 06, 2022. DOI: https://doi.org/10.1016/j.cgh.2022.05.044 (Full text)