• COVID-19
• Immunomodulator therapy
• Inflammatory Bowel Disease
• Papain-like protease (PLpro)
• SARS-CoV-2 protease inhibitor
• Thiopurine therapy

• Humans
• Pandemics
• Tumor Necrosis Factor Inhibitors/therapeutic use
• COVID-19
• Inflammatory Bowel Diseases/drug therapy
• Crohn Disease/drug therapy

• COVID-19
• Pandemic
• Selenite sodium
• Selenium

• Humans
• SARS-CoV-2
• COVID-19/prevention & control
• Selenium/therapeutic use
• Hydroxychloroquine
• Ivermectin

Inflammatory bowel diseases (IBDs), with blurred etiology, show a rising trend and are of global concern. Of various factors involved in IBD pathogenesis and development, inflammation has been shown to play a major role. Recognition of the molecular and cellular pathways that induce IBD is an emerging subject to develop targeted therapies. Mammalian target of rapamycin (mTOR) is one the most common receptors of many inflammatory pathways, including that of IBD. To this end, we intend to overview the mTOR inhibitors for their possible efficacy in present and future approaches to treatment of IBD.

• Inflammatory bowel diseases
• Inflammation
• Mammalian target of rapamycin
• Mammalian target of rapamycin inhibitors

• Coronavirus disease 2019
• Dexamethasone
• Gastrointestinal symptoms
• Inflammatory bowel disease
• Mutation

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is spreading at an alarming rate, and it has created an unprecedented health emergency threatening tens of millions of people worldwide. Previous studies have indicated that SARS-CoV-2 ribonucleic acid could be detected in the feces of patients even after smear-negative respiratory samples. However, demonstration of confirmed fecal-oral transmission has been difficult. Clinical studies have shown an incidence rate of gastrointestinal (GI) symptoms ranging from 2% to 79.1% in patients with COVID-19. They may precede or accompany respiratory symptoms. The most common GI symptoms included nausea, diarrhea, and abdominal pain. In addition, some patients also had liver injury, pancreatic damage, and even acute mesenteric ischemia/thrombosis. Although the incidence rates reported in different centers were quite different, the digestive system was the clinical component of the COVID-19 section. Studies have shown that angiotensin-converting enzyme 2, the receptor of SARS-CoV-2, was not only expressed in the lungs, but also in the upper esophagus, small intestine, liver, and colon. The possible mechanism of GI symptoms in COVID-19 patients may include direct viral invasion into target cells, dysregulation of angiotensin-converting enzyme 2, immune-mediated tissue injury, and gut dysbiosis caused by microbiota. Additionally, numerous experiences, guidelines, recommendations, and position statements were published or released by different organizations and societies worldwide to optimize the management practice of outpatients, inpatients, and endoscopy in the era of COVID-19. In this review, based on our previous work and relevant literature, we mainly discuss potential fecal-oral transmission, GI manifestations, abdominal imaging findings, relevant pathophysiological mechanisms, and infection control and prevention measures in the time of COVID-19.

• COVID-19
• SARS-CoV-2
• Gastrointestinal manifestations
• Abdominal imaging
• Mechanisms
• Prevention

Coronavirus disease 2019 (COVID‐19), caused by coronavirus severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), has caused extensive disruption and mortality since its recent emergence. Concomitantly, there has been a race to understand the virus and its pathophysiology. The clinical manifestations of COVID‐19 are manifold and not restricted to the respiratory tract. Extrapulmonary manifestations involving the gastrointestinal tract, hepatobiliary system, cardiovascular and renal systems have been widely reported. However, the pathophysiology of many of these manifestations is controversial with questionable support for direct viral invasion and an abundance of alternative explanations such as pre‐existing medical conditions and critical illness. Prior research on SARS‐Co‐V and NL63 was rapidly leveraged to identify angiotensin‐converting enzyme 2 (ACE2) receptor as the key cell surface receptor for SARS‐CoV‐2. The distribution of ACE2 has been used as a starting point for estimating vulnerability of various tissue types to SARS‐CoV‐2 infection. Sophisticated organoid and animal models have been used to demonstrate such infectivity of extrapulmonary tissues in vitro, but the clinical relevance of these findings remains uncertain. Clinical autopsy studies are typically small and inevitably biased towards patients with severe COVID‐19 and prolonged hospitalization. Technical issues such as delay between time of death and autopsy, use of inappropriate antibodies for paraffin‐embedded tissue sections and misinterpretation of cellular structures as virus particles on electron micrograph images are additional problems encountered in the extant literature. Given that SARS‐CoV‐2 is likely to circulate permanently in human populations, there is no doubt that further work is required to clarify the pathobiology of COVID‐19.

• COVID-19
• SARS-CoV-2
• pathophysiology
• transmission

• COVID-19
• MFS
• Miller Fisher syndrome
• SARS-CoV-2

• COVID-19
• Europe
• Humans
• Miller Fisher Syndrome
• SARS-CoV-2
• Spain