Anosmia & ageusia/dysgeusia |
Very common. Often the first symptom to manifest with COVID-19 infection and the last symptom to resolve. Bothersome symptoms but not life-threatening. Proposed, unproven therapies include corticosteroids and Paxlovid. |
Not associated with nasopharyngitis, nasal obstruction, glossitis, zinc deficiency, or rhinorrhea. Postulated decreased sensitivity of olfactory neurons associated with expression of ACE-2 in alveolar epithelial cells. |
Geographic (COVID) tongue |
Affects about 4% of infected patients. Associated with minor symptoms. |
Loss of filiform papillae in rear of tongue from damage caused by high expression of ACE-2 in epithelial cells. |
GERD (gastroesophageal reflux disease) |
Very common with COVID-19 infection but also very common without COVID-19 infection. GERD likely does not arise from acute COVID-19 infection but likely arises from shared risk factors, such as obesity. |
COVID-19 may preferentially infect Barrett’s epithelium over normal esophageal mucosa, and PPI therapy may be associated with increased COVID-19 susceptibility. |
Esophageal candidiasis |
Risk factors include acute respiratory distress syndrome, chronic corticosteroid therapy, and prolonged endotracheal intubation. Often associated with severe COVID-19 infection and has a high mortality due to this association. Typical symptoms are dysphagia and odynophagia. EGD classically demonstrates a cheesy exudate in esophagus. Endoscopic brushings are usually diagnostic. Primary therapies are echinocandins and azoles. |
Associated with profound immune dysregulation with COVID-19 infection, but the specific underlying immunologic defects are unknown. |
Pill-induced esophagitis |
More prevalent in COVID-19 infected patients. |
Partly related to increased use of doxycycline antibiotics to treat COVID-19 infection and increased corrosive ingestion due to COVID-19 pandemic–related stress. |
Eosinophilic esophagitis |
Apparently eosinophilic esophagitis does not increase the frequency or severity of COVID-19 infection. Acute COVID-19 infection does not apparently cause flares of eosinophilic esophagitis. |
Patients with eosinophilic esophagitis typically have mild COVID-19 infection. COVID-19 esophageal infection might be related to oral corticosteroid therapy for eosinophilic esophagitis. |
Gastric ulcers |
Gastric ulcers very common in patients with COVID-19 infection who are undergoing EGD. |
H pylori does not apparently affect the severity of COVID-19 infection. Several patients had esophageal or gastric ulcers from primary COVID-19 infection, as demonstrated by electron microscopy. |
GI hemorrhage |
Occurs in about 9% or less of hospitalized COVID-19–infected patients. Often the GI bleeding is mild and does not mandate endoscopy. Patients with GI bleeding often have a worse prognosis from COVID-19 infection than nonbleeding COVID-19–infected patients. GI hemorrhage in patients with COVID-19 is often from gastric ulcers. GI bleeding may sometimes arise from anticoagulation used to treat a hypercoagulopathy associated with COVID-19 infection. |
GI bleeding rarely due to ulcers associated with primary COVID-19 infection. |
Celiac disease |
Celiac patients do not have increased susceptibility to COVID-19 infection and do not have a worse outcome from COVID-19 infection. The mainstay of therapy in COVID-19–infected patients is maintenance of a gluten-free diet. |
The 2 different diseases do not seem to significantly interact. |
Multisystem inflammatory syndrome |
Rare syndrome that occurs in children. Clinically can resemble regional enteritis. Can cause GI obstruction, fistula, or contained GI perforation. |
Syndrome associated with an abnormal immune response due to viral cytopathic effects. |
Mesenteric ischemia |
COVID-19 infection likely increases the risk of mesenteric ischemia. Mesenteric ischemia has a high mortality in COVID-19–infected patients. |
Most likely increased frequency of mesenteric ischemia due to microcirculatory thrombosis, but sometimes can occur from large vessel thrombosis. COVID-19 can produce a hypercoagulopathy. High mortality from mesenteric ischemia attributed to delayed diagnosis because symptoms can be confused with acute COVID-19 infection. |
Small bowel intussusception |
Frequency may increase with COVID-19 infection. |
Attributed to bowel wall or mesenteric lymph node inflammation, edema and thickening from local viral infection that forms a lead point for the intussusception. |
GI infection with mucormycosis |
Increased risk with advanced COVID-19 infection due to immunosuppression. Associated with high mortality. |
Increased risk attributed to high-dose corticosteroid therapy, exposure to mechanical ventilation, and advanced COVID-19 infection. |
Collagenous colitis |
Significantly higher rate of contracting COVID-19 infection, having severe COVID-19 infection, and of being hospitalized for COVID-19 infection than patients with lymphocytic colitis or controls. |
May relate to genetic factors associated with predisposition to developing collagenous colitis such as an extended HLA haplotype or the rs13071258 A variant on genetic locus 3p21.31 associated with collagenous colitis. This genetic locus harbors 6 genes potentially affecting the immune defense against viral infections. |
Lymphocytic colitis |
Has similar rate of contracting COVID-19 infection and developing severe infection as controls. Lymphocytic colitis should be considered in the differential of watery diarrhea after contracting acute COVID-19 infection. |
Unlike collagenous colitis, lymphocytic colitis is not associated with genetic abnormalities affecting host defenses against viruses. |
Tocilizumab-associated colonic perforation |
Case report of developing terminal ileal and cecal ulcers that caused colonic perforation after initiating tocilizumab therapy for suspected cytokine release syndrome in a patient with COVID-19 infection. |
Tocilizumab has previously been associated with lower GI perforation and colonic diverticular perforation after its use to treat rheumatoid arthritis. |
Acute appendicitis and acute diverticulitis |
COVID-19 infection does not affect the frequency of hospitalization, colonic perforation, or surgery from these 2 diseases. |
COVID-19 infection does not seem to affect the natural history of these 2 diseases. |
Irritable bowel syndrome |
During pandemic patients with irritable bowel syndrome experienced more severe GI symptoms, more severe extraintestinal symptoms, and more sleep difficulties than before the COVID-19 pandemic. |
Patients likely experience more severe symptoms of irritable bowel syndrome due to anxiety related to the pandemic. |
Inflammatory bowel disease |
COVID-19–infected patients have a worse outcome from inflammatory bowel disease when treated with corticosteroids but not when treated with tumor necrosis factor antagonists. |
Corticosteroids may decrease immunologic defenses against COVID-19 infection. Another chapter in this monograph is devoted to COVID-19 infection in patients with inflammatory bowel disease. |