The gold standard for the diagnosis of checkpoint inhibitor induced colitis is colonoscopy with evaluation of the terminal ileum.
Infection should be ruled out with stool studies, including Clostridioides difficile, bacterial culture, ova and parasites.
Mild cases by managed with temporary interruption of immune checkpoint inhibitor therapy, dietary modification (low residue), and/or loperamide.
The most common symptom is diarrhea, which occurs in 92 percent of cases, followed by abdominal pain (82%) and rectal bleeding (64%).
Grade 4 colitis is defined by life-threatening consequences, including perforation, ischemia, necrosis, bleeding, or toxic megacolon.
High grade colitis may lead to severe complications, including perforation, toxic megacolon and death.
Mice with the CTLA-4 gene removed (e.g. CTLA-4 knockout) develop severe autoimmune disease, with diffuse infiltration of T cells in multiple organs and fatal enterocolitis.
[4] Histologic inflammation may occur as early as 1–2 weeks after immune checkpoint inhibitor therapy, well before the onset of symptoms.
In addition, a higher rate of checkpoint inhibitor induced colitis is associated with the presence of Faecalibacterium in the fecal microbiota.
[5] Colonoscopy with evaluation of the terminal ileum is the gold standard in the diagnosis of checkpoint inhibitor induced colitis.
[4][2][6] Endoscopic findings may include loss of vascular pattern, erythema, edema, erosions, ulcers, exudates, granularity, and bleeding.
For mild disease, supportive care may be sufficient, including loperamide and a low residue or bland diet.
Corticosteroid therapy is used to decrease inflammation, at a dose of roughly prednisone 1–2 mg per kg of body weight per day.
[9] Surgery with resection of the colon (colectomy) is necessary in some instances,[10] particularly if severe complications occur, such as perforation[1] or toxic megacolon.