Radiol Oncol 2024; 58(2): 179-185. doi: 10.2478/raon-2024-0022
179
review
Colitis due to cancer treatment with immune 
check-point inhibitors − review of literature 
and presentation of clinical cases
Andreja Ocepek
Department of Gastroenterology, Division of Internal Medicine, University Medical Centre Maribor, Maribor, Slovenia 
Radiol Oncol 2024; 58(2): 179-185.
Received 10 Avgust 2023 
Accepted 29 January 2024
Correspondence to: Andreja Ocepek, M.D., Department of Gastroenterology, Division of Internal Medicine, University Medical Centre Maribor, 
Ljubljanska 5, SI-2000 Maribor, Slovenia. E-mail: andreja.ocepek@ukc-mb.si
Disclosure: No potential conflicts of interest were disclosed.
This is an open access article distributed under the terms of the CC-BY license (https://creativecommons.org/licenses/by/4.0/).
Treatment with immune checkpoint inhibitors is effective in various cancers, but may be associated with immune-
mediated side effects in other organs. Among the more common ones is gastrointestinal tract involvement, especially 
colitis. In most patients, colitis is mild or responds to corticosteroid treatment. A smaller proportion of patients, more 
often those treated with cytotoxic T lymphocyte antigen-4 inhibitors, may have a more severe course of colitis, even 
life-threatening complications. In these patients, prompt action, timely diagnosis with endoscopic evaluation and 
early treatment with high-dose corticosteroids and, if ineffective, rescue therapy with biologic agents such as inflixi-
mab and vedolizumab are needed. We present three cases from our clinical practice, data on incidence and clini-
cal presentation, current recommendations regarding diagnostic approach and treatment of immune checkpoint 
inhibitors induced colitis.
Key words: immune checkpoint inhibitors; immune checkpoint inhibitors induced colitis; immune-mediated micro-
scopic colitis; corticosteroid therapy; infliximab; vedolizumab 
Introduction
Inhibition of immune checkpoints strengthens the 
body’s own defences against cancer, which can be 
exploited to great advantage in the treatment of ma-
lignant diseases. Such drugs are antibodies against 
inhibitory immune regulators such as cytotoxic T 
lymphocyte antigen-4 (CTLA-4), programmed cell 
death protein-1 (PD-1) and programmed death 
protein-1 ligand (PD-L1). Due to their involvement 
in the immune response, immune checkpoint in-
hibitors (ICPI) can trigger other immune-mediated 
diseases as a side effect, affecting many other or-
gans and tissues, e.g. skin, lung, liver and gastro-
intestinal tract. The most common side effect of 
immunotherapy for cancer of the gastrointestinal 
tract is immune-mediated or ICPI-induced colitis.1,2
Incidence
The incidence of ICPI-induced colitis depends 
on three factors: the type of immunotherapy, the 
characteristics of the patient and the characteristics 
of the cancer. Colitis occurs more frequently with 
CTLA-4 inhibitors than with PD-1 and PD-L1 in-
hibitors, with combination therapy with two ICPIs, 
and with higher doses, although a clear dose-de-
pendence of the occurrence and severity of colitis 
has not been confirmed.3 The incidence of colitis is 
3.4–22% with CTLA-4 inhibitor therapy, 0.7–12.8% 
with combined CTLA-4 and PD-1 inhibitor thera-
py, and 0.7–2.6% with PD-1/PD-L1 inhibitor mono-
therapy.1,2 Another important factor is cancer itself. 
According to data known so far, the incidence of 
colitis is higher in patients with melanoma than 
Radiol Oncol 2024; 58(2): 179-185.
Ocepek A / Colitis due to cancer treatment with immune check-point inhibitors180
in patients with other cancers. For example, ipili-
mumab treatment causes diarrhoea in 41% of mela-
noma patients compared with up to 27% of lung 
cancer patients.3 The stage of cancer may also in-
fluence the incidence of side-effects, although the 
underlying mechanism is unknown. Thus, the in-
cidence of diarrhoea and colitis is lower in stage 
IV (35.3%) than in stage III (72%) of the same can-
cer.1 Third factor is the patient himself. The risk of 
ICPI-induced colitis is higher in Caucasians and in 
patients with known inflammatory bowel disease 
(IBD), but the influence of sex, age, gut microbiota 
and possibly genetic predisposition (e.g. human 
leukocyte antigen (HLA) status) remains unclear.1,3
Clinical presentation
Symptoms and signs of ICPI-induced colitis most 
commonly include diarrhoea, abdominal pain, 
bloating, haemochesia, mucus discharge, fever 
and vomiting.1,3 Diarrhoea occurs in most cases 
4–8 weeks after the start of ICPI, but in some pa-
tients it may be as early as 1 week, and in others it 
may occur months or up to 2 years after the end of 
treatment.1 The severity of colitis may range from 
mild, self-limiting diarrhoea to life-threatening co-
litis with the risk of rapid onset of complications 
such as ileus, toxic megacolon and intestinal per-
foration.1,2 The severity of diarrhoea and colitis 
is defined by the Common Terminology Criteria 
for Adverse Events (CTCAE) in 5 grades shown 
in Table 1.2,4,5 A more severe course of colitis can 
be expected in patients receiving CTLA-4 inhibi-
tors (e.g. ipilimumab) and in patients with known 
IBD.2,3
Diagnosis
ICPI-induced colitis should be considered in all 
cancer patients receiving ICPI. Because of non-
specific symptoms, diagnosis is based on exclu-
sion of other conditions with a similar clinical 
presentation. In the differential diagnosis, we must 
consider infectious causes (e.g. clostridial diar-
rhoea, cytomegalovirus reactivation, etc.), drug-
induced colitis (e.g. non-steroidal antirheumatic 
drugs, chemotherapeutic drugs, mycophenolate 
mofetil...), microscopic colitis, IBD flare, diverticu-
litis, ischaemic colitis, graft-versus-host disease, 
ICPI-induced pancreatitis, exocrine pancreatic in-
sufficiency, ICPI-induced coeliac disease, thyroid 
dysfunction1,4,6,7. The recommended set of diagnos-
tic tests and procedures is shown in Table 2.1-3,8 In 
case of severe abdominal pain or suspected com-
plications, imaging is required, most commonly 
with computed tomography (CT) and/or magnetic 
resonance imaging (MRI). Both CT and MRI are in-
sufficiently sensitive and specific for the diagnosis 
of ICPI-induced colitis.2-4
Endoscopic and 
histopathological features
Endoscopic findings are non-specific. Up to 37% 
of patients with ICPI-induced colitis have normal 
endoscopic findings, but up to 90% of patients 
with grade 1 colitis have microscopic changes, so 
even macroscopically normal mucosa needs to be 
biopsied for histological analysis. Endoscopically, 
mucosal oedema, erythema, erosions, loss of vas-
cular permeation, superficial or deep ulcers may be 
found.2 Lesions may be present diffusely, segmen-
tally or irregularly along the bowel. Single atypical 
cases of colonic pseudolipomatosis and collagen-
ous colitis after atezolizumab treatment have also 
been described.9,10 The Mayo endoscopic scoring 
system, which is routinely used to describe ul-
cerative colitis, can be used to describe endoscopic 
changes (Table 3).4,11
Clinical studies have shown the importance 
of endoscopic diagnosis in patients with CTCAE 
grade > 1 in predicting the need for biologic thera-
py, as patients with a more severe endoscopic pic-
ture according to Mayo endoscopic score of grade 
3 were statistically significantly more likely to re-
quire treatment with infliximab.12,13
Histo-pathological features vary from acute co-
litis with intraepithelial neutrophilic infiltration, 
cryptitis and crypt abscesses, to chronic colitis 
with basal lymphocytic infiltration, Paneth cell 
metaplasia and disrupted crypt architecture, or 
both.3,10 Histo-pathological assessment of the se-
verity of inflammation using the Nancy score has 
also been shown to be a good predictor of the need 
for biologic therapy, with 50% of patients with 
Nancy grade 3 and 4 requiring salvage therapy 
with infliximab compared with 20% of patients 
with Nancy grade 1 and 2.1
Immune-mediated microscopic 
colitis
Immune-mediated microscopic colitis, recognised 
as a separate disease, presents with chronic wa-
Radiol Oncol 2024; 58(2): 179-185.
Ocepek A / Colitis due to cancer treatment with immune check-point inhibitors 181
tery diarrhoea. It usually occurs after treatment 
with anti-PD-1 or anti-CTLA-4. On colonoscopy, 
the intestinal mucosa is normal or mildly altered 
with oedema and/or erythema. Histopathological 
examination is the key to the diagnosis, and there-
fore random biopsies of apparently normal mu-
cosa should always be performed. There are two 
forms of microscopic colitis. Lymphocytic colitis is 
characterised by intraepithelial lymphocytosis and 
infiltration of the lamina propria. In collagenous 
colitis, however, thickening of the collagenous sub-
epithelial layer is visible on histopathology.16
Treatment
Treatment depends on the stage of CTCAE. In 
grade 1, treatment is supportive and symptomatic. 
Oral hydration, a soft, non-irritating diet with-
out lactose and caffeine, and antidiarrhoic drugs 
(e.g. loperamide) are advised after exclusion of 
infection.15,16 Treatment with mesalazine may be 
attempted.3,17 Discontinuation of ICPI is not nec-
essary. If symptoms do not resolve within 7–10 
days or the clinical picture worsens to grade ≥ 2, a 
consultation with a gastroenterologist and an en-
doscopic examination is recommended as a start-
ing point for further treatment.2,4,8 In the absence 
of blood in the stool and/or normal endoscopic 
findings (Mayo grade 0), especially in confirmed 
microscopic colitis treatment with the topically act-
ing corticosteroid, budesonide (extended-release 
tablets) at a dose of 9 mg daily may be attempt-
ed.4,8,16 Duration of treatment depends on whether 
ICPI is discontinued or not. If ICPI is discontin-
ued, budesonide treatment lasts for 8 weeks, but 
if ICPI is continued, budesonide treatment can be 
maintained continuously. In the event of a discon-
tinuation of budesonide, a gradual dose reduction 
from 9 mg to 6 mg for 14 days and then 3 mg for 14 
days is advised, with careful monitoring of symp-
toms and, if necessary, extending time intervals.4,16 
Mayo grade 1–2 colitis is treated primarily with a 
systemic corticosteroid. Patients without systemic 
signs of food-borne inflammation are prescribed 
TABLE 1. CTCAE gastrointestinal toxicity levels of ICPI2,4
Grade Diarrhoea Colitis
1 Increase in frequency of bowel movements < 4x above baseline; mild increase in ejection via stoma
Asymptomatic; clinical or diagnostic observation only; no 
action required
2 Increase in frequency of bowel movements 4−6x above baseline; moderate increase in ejection via stoma Abdominal pain; mucus or blood in stool
3
Increase in frequency of bowel movements ≥ 7x above baseline, 
incontinence, need for hospitalisation, impaired daily self-care; 
marked increase in ejection via stoma
Severe or persistent abdominal pain; change in bowel 
movements; fever, ileus, peritoneal irritation; medical 
intervention required
4 Life-threatening consequences; need for urgent action Life-threatening consequences; need for urgent action
5 Death Death
CTCAE = Common Terminology Criteria for Adverse Events; ICPI = immune checkpoint inhibitors
TABLE 2. Set of diagnostic tests1-3
Stool tests
Stool culture for pathogenic bacteria (e.g. Yersinia) and viruses
Clostridium difficile toxin
Parasites and parasite eggs
Pancreatic elastase
Inflammatory markers (calprotectin, lactoferrin)
PCR for CMV
Blood tests
Complete blood count
Biochemical tests (liver tests, renal function tests, amylase, lipase, albumin,...)
TSH
Inflammatory markers (CRP, ESR)
Serology for celiac disease (total IgA, tTG)
HIV serology
Imaging
CT scan of the abdomen (for severe abdominal pain)
Endoscopy of the lower GI tract (in all or at least patients with CTCAE grade 
≥ 2)
Investigations before immunosuppressive/biological treatment
Serology for HAV, HBV and HCV, HIV
Quantiferon test
Chest X-ray
CMV = cytomegalovirus; CRP = C-reactive protein; CT = computed tomography; CTCAE = 
Common Terminology Criteria for Adverse Events; ESR = erythrocyte sedimentation rate; GI = 
gastrointestinal; HAV = hepatitis A virus; HBV = hepatitis B virus; HCV = hepatitis C virus; HIV = 
human immunodeficiency virus; IgA = immunoglobulin A; PCR = polymerase chain reaction; 
TSH = thyroid-stimulating hormone; tTG = tissue transglutaminase
Radiol Oncol 2024; 58(2): 179-185.
Ocepek A / Colitis due to cancer treatment with immune check-point inhibitors182
the equivalent of prednisone 0.5–1 mg/kg/day, the 
dose of which is tapered (by 10 mg every 5–7 days) 
until discontinuation after symptoms subside. In 
case of systemic involvement, hospitalisation is 
usually necessary and intravenous methylpredni-
solone 0,5–1 mg/kg/day is recommended in a di-
vided dose every 12 hours. With long-term corti-
costeroid treatment, prophylaxis of pneumocystis 
infection, vitamin D and calcium replacement and 
blood sugar control are recommended.4,16 The most 
severe endoscopic Mayo grade 3 requires treat-
ment with higher doses of methylprednisolone 1–2 
mg/kg/day intravenously and early consideration 
of salvage biologic therapy. In approximately 2/3 
of patients, corticosteroid therapy is sufficient and 
is gradually weaned over 4–8 weeks.1,8,16 However, 
if the colitis does not resolve with corticosteroid 
treatment within 2−5 days, treatment with one of 
the biologic agents, TNF-a inhibitor infliximab or 
integrin a4b7 inhibitor vedolizumab, is indicated.2,6 
The recommended dose of infliximab is 5–10 mg/
kg infused at weeks 0, 2 and 6, and vedolizumab 
dose is 300 mg infused following the same re-
gime.1,3,4 Treatment can be continued with a main-
tenance dose every 8 weeks if needed, depending 
on endoscopic reassessment after 8−10 weeks and 
decision to continue treatment with ICPI.2 In all pa-
tients with colitis grade ≥ 2, at least temporary dis-
continuation of ICPI and consideration of perma-
nent discontinuation of CTLA-4 inhibitor or sub-
stitution with PD-1/PD-L1 inhibitor is necessary.3 
In rare cases, all treatments described so far are 
ineffective and refractory colitis is present. In such 
cases, infectious causes should be excluded again, 
and alternative treatments such as other immu-
nosuppressive drugs (e.g. mycophenolate mofetil, 
tacrolimus, cyclosporine), faecal transplantation or 
extracorporeal photopheresis are possible.1,3,4 Cases 
of treatment of refractory colitis with ustekinumab, 
tofacitinib and abatacept have also been described, 
but caution is advised due to the involvement of 
these drugs in anti-tumour response.2
Prognosis
Overall mortality from ICPI-induced colitis is 5%. 
A more severe disease course should be considered 
in patients treated with a CTLA-4 inhibitor or with 
dual ICPI therapy, as the disease can be progres-
sive and rapidly leads to life-threatening complica-
tions within 14 days.1 
In most cases, recurrence of ICPI-induced coli-
tis after treatment with corticosteroids or biologics 
does not occur if ICPI treatment is discontinued. 
The decision to restart ICPI treatment depends on 
the nature of cancer, severity and likelihood of re-
currence of colitis, and availability of alternative 
treatments. After mild grade 1 colitis has subsid-
ed, continuation with the same ICPI is advised. 
Likelihood of recurrence of colitis is higher with 
CTLA-4 inhibitor therapy or dual (CTLA-4 inhibi-
tor + PD-1/PD-L1 inhibitor) therapy, and therefore 
CTLA-4 inhibitor therapy is advised against after 
severe colitis has subsided. In this case, a switch to 
a PD-1/PD-L1 inhibitor in monotherapy is possible, 
and concomitant maintenance therapy with a bio-
logic may also be considered. At present, evidence 
for long-term safety of such combination therapy 
is limited.2,4
Clinical cases
Case 1
A 71-year-old man with metastatic non-small cell 
K-ras positive lung cancer was treated with the 
PD-1 inhibitor pembrolizumab as a second-line on-
cologic therapy. After the 3rd dose of immunother-
apy, diarrhoea occurred, grade 2. CRP was 5 mg/L 
or less, faecal calprotectin was not determined. 
After excluding an infectious cause, he was treated 
with loperamide, followed by oral mesalazine and 
methylprednisolone at a dose of 0.5 mg/kg/day 
orally. Colonoscopy showed mild hyperaemia and 
oedema of the sigmoid mucosa, endoscopic Mayo 
TABLE 3. Mayo endoscopic score14
Mayo score 0 Mayo score 1 Mayo score 2 Mayo score 3
Disease activity Inactive disease Mild activity Medium activity High activity
Features normal mucosa
erythema,
decreased vascular 
pattern,
mild friability
marked erythema,
absent vascular pattern,
friability,
erosions
spontaneous bleeding, 
ulceration
Radiol Oncol 2024; 58(2): 179-185.
Ocepek A / Colitis due to cancer treatment with immune check-point inhibitors 183
score 1 (Figure 1), with normal mucosa in the rest 
of the colon. 
Random biopsies of endoscopically normal mu-
cosa and biopsies of sigmoid mucosa were histo-
pathologically defined as moderate-to-intense 
aetiologically undefined chronic colitis with pre-
dominant plasma-cell mixed-cell inflammatory 
infiltrate. Following the decision of the multidis-
ciplinary team, the patient received infliximab 
5 mg/kg at standard time intervals on weeks 0 
and 2, which resulted in normalisation of bowel 
movements. Due to concomitant progression of 
malignant disease, treatment was not continued. 
The patient was considered for third line systemic 
oncological therapy, but his general health dete-
riorated and he died 6 months later due to septic 
pneumonia.
Case 2
A 75-year-old man with primary metastatic lung 
adenocarcinoma received the PD-1 inhibitor pem-
brolizumab as first-line systemic oncologic treat-
ment. After 2 applications of pembrolizumab, he 
developed frequent discharges of small amounts 
of mucus. Immunotherapy was stopped, stool cul-
tures were performed and were negative. Despite 
supportive symptomatic treatment and lopera-
mide, the condition worsened and due to diarrhoea 
grade 3, systemic corticosteroid methylpredniso-
lone was started at a dose of 1 mg/kg/day orally. 
After normalisation of bowel movements, the dose 
of methylprednisolone was tapered and discon-
tinued after 6 weeks. 5 days after discontinuation, 
mucous discharge recurred up to 5 times daily and 
abdominal pain appeared, with a CRP of 157 mg/L, 
mild leucocytosis (10.27x109), and normal procalci-
tonin levels (0.11 mg/L). Emergency imaging (plain 
abdominal X-ray, chest X-ray, and abdominal CT) 
excluded life-threatening complications, and signs 
of pancolitis were described. The patient was ad-
mitted to hospital where, after serological investi-
gations (viral hepatitis, HIV and Quantiferon test), 
he received methylprednisolone at a dose of 2 mg/
kg/day intravenously. Endoscopic examination 
showed diffuse mucosal inflammation with ulcera-
tions, endoscopic Mayo score 3 (Figure 2). 
Histology confirmed marked active colitis with 
ulceration, architectural changes of the crypts, 
with extensive areas of acute cryptitis and crypt 
abscesses. Decision of multidisciplinary team was 
to treat the patient with infliximab at a dose of 5 
mg/kg at standard time intervals (weeks 0, 2 and 
6). After only one dose of infliximab, CRP dropped 
to 16 mg/L and after the 2nd dose to normal levels, 
the bowel movements normalised. After the 3rd 
dose of infliximab, the treatment was stopped and 
the patient is being further managed by the treat-
ing oncologist. 
FIGURE 1. Endoscopic image of sigmoid colon in case 1.
FIGURE 2. Endoscopic finding in case 2.
Radiol Oncol 2024; 58(2): 179-185.
Ocepek A / Colitis due to cancer treatment with immune check-point inhibitors184
Case 3
A 72-year-old man received the PD-1 inhibitor 
nivolumab at 14-day intervals as second-line sys-
temic oncologic treatment for metastatic renal 
cell carcinoma. After the first month of treatment, 
diarrhoea, initially grade 2, started. Due to the 
escalation of diarrhoea to grade 3 despite immu-
notherapy withdrawal and supportive treatment 
(dietary measures, oral rehydration, loperamide), 
methylprednisolone was introduced at a dose of 
1 mg/kg/day, to which he responded well. The 
dose of methylprednisolone was gradually tapered 
and discontinued. 10 days after discontinuation, 
diarrhoea recurred and he was restarted on cor-
ticosteroid therapy and referred for colonoscopy. 
Endoscopy showed erythema of the sigmoid mu-
cosa and hyperaemia of the rectal mucosa, endo-
scopic Mayo score 1 (Figure 3). 
Histology showed infiltrates of plasma cells in 
the lamina propria, few lymphocytes, eosinophil-
ic and neutrophilic granulocytes with minimal 
signs of cryptitis, without crypt micro-abscesses. 
Although histological picture was non-specific, 
the pathologist considered it to be consistent with 
ICPI-induced colitis. Following the decision of the 
multidisciplinary team, the patient was treated 
with vedolizumab at a standard dose of 300 mg 
intravenously at time intervals week 0, 2, 6 and 14. 
CT of the chest and abdomen showed stagnation 
of malignant disease and no signs of colitis com-
plications. The patient continues follow-up by the 
treating oncologist.
Conclusions
Immunotherapy represents a breakthrough in 
treatment of various cancers, but can trigger im-
mune-mediated side effects, of which ICPI-induced 
colitis is most common. In most cases, the course 
of colitis is mild or may be effectively treated with 
corticosteroid therapy. Small proportion of pa-
tients require treatment with biologic agents, and 
rarely, more severe form of colitis may trigger life-
threatening complications. In these cases, coopera-
tion between oncologist and gastroenterologist is 
vital to establish a rapid diagnosis with endoscopic 
evaluation and timely escalation of treatment.
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