Characteristics of Immune Checkpoint Inhibitor-Associated Gastritis: Report from a Major Tertiary Care Center

Abstract

Background: Immune checkpoint inhibitors (ICIs) have increased our ability to treat an ever-expanding number of cancers. We describe a case series of 25 patients who were diagnosed with gastritis following ICI therapy.

Materials and methods: This was a retrospective study involving 1712 patients treated for malignancy with immunotherapy at Cleveland Clinic from January 2011 to June 2019 (IRB 18-1225). We searched electronic medical records using ICD-10 codes for gastritis diagnosis confirmed on endoscopy and histology within 3 months of ICI therapy. Patients with upper gastrointestinal tract malignancy or documented Helicobacter pylori-associated gastritis were excluded.

Results: Twenty-five patients were found to meet the criteria for diagnosis of gastritis. Of these 25 patients, most common malignancies were non-small cell lung cancer (52%) and melanoma (24%). Median number of infusions preceding symptoms was 4 (1-30) and time to symptom onset 2 (0.5-12) weeks after last infusion. Symptoms experienced were nausea (80%), vomiting (52%), abdominal pain (72%), and melena (44%). Common endoscopic findings were erythema (88%), edema (52%), and friability (48%). The most common diagnosis of pathology was chronic active gastritis in 24% of patients. Ninety-six percent received acid suppression treatment and 36% of patients also received steroids with an initial median dose of prednisone 75 (20-80) mg. Within 2 months, 64% had documented complete resolution of symptoms and 52% were able to resume immunotherapy.

Conclusion: Patients presenting with nausea, vomiting, abdominal pain, or melena following immunotherapy should be assessed for gastritis and if other causes are excluded, may require treatment as consideration for complication of immunotherapy.

Figure 1.

A. Chronic active gastritis: This case exemplifies a severe chronic active gastritis with extensive surface ulceration. Residual glands are present (arrow) and reveal neutrophilic microabscesses. The lamina propria is replaced by mixed inflammatory infiltrate including numerous plasma cells (H&E stain, 200×). B. Focally enhanced gastritis. The sections show lamina propria expansion by plasma cells, scattered lymphocytes, and eosinophils. There is neutrophil mediated injury (arrow). In addition, the surrounding glands demonstrate patchy intraepithelial lymphocytosis (H&E stain, 200×). C. Acute gastritis: gastric mucosa with florid neutrophilic mediated injury, including neutrophilic micro-abscesses and surface erosion (H&E stain, 10×). D. Chronic inactive gastritis: superficial band-like chronic inflammatory infiltrated in the lamina propria with foci of neutrophilic mediated injury, characteristic of chronic inactive gastritis (H&E stain 10×). E. Lymphocytic gastritis: prominent intraepithelial lymphocytes accompanied by a mild infiltrate in the lamina propria (H&E stain, 20×). F. Reactive gastropathy: marked reactive mucin loss in the foveolar epithelium with corkscrewing of gastric pits, capillary congestion and sparse lymphocytes and plasma cells in the lamina propria (H&E stain, 10×).