Checkpoint Inhibitor-Induced Gastroduodenitis: An Unusual Manifestation

A 44-year-old male presented with an 8-week course of progressively worsening bloating, dysphagia, regurgitation, vomiting, and weight loss (10 kg). He denied any other symptoms. He was diagnosed with metastatic nonsmall cell lung cancer 1 year before and was receiving pembrolizumab infusions every 3 weeks since then. Medication history included omeprazole, duloxetine, and pregabalin. He underwent an elective esophagogastroduodenoscopy that revealed a diffusely swollen and friable gastric mucosa from the cardia to the pylorus, covered with an off-white material due to exudate and sloughing mucosa along with scant food remains (Fig. 1a–c). Additionally, small patches of white exudate were identified in the duodenal bulb (Fig. 1d). Gastric and duodenal biopsies revealed a diffusely active gastroduodenitis with mixed inflammatory infiltration of the lamina propria and glandular distortion associated with ulceration of the mucosa (Fig. 2a). Prominent intraepithelial lymphocytosis, crypt abscess foci, and apoptotic bodies were also seen (Fig. 2b). No evidence of intestinal metaplasia or dysplasia was found. Immunohistochemistry for Helicobacter pylori and cytomegalovirus detection were negative. Checkpoint inhibitor-induced gastroduodenitis was then presumed. Pembrolizumab was withheld, and oral prednisolone was initiated on 1 mg/kg and maintained for 2 weeks, with a subsequent taper dose of 5 mg/week. Symptomatic improvement was seen within days after initiation. Esophagogastroduodenoscopy was repeated 12 weeks later, showing only mild endoscopic improvement. Thus, corticosteroids were reinitiated as previously. Esophagogastroduodenoscopy was repeated at 24 weeks revealing marked endoscopic and histopathologic improvement. Immune-checkpoint inhibitors (ICI) are a class of immunotherapy drugs that lead to an antineoplastic immune response by blocking signalling via either the cyto-