Antitumor response to microscopic melanoma in the gastric mucosa mimicking ipilimumab-induced gastritis

• Main Authors: Elisa Bello, Justine V. Cohen, Mari Mino-Kenudson, Michael Dougan
• Format: Article
• Language: English
• Published: BMJ Publishing Group 2019-02-01
• Series: Journal for ImmunoTherapy of Cancer
• Online Access: http://link.springer.com/article/10.1186/s40425-019-0524-1

Abstract Background Alongside its clinical success, checkpoint blockade has also given rise to a set of immune-related adverse events (irAEs). In addition to causing considerable morbidity and even mortality, irAEs may limit the success and scope of immunotherapy. Most irAEs arise at mucosal barriers, including the gastrointestinal mucosa, leading most commonly to colitis, though both gastritis and enteritis can result from checkpoint blockade. While guidelines generally recommend confirmatory testing for suspected severe irAEs, the role of endoscopy in diagnosing more moderate irAEs is less clear. Many patients with suspected gastrointestinal irAEs are treated empirically with glucocorticoids based on typical symptoms. Although efficient, this approach may miss less common underlying etiologies, and may expose patients unnecessarily to an increased risk of infection, and a potentially dampened antitumor response. Case presentation We report a case of ipilimumab-induced antitumor immunity targeting microscopic gastric melanoma metastases, mimicking checkpoint blockade induced gastritis. Immune suppression was avoided and the immunotherapy was continued. Conclusion Checkpoint blockade can induce rapid inflammatory responses to tumor tissue present throughout the body. These responses are desirable, but may also lead to local tissue injury, causing symptoms that may mimic adverse events. This is particularly important to consider in organs where metastatic disease may be unappreciated at the time of treatment, and where irAEs are otherwise common, such as the gastrointestinal tract. In this setting, empiric immune suppression may inhibit antitumor responses, improving symptoms but at a potential cost to therapeutic efficacy.