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Dietary Considerations for Inflammatory Bowel Disease Are Useful for Treatment of Checkpoint Inhibitor-Induced Colitis

SIMPLE SUMMARY: We will briefly review the pathophysiologic, dietary, and genetic factors associated with inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis. This review will elaborate on how the principles developed for the treatment of inflammatory bowel disease can be app...

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Detalles Bibliográficos
Autores principales: Saha, Aditi, Dreyfuss, Isabella, Sarfraz, Humaira, Friedman, Mark, Markowitz, Joseph
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9817715/
https://www.ncbi.nlm.nih.gov/pubmed/36612082
http://dx.doi.org/10.3390/cancers15010084
Descripción
Sumario:SIMPLE SUMMARY: We will briefly review the pathophysiologic, dietary, and genetic factors associated with inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis. This review will elaborate on how the principles developed for the treatment of inflammatory bowel disease can be applied to patients experiencing inflammatory bowel toxicity secondary to checkpoint blockade. The medical oncology and gastroenterology perspectives are presented in this review. ABSTRACT: Checkpoint molecules are cell surface receptors on immune cells that mitigate excessive immune responses, but they have increased expression levels in cancer to facilitate immune escape. Checkpoint blockade therapies (e.g., anti–PD-1, anti–CTLA-4, and anti–LAG-3 therapy, among others) have been developed for multiple cancers. Colitis associated with checkpoint blockade therapy has pathophysiological similarities to inflammatory bowel disease (IBD), such as Crohn’s disease and ulcerative colitis. Current therapeutic guidelines for checkpoint blockade-induced colitis include corticosteroids and, if the patient is refractory to steroids, immunomodulating antibodies, such as anti-TNF and anti-integrin agents. Interestingly, immunomodulatory molecules, such as TNFα, are upregulated in both IBD and checkpoint-mediated colitis. The inflammatory colitis toxicity symptoms from checkpoint blockade are similar to clinical symptoms experienced by patients with IBD. The pathophysiologic, dietary, and genetic factors associated with IBD will be reviewed. We will then explain how the principles developed for the treatment of IBD can be applied to patients experiencing inflammatory bowel toxicity secondary to checkpoint blockade.