NSAIDs and EGFR Inhibitors for Duodenal Polyp Prevention.

Abstract

Familialadenomatouspolyposis (FAP)andattenuatedFAP(AFAP) are relatedgeneticconditions thatarecharacterizedbymultiple synchronous and metachronous colorectal adenomas with a 70% to 100%riskofdevelopingcolorectal cancer (CRC)and, lessoften,duodenal neoplasia. Although both of these conditions are caused by mutations in the coding region of the adenomatous polyposis coli (APC) tumor suppressor gene, thephenotypespresentquitedistinctly in correlationwith the position of the mutation within the coding region. In classic FAP, which presents with amuch greater polyp burden at an earlier age and a greater risk of CRC than AFAP, the mutation occurs in the central region of the protein, whereas mutations in the Nor CterminusareassociatedwithAFAP.TheAmericanGastroenterological Association recommends an annual sigmoidoscopy, beginning at ages 10 to 12 years, for patients with a genetic diagnosis of FAP, or at-risk familymemberswhohavenotundergonegenetic testing.1 Genetic and endoscopic screening of patients and family members, followed by timely treatment, has led to a 55% reduction in the occurrence of CRC at diagnosis of FAP, and improved cumulative survival amongall FAPpatients. In fact, duodenal cancer is now amore common cause of death than CRC in this population. TreatJAMA