Ingrid C A W Konings1, Femme Harinck, Jan-Werner Poley, Cora M Aalfs, Anja van Rens, Nanda C Krak, Anja Wagner, C Yung Nio, Rolf H Sijmons, Hendrik M van Dullemen, Frank P Vleggaar, Margreet G E M Ausems, Paul Fockens, Jeanin E van Hooft, Marco J Bruno. 1. From the *Department of Gastroenterology and Hepatology, Erasmus MC, University Medical Center, Rotterdam; †Department of Clinical Genetics, Academic Medical Center; and ‡Family Cancer Clinic Cancer Institute, Amsterdam; Departments of §Radiology and ∥Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam; ¶Department of Radiology, Academic Medical Center, Amsterdam; #Department of Genetics, University of Groningen, and **Department of Gastroenterology and Hepatology, University Medical Center, Groningen; Departments of ††Gastroenterology and Hepatology and ‡‡Clinical Genetics, University Medical Center, Utrecht; and §§Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, the Netherlands.
Abstract
OBJECTIVES: The aim of this study was to compare the prevalence of cystic pancreatic lesions and their natural behavior in 2 distinct high-risk groups for developing pancreatic ductal adenocarcinoma (PDAC): (1) carriers of a mutation that predisposes to PDAC and (2) individuals without a known gene mutation but with a family history of PDAC (familial pancreatic cancer [FPC]). METHODS: Pancreatic surveillance by annual magnetic resonance imaging and endoscopic ultrasound was performed in individuals with an estimated lifetime risk of developing PDAC of 10% or greater. Progression of a lesion was defined as growth 4 mm or greater or the development of worrisome features. RESULTS: We included 186 individuals: 98 mutation carriers and 88 FPC individuals (mean follow-up, 51 months). Individuals with FPC were significantly more likely than mutation carriers to have a pancreatic cyst 10 mm or greater (16% vs 5%, P = 0.045). Pancreatic cysts detected in mutation carriers, however, were significantly more likely to progress than those in FPC individuals (16% vs 2%, P = 0.050). CONCLUSIONS: This study provides evidence that the prevalence and growth characteristics of pancreatic cysts differ between distinct high-risk groups: individuals with FPC have a higher prevalence of pancreatic cysts 10 mm or greater, whereas cysts in mutation carriers are more likely to progress. These observations may help to develop more optimally tailored surveillance strategies in specific high-risk populations.
OBJECTIVES: The aim of this study was to compare the prevalence of cystic pancreatic lesions and their natural behavior in 2 distinct high-risk groups for developing pancreatic ductal adenocarcinoma (PDAC): (1) carriers of a mutation that predisposes to PDAC and (2) individuals without a known gene mutation but with a family history of PDAC (familial pancreatic cancer [FPC]). METHODS: Pancreatic surveillance by annual magnetic resonance imaging and endoscopic ultrasound was performed in individuals with an estimated lifetime risk of developing PDAC of 10% or greater. Progression of a lesion was defined as growth 4 mm or greater or the development of worrisome features. RESULTS: We included 186 individuals: 98 mutation carriers and 88 FPC individuals (mean follow-up, 51 months). Individuals with FPC were significantly more likely than mutation carriers to have a pancreatic cyst 10 mm or greater (16% vs 5%, P = 0.045). Pancreatic cysts detected in mutation carriers, however, were significantly more likely to progress than those in FPC individuals (16% vs 2%, P = 0.050). CONCLUSIONS: This study provides evidence that the prevalence and growth characteristics of pancreatic cysts differ between distinct high-risk groups: individuals with FPC have a higher prevalence of pancreatic cysts 10 mm or greater, whereas cysts in mutation carriers are more likely to progress. These observations may help to develop more optimally tailored surveillance strategies in specific high-risk populations.
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