Natural history of ampullary adenomas in familial adenomatous polyposis: a long-term follow-up study.


Journal

Gastrointestinal endoscopy
ISSN: 1097-6779
Titre abrégé: Gastrointest Endosc
Pays: United States
ID NLM: 0010505

Informations de publication

Date de publication:
03 2022
Historique:
received: 08 06 2021
accepted: 24 09 2021
pubmed: 9 10 2021
medline: 9 3 2022
entrez: 8 10 2021
Statut: ppublish

Résumé

Ampullary adenomas (AAs), common in familial adenomatous polyposis (FAP), are precursors to ampullary carcinoma. We assessed the natural history of AAs and factors associated with clinically significant progression (CSP). Consecutive FAP patients with AAs and at least 2 EGDs were identified from a hereditary GI cancer registry. We assessed the incidence of CSP (increase in size to ≥10 mm and/or development of advanced histology) of AAs. Clinical, endoscopic, and pathologic features between patients with CSP and nonprogressors were compared. One hundred forty-three patients with AAs were included. Over a median follow-up of 7.8 years (interquartile range, 4.3-11.1), 41 patients (28.6%) developed CSP for an incidence of 35 per 1000 patient-years. Of 143 patients, 22 (15.6%) progressed to AAs ≥10 mm, 12 (8.5%) progressed to advanced histology, and 7 (4.9%) progressed both in size and histology. Two patients (1.4%) developed ampullary cancer. Male gender, abnormal appearance of the papilla at initial AA detection, prior cholecystectomy, and personal history of extracolonic malignancy were associated with CSP. Neither Spigelman stage nor the adenomatous polyposis coli gene pathogenic variants were associated with CSP. An intervention specifically for AA and not duodenal polyposis was performed in 24% of patients with AAs, including endoscopic papillectomy in 23 patients and duodenectomy in 3 patients at a median observation of 8.2 years. Most FAP patients with AAs did not experience CSP or require resection over 8 years of surveillance. Ampullary cancer was rare. Male gender, abnormal appearance of the papilla at AA detection, cholecystectomy, and history of extracolonic malignancy were associated with CSP. Our findings favor endoscopic surveillance of AAs over expedited resection for most patients with FAP.

Sections du résumé

BACKGROUND AND AIMS
Ampullary adenomas (AAs), common in familial adenomatous polyposis (FAP), are precursors to ampullary carcinoma. We assessed the natural history of AAs and factors associated with clinically significant progression (CSP).
METHODS
Consecutive FAP patients with AAs and at least 2 EGDs were identified from a hereditary GI cancer registry. We assessed the incidence of CSP (increase in size to ≥10 mm and/or development of advanced histology) of AAs. Clinical, endoscopic, and pathologic features between patients with CSP and nonprogressors were compared.
RESULTS
One hundred forty-three patients with AAs were included. Over a median follow-up of 7.8 years (interquartile range, 4.3-11.1), 41 patients (28.6%) developed CSP for an incidence of 35 per 1000 patient-years. Of 143 patients, 22 (15.6%) progressed to AAs ≥10 mm, 12 (8.5%) progressed to advanced histology, and 7 (4.9%) progressed both in size and histology. Two patients (1.4%) developed ampullary cancer. Male gender, abnormal appearance of the papilla at initial AA detection, prior cholecystectomy, and personal history of extracolonic malignancy were associated with CSP. Neither Spigelman stage nor the adenomatous polyposis coli gene pathogenic variants were associated with CSP. An intervention specifically for AA and not duodenal polyposis was performed in 24% of patients with AAs, including endoscopic papillectomy in 23 patients and duodenectomy in 3 patients at a median observation of 8.2 years.
CONCLUSIONS
Most FAP patients with AAs did not experience CSP or require resection over 8 years of surveillance. Ampullary cancer was rare. Male gender, abnormal appearance of the papilla at AA detection, cholecystectomy, and history of extracolonic malignancy were associated with CSP. Our findings favor endoscopic surveillance of AAs over expedited resection for most patients with FAP.

Identifiants

pubmed: 34624304
pii: S0016-5107(21)01693-X
doi: 10.1016/j.gie.2021.09.036
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

455-467.e3

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 American Society for Gastrointestinal Endoscopy. Published by Elsevier Inc. All rights reserved.

Auteurs

Achintya D Singh (AD)

Department of Internal Medicine, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Amit Bhatt (A)

Department of Gastroenterology, Hepatology and Nutrition, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA; Sanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Abel Joseph (A)

Department of Internal Medicine, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Ruishen Lyu (R)

Department of Quantitative Health Sciences, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Brandie Heald (B)

Sanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA; Center for Personalized Genetic Healthcare, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Carole Macaron (C)

Department of Gastroenterology, Hepatology and Nutrition, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA; Sanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

David Liska (D)

Sanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA; Department of Colorectal Surgery, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Carol A Burke (CA)

Department of Gastroenterology, Hepatology and Nutrition, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA; Sanford R. Weiss MD Center for Hereditary Colorectal Neoplasia, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA; Department of Colorectal Surgery, Digestive Disease and Surgery Institute, Cleveland Clinic, Cleveland, Ohio, USA.

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