Aspirin exposure and its association with metal stent patency in malignant distal biliary obstruction: a large international multicenter propensity score-matched study.


Journal

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

Informations de publication

Date de publication:
Apr 2024
Historique:
received: 19 07 2023
revised: 12 10 2023
accepted: 01 11 2023
pubmed: 12 11 2023
medline: 12 11 2023
entrez: 11 11 2023
Statut: ppublish

Résumé

Stent dysfunction is common after ERCP with self-expandable metal stent (SEMS) insertion for malignant distal biliary obstruction (MDBO). Chronic aspirin (acetylsalicylic acid; ASA) exposure has been previously shown to potentially decrease this risk. We aim to further ascertain the protective effect of ASA and to identify other predictors of stent dysfunction. This multicenter retrospective cohort study was conducted at 9 sites in Canada and 1 in the United States. Patients with MDBO who underwent ERCP with SEMS placement between January 2014 and December 2019 were included and divided into 2 cohorts: ASA exposed (ASA-E) and ASA unexposed (ASA-U). Propensity-score matching (PSM) was performed to limit selection bias. Matched variables were age, sex, tumor stage, and type of metal stent. The primary outcome was the hazard rate of stent dysfunction. A multivariable Cox proportional hazards model was used to identify independent predictors of stent dysfunction. Of 1396 patients assessed, after PSM 496 patients were analyzed (248 ASA-E and 248 ASA-U). ERCP with SEMS placement was associated with a high clinical success of 82.2% in ASA-E and 81.2% in ASA-U cohorts (P = .80). One hundred eighty-four patients had stent dysfunction with a mean stent patency time of 229.9 ± 306.2 days and 245.4 ± 241.4 days in ASA-E and ASA-U groups, respectively (P = .52). On multivariable analysis, ASA exposure did not protect against stent dysfunction (hazard ratio [HR], 1.25; 95% confidence interval [CI], .96-1.63). An etiology of pancreatic cancer (HR, 1.36; 95% CI, 1.15-1.61) predicted stent dysfunction, whereas cancer therapy was protective (HR, .73; 95% CI, .55-.96). Chronic ASA use was not associated with an increased risk for adverse events including bleeding, post-ERCP pancreatitis, and perforation. In this large, multicenter study using PSM, chronic exposure to ASA did not protect against stent dysfunction in MDBO. Instead, the analysis revealed that the etiology of pancreatic cancer was an independent predictor of stent dysfunction and cancer therapy was protective.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
Stent dysfunction is common after ERCP with self-expandable metal stent (SEMS) insertion for malignant distal biliary obstruction (MDBO). Chronic aspirin (acetylsalicylic acid; ASA) exposure has been previously shown to potentially decrease this risk. We aim to further ascertain the protective effect of ASA and to identify other predictors of stent dysfunction.
METHODS METHODS
This multicenter retrospective cohort study was conducted at 9 sites in Canada and 1 in the United States. Patients with MDBO who underwent ERCP with SEMS placement between January 2014 and December 2019 were included and divided into 2 cohorts: ASA exposed (ASA-E) and ASA unexposed (ASA-U). Propensity-score matching (PSM) was performed to limit selection bias. Matched variables were age, sex, tumor stage, and type of metal stent. The primary outcome was the hazard rate of stent dysfunction. A multivariable Cox proportional hazards model was used to identify independent predictors of stent dysfunction.
RESULTS RESULTS
Of 1396 patients assessed, after PSM 496 patients were analyzed (248 ASA-E and 248 ASA-U). ERCP with SEMS placement was associated with a high clinical success of 82.2% in ASA-E and 81.2% in ASA-U cohorts (P = .80). One hundred eighty-four patients had stent dysfunction with a mean stent patency time of 229.9 ± 306.2 days and 245.4 ± 241.4 days in ASA-E and ASA-U groups, respectively (P = .52). On multivariable analysis, ASA exposure did not protect against stent dysfunction (hazard ratio [HR], 1.25; 95% confidence interval [CI], .96-1.63). An etiology of pancreatic cancer (HR, 1.36; 95% CI, 1.15-1.61) predicted stent dysfunction, whereas cancer therapy was protective (HR, .73; 95% CI, .55-.96). Chronic ASA use was not associated with an increased risk for adverse events including bleeding, post-ERCP pancreatitis, and perforation.
CONCLUSIONS CONCLUSIONS
In this large, multicenter study using PSM, chronic exposure to ASA did not protect against stent dysfunction in MDBO. Instead, the analysis revealed that the etiology of pancreatic cancer was an independent predictor of stent dysfunction and cancer therapy was protective.

Identifiants

pubmed: 37951281
pii: S0016-5107(23)03040-7
doi: 10.1016/j.gie.2023.11.004
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

557-565

Informations de copyright

Copyright © 2024 American Society for Gastrointestinal Endoscopy. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Disclosure The following author received research support for this study from the Fonds de Recherche du Québec–Santé: Y.-I Chen. In addition, the following authors disclosed financial relationships: N. Forbes: Consultant for Pentax Medical, Boston Scientific, and AstraZeneca; speaker for Pentax Medical. D. Pleskow: Consultant for Boston Scientific, Olympus, Fuji, Medtronic, Nine Point, and Allurion. Y.-I Chen: Consultant for Boston Scientific; shareholder of Chess Medical Inc. All other authors disclosed no financial relationships.

Auteurs

Kristina Candido (K)

Division of Gastroenterology and Hepatology, McGill University Health Center, Montreal, Quebec, Canada.

Simon Bouchard (S)

Division of Gastroenterology and Hepatology, Centre hospitalier de l'université de Montréal, Montreal, Quebec, Canada.

Christopher Hansen-Barkun (C)

Division of Gastroenterology and Hepatology, Providence Health Care, St Paul's Hospital, Vancouver, British Columbia, Canada.

Dora C Huang (DC)

Digestive Disease Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.

Avijit Chatterjee (A)

Division of Gastroenterology and Hepatology, The Ottawa Hospital, Ottawa, Ontario, Canada.

Charles Menard (C)

Division of Gastroenterology, Centre hospitalier universitaire de Sherbrooke, Sherbrooke, Quebec, Canada.

Corey Miller (C)

Digestive Disease Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.

Gurpal Sandha (G)

Division of Gastroenterology and Hepatology, University of Alberta Hospital, Edmonton, Alberta, Canada.

Fergal Donnellan (F)

Division of Gastroenterology and Hepatology, Vancouver Coastal Health Research Institute, Vancouver General Hospital, Vancouver, British Columbia, Canada.

Jennifer Telford (J)

Division of Gastroenterology and Hepatology, Providence Health Care, St Paul's Hospital, Vancouver, British Columbia, Canada.

Etienne Desilets (E)

Division of Gastroenterology, Hôpital Charles-Le Moyne, Longueuil, Quebec, Canada.

Nauzer Forbes (N)

Division of Gastroenterology and Hepatology, Peter Lougheed Centre, University of Calgary, Calgary, Alberta, Canada.

Andre Roy (A)

Division of Gastroenterology and Hepatology, Centre hospitalier de l'université de Montréal, Montreal, Quebec, Canada.

Natalia Calo (N)

Division of Gastroenterology and Hepatology, The Ottawa Hospital, Ottawa, Ontario, Canada.

Ian Gan (I)

Division of Gastroenterology and Hepatology, Vancouver Coastal Health Research Institute, Vancouver General Hospital, Vancouver, British Columbia, Canada.

Eric Lam (E)

Division of Gastroenterology and Hepatology, Providence Health Care, St Paul's Hospital, Vancouver, British Columbia, Canada.

Douglas Pleskow (D)

Digestive Disease Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.

Jeremy Liu Chen Kiow (JL)

Division of Gastroenterology and Hepatology, Centre hospitalier de l'université de Montréal, Montreal, Quebec, Canada.

Avi Sarker (A)

Division of Gastroenterology and Hepatology, The Ottawa Hospital, Ottawa, Ontario, Canada.

Etienne Cadieux-Genesse (E)

Division of Gastroenterology, Centre hospitalier universitaire de Sherbrooke, Sherbrooke, Quebec, Canada.

Avni Jain (A)

Division of Gastroenterology and Hepatology, Vancouver Coastal Health Research Institute, Vancouver General Hospital, Vancouver, British Columbia, Canada.

Felix Louis (F)

Division of Gastroenterology, Hôpital Charles-Le Moyne, Longueuil, Quebec, Canada.

Mohammad Bilal (M)

Digestive Disease Center, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.

Pape-Mamadou Sene (PM)

Division of Gastroenterology and Hepatology, Centre hospitalier de l'université de Montréal, Montreal, Quebec, Canada.

Jehovan Fairclough (J)

Division of Gastroenterology and Hepatology, The Ottawa Hospital, Ottawa, Ontario, Canada.

Jacqueline Reuangrith (J)

Division of Gastroenterology and Hepatology, Centre hospitalier de l'université de Montréal, Montreal, Quebec, Canada.

Amine Benmassaoud (A)

Division of Gastroenterology and Hepatology, McGill University Health Center, Montreal, Quebec, Canada.

Olivia Geraci (O)

Division of Gastroenterology and Hepatology, McGill University Health Center, Montreal, Quebec, Canada.

Myriam Martel (M)

Division of Gastroenterology and Hepatology, McGill University Health Center, Montreal, Quebec, Canada.

Yen-I Chen (YI)

Division of Gastroenterology and Hepatology, McGill University Health Center, Montreal, Quebec, Canada.

Classifications MeSH