Pancreatobiliary manifestations of nonalcoholic fatty liver disease: a retrospective case-control multicenter study.
Journal
European journal of gastroenterology & hepatology
ISSN: 1473-5687
Titre abrégé: Eur J Gastroenterol Hepatol
Pays: England
ID NLM: 9000874
Informations de publication
Date de publication:
01 05 2021
01 05 2021
Historique:
pubmed:
3
6
2020
medline:
10
8
2021
entrez:
3
6
2020
Statut:
ppublish
Résumé
Nonalcoholic fatty liver disease (NAFLD) has become a major cause of chronic liver disease. Several extrahepatic manifestations have been reported in relation to NAFLD. However, data regarding pancreatobiliary manifestation are scarce. We aimed to explore the association of pancreatobiliary manifestation with NAFLD. A retrospective multicenter study that included all patients who underwent an endoscopic ultrasound performed for hepatobiliary indications and for whom the endosonographer reported on the presence or absence of fatty liver. The endoscopic ultrasound reports were reviewed and all pathological findings were reported. Overall, 545 patients were included in the study, among them, 278 patients had fatty liver (group A) as compared to 267 who did not have (group B). The average age in group A was 64.5 ± 13.5 years vs. 61.2 ± 14.7 years in group B. Male sex constituted 49.6 and 58% in groups A and B, respectively. On multivariate analysis, fatty pancreas [odds ratio (OR) 4.02; P = 0.001], serous cystadenoma (SCA) (OR 5.1; P = 0.0009), mucinous cystadenoma (MCA) (OR 9.7; P = 0.005), side-branch intraductal papillary mucinous neoplasm (IPMN) (OR 2.76; P < 0.0001), mixed-type IPMN (OR 16.4; P = 0.0004), pancreatic neuroendocrine tumor (NET) (OR 8.76; P < 0.0001), gallbladder stones (OR 1.9; P = 0.02) and hilar lymphadenopathy (OR 6.8; P < 0.0001) were significantly higher among patients with NAFLD. After adjustment for fatty pancreas, the association remained significant for SCA (OR 3; P = 0.01), MCA (OR 4.6; P = 0.03), side-branch IPMN (OR 1.7; P = 0.02), mixed-type IPMN (OR 5.5; P = 0.01) and pancreatic NET (OR 4.5; P = 0.001). Pancreatobiliary manifestations are common among patients with NAFLD. Assessment of these coexistent manifestations should be considered in the setting of patients with NAFLD.
Sections du résumé
BACKGROUND
Nonalcoholic fatty liver disease (NAFLD) has become a major cause of chronic liver disease. Several extrahepatic manifestations have been reported in relation to NAFLD. However, data regarding pancreatobiliary manifestation are scarce.
AIM
We aimed to explore the association of pancreatobiliary manifestation with NAFLD.
METHODS
A retrospective multicenter study that included all patients who underwent an endoscopic ultrasound performed for hepatobiliary indications and for whom the endosonographer reported on the presence or absence of fatty liver. The endoscopic ultrasound reports were reviewed and all pathological findings were reported.
RESULTS
Overall, 545 patients were included in the study, among them, 278 patients had fatty liver (group A) as compared to 267 who did not have (group B). The average age in group A was 64.5 ± 13.5 years vs. 61.2 ± 14.7 years in group B. Male sex constituted 49.6 and 58% in groups A and B, respectively. On multivariate analysis, fatty pancreas [odds ratio (OR) 4.02; P = 0.001], serous cystadenoma (SCA) (OR 5.1; P = 0.0009), mucinous cystadenoma (MCA) (OR 9.7; P = 0.005), side-branch intraductal papillary mucinous neoplasm (IPMN) (OR 2.76; P < 0.0001), mixed-type IPMN (OR 16.4; P = 0.0004), pancreatic neuroendocrine tumor (NET) (OR 8.76; P < 0.0001), gallbladder stones (OR 1.9; P = 0.02) and hilar lymphadenopathy (OR 6.8; P < 0.0001) were significantly higher among patients with NAFLD. After adjustment for fatty pancreas, the association remained significant for SCA (OR 3; P = 0.01), MCA (OR 4.6; P = 0.03), side-branch IPMN (OR 1.7; P = 0.02), mixed-type IPMN (OR 5.5; P = 0.01) and pancreatic NET (OR 4.5; P = 0.001).
CONCLUSION
Pancreatobiliary manifestations are common among patients with NAFLD. Assessment of these coexistent manifestations should be considered in the setting of patients with NAFLD.
Identifiants
pubmed: 32483086
pii: 00042737-202105000-00019
doi: 10.1097/MEG.0000000000001780
doi:
Types de publication
Journal Article
Multicenter Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
722-726Informations de copyright
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
Références
Fassio E, Alvarez E, Domínguez N, Landeira G, Longo C. Natural history of nonalcoholic steatohepatitis: a longitudinal study of repeat liver biopsies. Hepatology. 2004; 40:820–826.
Ahmed A, Wong RJ, Harrison SA. Nonalcoholic fatty liver disease review: diagnosis, treatment, and outcomes. Clin Gastroenterol Hepatol. 2015; 13:2062–2070.
Byrne CD, Targher G. NAFLD: a multisystem disease. J Hepatol. 2015; 62:S47–S64.
Anstee QM, Targher G, Day CP. Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis. Nat Rev Gastroenterol Hepatol. 2013; 10:330–344.
VanWagner LB, Rinella ME. Extrahepatic manifestations of nonalcoholic fatty liver disease. Curr Hepatol Rep. 2016; 15:75–85.
Hou S, Tang X, Cui H, Liu C, Bai X, Shi L, Shi Y. Fatty liver disease is associated with the severity of acute pancreatitis:a systematic review and meta-analysis. Int J Surg. 2019; 65:147–153.
Mikolasevic I, Orlic L, Poropat G, Jakopcic I, Stimac D, Klanac A, et al. Nonalcoholic fatty liver and the severity of acute pancreatitis. Eur J Intern Med. 2017; 38:73–78.
Uygun A, Kadayifci A, Demirci H, Saglam M, Sakin YS, Ozturk K, et al. The effect of fatty pancreas on serum glucose parameters in patients with nonalcoholic steatohepatitis. Eur J Intern Med. 2015; 26:37–41.
Idilman IS, Tuzun A, Savas B, Elhan AH, Celik A, Idilman R, Karcaaltincaba M. Quantification of liver, pancreas, kidney, and vertebral body MRI-PDFF in non-alcoholic fatty liver disease. Abdom Imaging. 2015; 40:1512–1519.
Koller T, Kollerova J, Hlavaty T, Huorka M, Payer J. Cholelithiasis and markers of nonalcoholic fatty liver disease in patients with metabolic risk factors. Scand J Gastroenterol. 2012; 47:197–203.
Loria P, Lonardo A, Lombardini S, Carulli L, Verrone A, Ganazzi D, et al. Gallstone disease in non-alcoholic fatty liver: prevalence and associated factors. J Gastroenterol Hepatol. 2005; 20:1176–1184.
Al-Haddad M, Khashab M, Zyromski N, Pungpapong S, Wallace MB, Scolapio J, et al. Risk factors for hyperechogenic pancreas on endoscopic ultrasound: a case-control study. Pancreas. 2009; 38:672–675.
Sepe PS, Ohri A, Sanaka S, Berzin TM, Sekhon S, Bennett G, et al. A prospective evaluation of fatty pancreas by using EUS. Gastrointest Endosc. 2011; 73:987–993.
Das A, Ngamruengphong S, Nagendra S, Chak A. Asymptomatic pancreatic cystic neoplasm: a cost-effectiveness analysis of different strategies of management. Gastrointest Endosc. 2009; 70:690–699.e6.
Federico A, Dallio M, Masarone M, Persico M, Loguercio C. The epidemiology of non-alcoholic fatty liver disease and its connection with cardiovascular disease: role of endothelial dysfunction. Eur Rev Med Pharmacol Sci. 2016; 20:4731–4741.
Adams LA, Lymp JF, St Sauver J, Sanderson SO, Lindor KD, Feldstein A, Angulo P. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology. 2005; 129:113–121.
Angulo P, Kleiner DE, Dam-Larsen S, Adams LA, Bjornsson ES, Charatcharoenwitthaya P, et al. Liver fibrosis, but no other histologic features, is associated with long-term outcomes of patients with nonalcoholic fatty liver disease. Gastroenterology. 2015; 149:389–97.e10.
Li AA, Ahmed A, Kim D. Extrahepatic manifestations of nonalcoholic fatty liver disease. Gut Liver. 2020; 14:168–178.
Khoury T, Asombang AW, Berzin TM, Cohen J, Pleskow DK, Mizrahi M. The clinical implications of fatty pancreas: a concise review. Dig Dis Sci. 2017; 62:2658–2667.
Zerboni G, Capurso G, Di Pietropaolo M, Carbonetti F, Iannicelli E, Marignani M, Delle Fave G. The prevalence of pancreatic cystic lesions in patients with liver cirrhosis is double that in controls. United European Gastroenterol J. 2017; 5:1007–1014.
Kalaitzakis E, Gunnarsdottir SA, Josefsson A, Björnsson E. Increased risk for malignant neoplasms among patients with cirrhosis. Clin Gastroenterol Hepatol. 2011; 9:168–174.
Prystupa A, Kiciński P, Sak J, Boguszewska-Czubara A, Toruń-Jurkowska A, Załuska W. Proinflammatory cytokines (IL-1α, IL-6) and hepatocyte growth factor in patients with alcoholic liver cirrhosis. Gastroenterol Res Pract. 2015; 2015:532615.
Porowski D, Wirkowska A, Hryniewiecka E, Wyzgał J, Pacholczyk M, Pączek L. Liver failure impairs the intrahepatic elimination of interleukin-6, tumor necrosis factor-alpha, hepatocyte growth factor, and transforming growth factor-beta. Biomed Res Int. 2015; 2015:934065.
du Plessis J, van Pelt J, Korf H, Mathieu C, van der Schueren B, Lannoo M, et al. Association of adipose tissue inflammation with histologic severity of nonalcoholic fatty liver disease. Gastroenterology. 2015; 149:635–48.e14.
Daher S, Lev Cohen N, Massarwa M, Mahamid M, Nasser M, Hazou W, et al. Portal lymphadenopathy predicts non-alcoholic steatohepatitis and advanced fibrosis in non-alcoholic fatty liver disease. PLoS One. 2018; 13:e0207479.
Qiao QH, Zhu WH, Yu YX, Huang FF, Chen LY. Nonalcoholic fatty liver was associated with asymptomatic gallstones in a Chinese population. Medicine (Baltimore). 2017; 96:e7853.
Arrese M, Cortés V, Barrera F, Nervi F. Nonalcoholic fatty liver disease, cholesterol gallstones, and cholecystectomy: new insights on a complex relationship. Curr Opin Gastroenterol. 2018; 34:90–96.
Chen LY, Qiao QH, Zhang SC, Chen YH, Chao GQ, Fang LZ. Metabolic syndrome and gallstone disease. World J Gastroenterol. 2012; 18:4215–4220.
Lonardo A, Ballestri S, Marchesini G, Angulo P, Loria P. Nonalcoholic fatty liver disease: a precursor of the metabolic syndrome. Dig Liver Dis. 2015; 47:181–190.