Protective potential of the gallbladder in primary sclerosing cholangitis.
ABC, ATP-binding cassette transporter
Abcb4 knockout mice
BA, bile acid
Bile acids
C4, 7α-hydroxy-4-cholesten-3-one
CFTR, cystic fibrosis transmembrane conductance regulator
CK19, cytokeratin 19
Cholecystectomy
FGF19, fibroblast growth factor 19
Gallbladder volume
HPLC-MS/MS, high-performance liquid chromatography coupled to tandem mass spectrometry
IBD, inflammatory bowel disease
MRC, magnetic resonance cholangiography
Magnetic resonance imaging
PSC, primary sclerosing cholangitis
UDCA, ursodeoxycholic acid
ULN, upper limit of normal
Journal
JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237
Informations de publication
Date de publication:
Apr 2023
Apr 2023
Historique:
received:
12
08
2022
revised:
23
11
2022
accepted:
03
12
2022
entrez:
16
3
2023
pubmed:
17
3
2023
medline:
17
3
2023
Statut:
epublish
Résumé
Gallbladder enlargement is common in patients with primary sclerosing cholangitis (PSC). The gallbladder may confer hepatoprotection against bile acid overload, through the sequestration and cholecystohepatic shunt of bile acids. The aim of this study was to assess the potential impact of the gallbladder on disease features and bile acid homeostasis in PSC. Patients with PSC from a single tertiary center who underwent liver MRI with three-dimensional cholangiography and concomitant analyses of serum bile acids were included. Gallbladder volume was measured by MRI and a cut-off of 50 ml was used to define gallbladder enlargement. Bile acid profiles and PSC severity, as assessed by blood tests and MRI features, were compared among patients according to gallbladder size (enlarged Sixty-one patients with PSC, all treated with ursodeoxycholic acid (UDCA), were included. The gallbladder was enlarged in 30 patients, whereas 11 patients had been previously cholecystectomized. Patients with enlarged gallbladders had significantly lower alkaline phosphatase, a lower tauro- Altogether, our findings indicate that the gallbladder fulfills protective functions in PSC. In patients with primary sclerosing cholangitis (PSC), gallbladder status impacts on bile acid homeostasis and disease features. We found evidence of lessened bile acid toxicity in patients with PSC and enlarged gallbladders and of increased disease severity in those who were previously cholecystectomized. In the
Sections du résumé
Background & Aims
UNASSIGNED
Gallbladder enlargement is common in patients with primary sclerosing cholangitis (PSC). The gallbladder may confer hepatoprotection against bile acid overload, through the sequestration and cholecystohepatic shunt of bile acids. The aim of this study was to assess the potential impact of the gallbladder on disease features and bile acid homeostasis in PSC.
Methods
UNASSIGNED
Patients with PSC from a single tertiary center who underwent liver MRI with three-dimensional cholangiography and concomitant analyses of serum bile acids were included. Gallbladder volume was measured by MRI and a cut-off of 50 ml was used to define gallbladder enlargement. Bile acid profiles and PSC severity, as assessed by blood tests and MRI features, were compared among patients according to gallbladder size (enlarged
Results
UNASSIGNED
Sixty-one patients with PSC, all treated with ursodeoxycholic acid (UDCA), were included. The gallbladder was enlarged in 30 patients, whereas 11 patients had been previously cholecystectomized. Patients with enlarged gallbladders had significantly lower alkaline phosphatase, a lower tauro-
Conclusion
UNASSIGNED
Altogether, our findings indicate that the gallbladder fulfills protective functions in PSC.
Impact and implications
UNASSIGNED
In patients with primary sclerosing cholangitis (PSC), gallbladder status impacts on bile acid homeostasis and disease features. We found evidence of lessened bile acid toxicity in patients with PSC and enlarged gallbladders and of increased disease severity in those who were previously cholecystectomized. In the
Identifiants
pubmed: 36923239
doi: 10.1016/j.jhepr.2022.100649
pii: S2589-5559(22)00221-X
pmc: PMC10009728
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100649Informations de copyright
© 2022 The Authors.
Déclaration de conflit d'intérêts
Nora Cazzagon, Ester Gonzalez-Sanchez, Haquima El-Mourabit, Dominique Wendum, Dominique Rainteau, Lydie Humbert, Olivier Chazouillères, Lionel Arrivé, Chantal Housset and Sara Lemoinne declare no conflict of interest related to this paper. Christophe Corpechot declares the following conflicts of interest: Intercept, Arrow, Cymabay, Ipsen, Calliditas, Gilead. Please refer to the accompanying ICMJE disclosure forms for further details.
Références
Gut. 1996 Oct;39(4):594-9
pubmed: 8944571
Am J Gastroenterol. 2010 Jun;105(6):1364-73
pubmed: 20068558
Gastroenterology. 2004 Jul;127(1):261-74
pubmed: 15236191
Aliment Pharmacol Ther. 2014 Dec;40(11-12):1292-301
pubmed: 25316001
Semin Liver Dis. 2010 May;30(2):160-77
pubmed: 20422498
World J Gastroenterol. 2009 Jul 28;15(28):3498-503
pubmed: 19630104
Hepatology. 2021 Jul;74(1):281-295
pubmed: 33226645
Liver Int. 2016 Dec;36(12):1867-1875
pubmed: 26945698
Am J Gastroenterol. 2002 May;97(5):1138-42
pubmed: 12014717
Hepatology. 2017 Mar;65(3):907-919
pubmed: 27880989
Am J Gastroenterol. 2019 Dec;114(12):1878-1885
pubmed: 31738286
J Hepatol. 2017 Dec;67(6):1298-1323
pubmed: 28802875
J Gastroenterol. 2020 May;55(5):523-532
pubmed: 31932891
Gastroenterology. 2020 Sep;159(3):915-928
pubmed: 32445859
J Hepatol. 2013 Feb;58(2):329-34
pubmed: 23085647
J Hepatol. 2022 Sep;77(3):761-806
pubmed: 35738507
Compr Physiol. 2016 Jun 13;6(3):1549-77
pubmed: 27347902
Gut. 1973 Oct;14(10):753-62
pubmed: 4758655
Clin Gastroenterol Hepatol. 2013 Jul;11(7):841-6
pubmed: 23353641
Mayo Clin Proc. 2000 Jul;75(7):688-94
pubmed: 10907383
Gut. 2018 Oct;67(10):1864-1869
pubmed: 28739581
Hepatology. 1996 Aug;24(2):289-93
pubmed: 8690394
J Hepatol. 2009 Aug;51(2):237-67
pubmed: 19501929
J Hepatol. 2008 Apr;48(4):598-605
pubmed: 18222013
Gastroenterology. 2017 Jun;152(8):1975-1984.e8
pubmed: 28274849
Biochim Biophys Acta Mol Basis Dis. 2021 Apr 1;1867(4):166067
pubmed: 33418034
Hepatology. 2017 Nov;66(5):1675-1688
pubmed: 28555945
Am J Pathol. 1994 Nov;145(5):1237-45
pubmed: 7977654
Hepatology. 2014 Jan;59(1):242-50
pubmed: 23857427
Eur Radiol. 2022 May;32(5):3358-3368
pubmed: 34918177
Gastroenterology. 2014 Apr;146(4):970-9; quiz e15-6
pubmed: 24389304
AJR Am J Roentgenol. 1988 Mar;150(3):571-4
pubmed: 3277348
Hepatology. 2013 Dec;58(6):2045-55
pubmed: 23775876
Nat Rev Gastroenterol Hepatol. 2022 Jul;19(7):432-450
pubmed: 35165436
Gastroenterology. 2012 Jun;142(7):1581-91.e6
pubmed: 22370478
Autoimmun Rev. 2017 Sep;16(9):885-896
pubmed: 28698093
Hepatology. 2020 Feb;71(2):741-748
pubmed: 31833071
Clin Gastroenterol Hepatol. 2019 Dec;17(13):2785-2792.e3
pubmed: 30880273
Nat Med. 2006 Nov;12(11):1253-5
pubmed: 17072310
J Hepatol. 1997 Jan;26(1):138-45
pubmed: 9148004
J Hepatol. 2014 Jun;60(6):1290-303
pubmed: 24560657
J Chromatogr B Analyt Technol Biomed Life Sci. 2012 Jun 15;899:135-45
pubmed: 22664055
JHEP Rep. 2020 Nov 11;3(2):100214
pubmed: 33604531