Primary biliary cholangitis with metabolic associated fatty liver disease： Clinical features and risk factors

Linna YUAN; Yihui CHEN; Hengbin NA; Jie LU; Ye LIU; Wu LI

doi:10.12449/JCH240815

Volume 40 Issue 8

Aug. 2024

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Article Navigation > Journal of Clinical Hepatology > 2024 > 40(8): 1598-1604

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Primary biliary cholangitis with metabolic associated fatty liver disease： Clinical features and risk factors

DOI: 10.12449/JCH240815

Linna YUAN¹,
Yihui CHEN²,
Hengbin NA¹,
Jie LU¹,
Ye LIU¹,
Wu LI^{2
,
,
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1.
Department of Psychiatry ‍I‍，Yunnan Provincial Hospital of Infectious Diseases/Yunnan Mental Health Center，Anning，Yunnan 650302，China
2.
Department of Infection and Liver Diseases，The First Affiliated Hospital of Kunming Medical University，Kunming 650032，China

Research funding:

National Natural Science Foundation of China (82160801);

Yunnan Province Famous Doctor Project (Yunrenweifa（2020）20);

Yunnan Province Famous Doctor Project (RLMY20200015);

Yunnan Provincial Department of Science and Technology-Applied Basic Research Joint Special Fund Project (2018FE001（-214）)

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Corresponding author: LI Wu， liwukm@qq.com （ORCID： 0000-0002-1222-3629）
Received Date: 2023-04-22
Accepted Date: 2023-05-18
Published Date: 2024-08-25

Abstract

Abstract

Objective To investigate the clinical features and risk factors of primary biliary cholangitis （PBC） comorbid with metabolic associated fatty liver disease （MAFLD） and the interaction between the two diseases. Methods A total of 187 patients who were diagnosed with PBC， MAFLD， or PBC with MAFLD in The First Affiliated Hospital of Kunming Medical University from January 2019 to December 2022 were enrolled and divided into PBC group with 70 patients， PBC+MAFLD group with 38 patients， and MAFLD group with 79 patients. Related data were collected， including general information， clinical symptoms， serological parameters， transient elastography （FibroScan）， and non-invasive fibrosis markers， which were compared between the three groups. A one-way analysis of variance or the Kruskal-Wallis H test was used for comparison of continuous data between groups， the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups， and the binary Logistic regression analysis was used for multivariate analysis. Results There were significant differences between the three groups in sex， age， height， weight， body mass index （BMI）， and history of autoimmune diseases （P<0.05）. In the PBC+MAFLD group， female patients accounted for 89.5%， with a mean age of 57.26±12.72 years and a BMI of 23.35±3.70 kg/m²， and in the PBC group， the detection rate of autoimmune diseases was 25.7% （18 patients）. There were significant differences between the three groups in the incidence rates of weakness， poor appetite， pruritus， jaundice， varices， ascites， and splenomegaly （all P<0.05）. The PBC+MAFLD group had the common symptoms of weakness in 18 patients （47.4%）， poor appetite in 15 patients （39.5%）， abdominal pain in 14 patients （36.8%）， and abdominal distension in 16 patients （42.1%）； the MAFLD group had the common symptoms of abdominal pain in 34 patients （43%） and abdominal distension in 32 patients （40.5%）； the PBC group had the common symptoms of weakness in 37 patients （52.9%）， poor appetite in 25 patients （35.7%）， jaundice in 25 patients （35.7%）， abdominal pain in 18 patients （25.7%）， abdominal distension in 25 patients （35.7%）， varices in 19 patients （27.9%）， ascites in 23 patients （32.9%）， and splenomegaly in 44 patients （62.9%）. The PBC+MAFLD group had a controlled attenuation parameter （CAP）， which was higher than that of the PBC group， and the PBC group had significantly higher levels of liver stiffness measurement， aspartate aminotransferase-to-platelet ratio index （APRI）， and fibrosis-4 （FIB-4） than the MAFLD group （all P<0.05）. The factors without multicollinearity were included in the regression analysis， and with the PBC group as the reference group， FIB-4 （odds ratio ［OR］=0.218， 95% confidence interval ［CI］： 0.069 ‍—‍ 0.633， P<0.05） and history of autoimmune diseases （OR=0.229， 95%CI： 0.067‍ — ‍0.810， P<0.05） were influencing factors for the onset of PBC with MAFLD； with the MAFLD group as the reference group， ALT （OR=0.157， 95%CI： 0.025‍ —‍ ‍1.000， P<0.05） and TBil （OR=0.995， 95%CI： 0.990‍‍ — ‍0.999， P<0.05） were influencing factors for the onset of PBC with MAFLD. Conclusion PBC with MAFLD lacks specific clinical manifestations， and PBC patients tend to have more severe clinical manifestations and a higher incidence rate of liver function decompensation. PBC comorbid with MAFLD may not aggravate the disease progression of PBC.
- Primary Biliary Cholangitis,
- Metabolism Associated Fatty Liver Disease,
- Risk Factors

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References

[1]	Chinese Society of Hepatology, Chinese Medical Association. Guidelines on the diagnosis and management of primary biliary cholangitis(2021)[J]. J Clin Hepatol, 2022, 38( 1): 35- 41. 中华医学会肝病学分会. 原发性胆汁性胆管炎的诊断和治疗指南(2021)[J]. 临床肝胆病杂志, 2022, 38( 1): 35- 41.
[2]	XUE R, FAN JG. Brief introduction of an international expert consensus statement: A new definition of metabolic associated fatty liver disease[J]. J Clin Hepatol, 2020, 36( 6): 1224- 1227. DOI: 10.3969/j.issn.1001-5256.2020.06.007. 薛芮, 范建高. 代谢相关脂肪性肝病新定义的国际专家共识简介[J]. 临床肝胆病杂志, 2020, 36( 6): 1224- 1227. DOI: 10.3969/j.issn.1001-5256.2020.06.007
[3]	BRUNT EM, RAMRAKHIANI S, CORDES BG, et al. Concurrence of histologic features of steatohepatitis with other forms of chronic liver disease[J]. Mod Pathol, 2003, 16( 1): 49- 56. DOI: 10.1097/01.MP.0000042420.21088.C7.
[4]	JEFFERY ND, HAMILTON L, GRANGER N. Designing clinical trials in canine spinal cord injury as a model to translate successful laboratory interventions into clinical practice[J]. Vet Rec, 2011, 168( 4): 102- 107. DOI: 10.1136/vr.d475.
[5]	SEIKE T, KOMURA T, SHIMIZU Y, et al. A young man with non-alcoholic steatohepatitis and serum anti-mitochondrial antibody positivity[J]. Intern Med, 2018, 57( 21): 3093- 3097. DOI: 10.2169/internalmedicine.0405-17.
[6]	ESLAM M, SARIN SK, WONG VWS, et al. The Asian Pacific Association for the Study of the Liver clinical practice guidelines for the diagnosis and management of metabolic associated fatty liver disease[J]. Hepatol Int, 2020, 14( 6): 889- 919. DOI: 10.1007/s12072-020-10094-2.
[7]	ILUZ-FREUNDLICH D, UHANOVA J, GRUBERT VAN IDERSTINE M, et al. The impact of primary biliary cholangitis on non-alcoholic fatty liver disease[J]. Eur J Gastroenterol Hepatol, 2021, 33( 4): 565- 570. DOI: 10.1097/MEG.0000000000001782.
[8]	LAN RY, CHENG CM, LIAN ZX, et al. Liver-targeted and peripheral blood alterations of regulatory T cells in primary biliary cirrhosis[J]. Hepatology, 2006, 43( 4): 729- 737. DOI: 10.1002/hep.21123.
[9]	SÖDERBERG C, MARMUR J, ECKES K, et al. Microvesicular fat, inter cellular adhesion molecule-1 and regulatory T-lymphocytes are of importance for the inflammatory process in livers with non-alcoholic steatohepatitis[J]. APMIS, 2011, 119( 7): 412- 420. DOI: 10.1111/j.1600-0463.2011.02746.x.
[10]	ODIN JA, HUEBERT RC, CASCIOLA-ROSEN L, et al. Bcl-2-dependent oxidation of pyruvate dehydrogenase-E2, a primary biliary cirrhosis autoantigen, during apoptosis[J]. J Clin Invest, 2001, 108( 2): 223- 232. DOI: 10.1172/JCI10716.
[11]	MA C, KESARWALA AH, EGGERT T, et al. NAFLD causes selective CD4(+‍) T lymphocyte loss and promotes hepatocarcinogenesis[J]. Nature, 2016, 531( 7593): 253- 257. DOI: 10.1038/nature16969.
[12]	HÍNDI M, LEVY C, COUTO CA, et al. Primary biliary cirrhosis is more severe in overweight patients[J]. J Clin Gastroenterol, 2013, 47( 3): e28- e32. DOI: 10.1097/MCG.0b013e318261e659.
[13]	FRIEDRICH-RUST M, MÜLLER C, WINCKLER A, et al. Assessment of liver fibrosis and steatosis in PBC with FibroScan, MRI, MR-spectroscopy, and serum markers[J]. J Clin Gastroenterol, 2010, 44( 1): 58- 65. DOI: 10.1097/MCG.0b013e3181a84b8d.
[14]	SORRENTINO P, TERRACCIANO L, D’ANGELO S, et al. Oxidative stress and steatosis are cofactors of liver injury in primary biliary cirrhosis[J]. J Gastroenterol, 2010, 45( 10): 1053- 1062. DOI: 10.1007/s00535-010-0249-x.
[15]	BERZIGOTTI A, GARCIA-TSAO G, BOSCH J, et al. Obesity is an independent risk factor for clinical decompensation in patients with cirrhosis[J]. Hepatology, 2011, 54( 2): 555- 561. DOI: 10.1002/hep.24418.
[16]	TSUNEYAMA K, BABA H, KIKUCHI K, et al. Autoimmune features in metabolic liver disease: A single-center experience and review of the literature[J]. Clin Rev Allergy Immunol, 2013, 45( 1): 143- 148. DOI: 10.1007/s12016-013-8383-x.
[17]	ALEFFI S, PETRAI I, BERTOLANI C, et al. Upregulation of proinflammatory and proangiogenic cytokines by leptin in human hepatic stellate cells[J]. Hepatology, 2005, 42( 6): 1339- 1348. DOI: 10.1002/hep.20965.
[18]	MARRA F, BERTOLANI C. Adipokines in liver diseases[J]. Hepatology, 2009, 50( 3): 957- 969. DOI: 10.1002/hep.23046.
[19]	ZHANG Y, HU X, CHANG J, et al. The liver steatosis severity and lipid characteristics in primary biliary cholangitis[J]. BMC Gastroenterol, 2021, 21( 1): 395. DOI: 10.1186/s12876-021-01974-4.
[20]	KAZANKOV K, JØRGENSEN SMD, THOMSEN KL, et al. The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis[J]. Nat Rev Gastroenterol Hepatol, 2019, 16( 3): 145- 159. DOI: 10.1038/s41575-018-0082-x.
[21]	LOAEZA-DEL CASTILLO AM, GAYTÁN-SANTILLÁN A, LÓPEZ-TELLO A, et al. Patterns of serum lipids derangements and cardiovascular risk assessment in patients with primary biliary cholangitis[J]. Ann Hepatol, 2019, 18( 6): 879- 882. DOI: 10.1016/j.aohep.2019.07.006.
[22]	FRITHIOFF-BØJSØE C, LUND MAV, LAUSTEN-THOMSEN U, et al. Leptin, adiponectin, and their ratio as markers of insulin resistance and cardiometabolic risk in childhood obesity[J]. Pediatr Diabetes, 2020, 21( 2): 194- 202. DOI: 10.1111/pedi.12964.
[23]	Authors/Task Force Members; ESC Committee for Practice Guidelines(CPG); National Cardiac Societies ESC. 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk[J]. Atherosclerosis, 2019, 290: 140- 205. DOI: 10.1016/j.atherosclerosis.2019.08.014.
[24]	RESHETNYAK VI. Primary biliary cirrhosis: Clinical and laboratory criteria for its diagnosis[J]. World J Gastroenterol, 2015, 21( 25): 7683- 7708. DOI: 10.3748/wjg.v21.i25.7683.
[25]	LIU WY, XIE DM, ZHU GQ, et al. Targeting fibroblast growth factor 19 in liver disease: A potential biomarker and therapeutic target[J]. Expert Opin Ther Targets, 2015, 19( 5): 675- 685. DOI: 10.1517/14728222.2014.997711.
[26]	YANG L, XU LH. Research progress of gut microbiota and primary biliary cholangitis[J]. J Med Postgrad, 2019, 32( 12): 1324- 1328. DOI: 10.16571/j.cnki.1008-8199.2019.12.018. 杨柳, 徐丽红. 肠道菌群与原发性胆汁性胆管炎的研究进展[J]. 医学研究生学报, 2019, 32( 12): 1324- 1328. DOI: 10.16571/j.cnki.1008-8199.2019.12.018.
[27]	LEMOINNE S, KEMGANG A, BELKACEM K BEN, et al. Fungi participate in the dysbiosis of gut microbiota in patients with primary sclerosing cholangitis[J]. Gut, 2020, 69( 1): 92- 102. DOI: 10.1136/gutjnl-2018-317791.

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Primary biliary cholangitis with metabolic associated fatty liver disease： Clinical features and risk factors

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