Clinical and Molecular Hepatology

"Cholestasis"

Original Article

Cholestatic liver disease

JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis: Li Xie, Hui Chen, Li Zhang, Yue Ma, Yuan Zhou, Yong-Yu Yang, Chang Liu, Yu-Li Wang, Ya-Jun Yan, Jia Ding, Xiao Teng, Qiang Yang, Xiu-Ping Liu, Jian Wu; Clin Mol Hepatol 2024;30(2):206-224.
Published online January 8, 2024; DOI: https://doi.org/10.3350/cmh.2023.0506

Background/Aims
Cholestatic liver diseases including primary biliary cholangitis (PBC) are associated with active hepatic fibrogenesis, which ultimately progresses to cirrhosis. Activated hepatic stellate cells (HSCs) are the main fibrogenic effectors in response to cholangiocyte damage. JCAD regulates cell proliferation and malignant transformation in nonalcoholic steatoheaptitis-associated hepatocellular carcinoma (NASH-HCC). However, its participation in cholestatic fibrosis has not been explored yet.
Methods
Serial sections of liver tissue of PBC patients were stained with immunofluorescence. Hepatic fibrosis was induced by bile duct ligation (BDL) in wild-type (WT), global JCAD knockout mice (JCAD-KO) and HSC-specific JCAD knockout mice (HSC-JCAD-KO), and evaluated by histopathology and biochemical tests. In situ-activated HSCs isolated from BDL mice were used to determine effects of JCAD on HSC activation.
Results
In consistence with staining of liver sections from PBC patients, immunofluorescent staining revealed that JCAD expression was identified in smooth muscle α-actin (α-SMA)-positive fibroblast-like cells and was significantly up-regulated in WT mice with BDL. JCAD deficiency remarkably ameliorated BDL-induced hepatic injury and fibrosis, as documented by liver hydroxyproline content, when compared to WT mice with BDL. Histopathologically, collagen deposition was dramatically reduced in both JCAD-KO and HSC-JCAD-KO mice compared to WT mice, as visualized by Trichrome staining and semi-quantitative scores. Moreover, JCAD deprivation significantly attenuated in situ HSC activation and reduced expression of fibrotic genes after BDL.
Conclusions
JCAD deficiency effectively suppressed hepatic fibrosis induced by BDL in mice, and the underlying mechanisms are largely through suppressed Hippo-YAP signaling activity in HSCs.

Citations

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Biliary YB-1/GLI2 axis facilitates ductular reaction and promotes HSC activation via SPP1/integrin αvβ1 signaling during liver fibrogenesis
Yuecheng Guo, Qingqing Zhang, Binghang Li, Weiming Dai, Bo Shen, Zhenyang Shen, Junjun Wang, Qichao Ge, Hanjing Zhangdi, Guangwen Chen, Qidi Zhang, Xiaobo Cai, Hui Dong, Guangjian Fan, Lungen Lu, Fei Li
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Zi-Rong Li, Yong-Yan Wang, Chao Zhang, Jin-Sha Shi, Xiao Yu, Ni-Tong Ying, Xiao-Ke Xu, Juan-Juan Li, Tao Guo
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Huanggan decoction ameliorates cholestatic hepatic fibrosis in rats via TGF-β1/Smad3 signaling pathway
Yaya Lei, Xueli Ma, Xiaohui Jin, Yanping He, Jianhong Yang, Yuna Zhao, Jing Chen, Ting Gao, Sharon DeMorrow
PLOS One.2026; 21(3): e0344168. CrossRef
Underestimated and Overlooked Factors in PBC Progression: Bacterial and Fungal Infections
Yaxin Zhu, Sumeng Li, Shiqi Li, Yichen Wang, Yanqin Du, Xin Zheng, Jun Wu
International Journal of Molecular Sciences.2026; 27(6): 2766. CrossRef
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Acta Tropica.2026; : 108160. CrossRef
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Xixi Zeng, Yanhong Liao, Weiyi Cheng
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Shenglu Liu, Peng Tan, Jiatong Chen, Zhiwei Huang, Bingyu Ren, Zhonghao Jiang, Boyuan Gu, Wenhao Yu, Lei Sun, Yingjun Chen, Jian Ruan, Wenguang Fu
Cellular and Molecular Gastroenterology and Hepatology.2025; 19(10): 101559. CrossRef
JCAD deficiency delayed liver regenerative repair through the Hippo–YAP signalling pathway
Li Zhang, Yong‐Yu Yang, Li Xie, Yuan Zhou, Zhenxing Zhong, Jia Ding, Zhong‐Hua Wang, Yu‐Li Wang, Xiu‐Ping Liu, Fa‐Xing Yu, Jian Wu
Clinical and Translational Medicine.2024;[Epub] CrossRef
JCAD, a new potential therapeutic target in cholestatic liver disease
Byoung Kuk Jang
Clinical and Molecular Hepatology.2024; 30(2): 166. CrossRef
Correspondence on Letter regarding “Both liver parenchymal and non-parenchymal cells express JCAD proteins under various circumstances”
Byoung Kuk Jang
Clinical and Molecular Hepatology.2024; 30(2): 297. CrossRef
Both liver parenchymal and non-parenchymal cells express JCAD protein under various circumstances
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Clinical and Molecular Hepatology.2024; 30(2): 279. CrossRef

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Case Reports

Hepatic involvement of systemic disease

A case of Alagille syndrome presenting with chronic cholestasis in an adult: Jihye Kim, Bumhee Yang, Namyoung Paik, Yon Ho Choe, Yong-Han Paik; Clin Mol Hepatol 2017;23(3):260-264.
Published online July 7, 2017; DOI: https://doi.org/10.3350/cmh.2016.0057

Abstract
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Alagille syndrome (AGS) is a complex multisystem disorder that involves mainly the liver, heart, eyes, face, and skeleton. The main associated clinical features are chronic cholestasis due to a paucity of intrahepatic bile ducts, congenital heart disease primarily affecting pulmonary arteries, vertebral abnormalities, ocular embryotoxon, and peculiar facies. The manifestations generally become evident at a pediatric age. AGS is caused by defects in the Notch signaling pathway due to mutations in JAG1 or NOTCH2. It is inherited in an autosomal dominant pattern with a high degree of penetrance, but variable expressivity results in a wide range of clinical features. Here we report on a 31-year-old male patient who presented with elevated serum alkaline phosphatase and gamma-glutamyl transpeptidase, and was diagnosed with AGS associated with the JAG1 mutation after a comprehensive workup.

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Alagille Syndrome Nowadays: “One, no-One and One Hundred Thousand”
M. Arrabito, S. D’Amico, C. Gulizia, L. Marino, G.F. Parisi, M. Papale, S. Manti, S. Leonardi
International Journal of Pediatrics and Child Health.2022; 10: 30. CrossRef
Alagille syndrome caused by NOTCH2 mutation presented atypical pathological changes
Yiling ShenTu, Xiaoxiao Mi, Dong Tang, Yanming Jiang, Ling Gao, Xiaojie Ma, Bing Zhou, Wenjun Yang, Junping Shi, Dixiang Lan, Gongying Chen, Ling Gong
Clinica Chimica Acta.2021; 521: 258. CrossRef
A rare cause of ductopenia: adult onset Alagille syndrome
Sameera Ansar, Kim Tran, Jason Pinner, Avik Majumdar, Catriona McKenzie
Pathology.2020; 52(5): 610. CrossRef
Alagille syndrome: an uncommon cause of intrahepatic cholestasis in adults
Wei Zhang, Xinyan Zhao, Jian Huang, Xiaojuan Ou, Jidong Jia
Revista Española de Enfermedades Digestivas.2019;[Epub] CrossRef
Persistent cholestasis resulting from duodenal papillary carcinoma in an adolescent male
Haiyan Fu, Yingchao Li, Gelan Bai, Runkai Yin, Chunlan Yin, Weina Shi, Lili Zhang, Rongpin Li, Ruiqin Zhao
Medicine.2019; 98(22): e15708. CrossRef
Alagille syndrome mutation update: Comprehensive overview ofJAG1andNOTCH2mutation frequencies and insight into missense variant classification
Melissa A. Gilbert, Robert C. Bauer, Ramakrishnan Rajagopalan, Christopher M. Grochowski, Grace Chao, Deborah McEldrew, James A. Nassur, Elizabeth B. Rand, Bryan L. Krock, Binita M. Kamath, Ian D. Krantz, David A. Piccoli, Kathleen M. Loomes, Nancy B. Spi
Human Mutation.2019; 40(12): 2197. CrossRef
Novel JAG1 Deletion Variant in Patient with Atypical Alagille Syndrome
Emanuele Micaglio, Andreea Alina Andronache, Paola Carrera, Michelle M. Monasky, Emanuela T. Locati, Barbara Pirola, Silvia Presi, Mario Carminati, Maurizio Ferrari, Alessandro Giamberti, Carlo Pappone
International Journal of Molecular Sciences.2019; 20(24): 6247. CrossRef

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Drug induced liver injury

A case of levocetirizine-induced liver injury: Moon Chan Jung, Ja Kyung Kim, Jae Yeon Cho, Jae Won Song, Bohyun Lee, Ji Won Park, Jinwon Seo, Sung Eun Kim; Clin Mol Hepatol 2016;22(4):495-498.
Published online December 25, 2016; DOI: https://doi.org/10.3350/cmh.2016.0023

Abstract
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Levocetirizine is a second-generation nonsedative antihistaminic agent that has been demonstrated to be safe and effective for treating allergic disease. There was only one case report of levocetirizine-induced liver toxicity, but a liver biopsy was not performed. In this article, we present the first case of levocetirizine-induced liver injury with histologic findings. A 48-year-old man was hospitalized with jaundice and generalized pruritus that had developed after 2 months of therapy with levocetirizine for prurigo nodularis. Laboratory findings revealed acute hepatitis with cholestasis. A liver biopsy demonstrated portal inflammation and hepatitis with apoptotic hepatocytes. The patient fully recovered 3 weeks after withdrawing levocetirizine. Although levocetirizine is safe and effective, physicians should be aware of its potential hepatotoxicity.

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Clinical courses after administration of oral corticosteroids in patients with severely cholestatic acute hepatitis A; three cases: Eileen L. Yoon, Hyung Joon Yim, Seung Young Kim, Jeong Han Kim, Ju-Han Lee, Young Sun Lee, Hyun Jung Lee, Sung Woo Jung, Sang Woo Lee, Jai Hyun Choi; Korean J Hepatol 2010;16(3):329-333.
Published online September 30, 2010; DOI: https://doi.org/10.3350/kjhep.2010.16.3.329

Abstract
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Acute hepatitis A is currently outbreaking in Korea. Although prognosis of acute hepatitis A is generally favorable, a minority of patients are accompanied by fatal complications. Severe cholestasis is one of the important causes of prolonged hospitalization in patients with acute hepatitis A. In such cases, higher chances of additional complications and increased medical costs are inevitable. We report three cases of severely cholestatic hepatitis A, who showed favorable responses to oral corticosteroids. Thirty milligram of prednisolone was initiated and tapered according to the responses. Rapid improvement was observed in all cases without side effects. We suggest that corticosteroid administration can be useful in hepatitis A patients with severe cholestasis who do not show improvement by conservative managements. Clinical trial will be needed to evaluate effectiveness of corticosteroids in these patients.

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Paediatrica Indonesiana.2021; 61(6): 317. CrossRef
Two case reports of corticosteroid administration-prolonged and pulsed therapy-in treatment of pruritus in cholestatic hepatitis A patients
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Adrenal Insufficiency Associated with Cholestatic Jaundice: A Case Report
Wei-Cheng Lee, Shou-Chuan Shih, Horng-Yuan Wang, Chien-Liang Wu, Shih-Yi Lee, Hui-Chun Ku
International Journal of Gerontology.2018; 12(2): 164. CrossRef
Current opinion in epidemiology and approaches to the treatment of viral hepatitis A and E.
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S Vita, G Tebano, A M Rossomando, Rosa A De, E N Cavallari, E Caraffa, C Ajassa, V Vullo
Journal of Medical Laboratory and Diagnosis.2016; 7(1): 1. CrossRef

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A case of acute cholestatic hepatitis induced by Corydalis speciosa Max.: Hyun Seok Kang , Hyuk Soon Choi , Tae Jung Yun , Kwang Gyun Lee , Yeon Seok Seo , Jong Eun Yeon , Kwan Soo Byun , Soon Ho Um , Chang Duck Kim , Ho Sang Ryu; Korean J Hepatol 2009;15(4):517-523.
Published online December 31, 2009; DOI: https://doi.org/10.3350/kjhep.2009.15.4.517

Abstract
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Herbs are widely used as treatments for various symptoms. However, several herbs have been reported to be inducers of liver injury. We report herein a case of hepatotoxicity induced by Corydalis speciosa Max. A 37-year-old male complained of jaundice and mild abdominal discomfort. A thorough history was taken, and laboratory investigation, diagnostic imaging studies, and percutaneous liver biopsy sampling were conducted to determine the cause of liver injury. An accurate cause was not revealed. We administered supportive management for acute cholestatic hepatitis of unknown origin, after which his symptoms disappeared and serum aminotransferase levels decreased gradually to near normal levels. However, at 2 months after discharge, the symptoms and the elevation of aminotransferase levels recurred. At that time he told us that he had repeatedly but unintentionally eaten a herb called “Hwang-geun cho”(Corydalis speciosa Max.). Thus, we diagnosed his case as herbal hepatotoxicity. (Korean J Hepatol 2009;15:517-523)

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Herb-induced Liver Injury in Asia and Current Role of RUCAM for Causality Assessment in 11,160 Published Cases
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Rolf Teschke, Gaby Danan
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Herbal Hepatotoxicity: Clinical Characteristics and Listing Compilation
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International Journal of Molecular Sciences.2016; 17(5): 588. CrossRef
Traditional Chinese Medicine (TCM) and Herbal Hepatotoxicity: RUCAM and the Role of Novel Diagnostic Biomarkers Such as MicroRNAs
Rolf Teschke, Dominique Larrey, Dieter Melchart, Gaby Danan
Medicines.2016; 3(3): 18. CrossRef
Systematic review on herb-induced liver injury in Korea
Woo-Jin Lee, Hae-Won Kim, Hyun-Yong Lee, Chang-Gue Son
Food and Chemical Toxicology.2015; 84: 47. CrossRef
RUCAM in Drug and Herb Induced Liver Injury: The Update
Gaby Danan, Rolf Teschke
International Journal of Molecular Sciences.2015; 17(1): 14. CrossRef
Traditional Chinese Medicine and herbal hepatotoxicity: a tabular compilation of reported cases
Rolf Teschke, Li Zhang, Hongzhu Long, Alexander Schwarzenboeck, Wolfgang Schmidt-Taenzer, Alexander Genthner, Albrecht Wolff, Christian Frenzel, Johannes Schulze, Axel Eickhoff
Annals of Hepatology.2015; 14(1): 7. CrossRef
A Pediatric Case of Toxic Hepatitis Induced by Hovenia Dulcis
Yun Ji Kim, Seung Lok Ryu, Jae Won Shim, Duk Soo Kim, Jung Yeon Shim, Moon Soo Park, Hye Lim Jung
Pediatric Gastroenterology, Hepatology & Nutrition.2012; 15(2): 111. CrossRef
A Pediatric Case of Toxic Hepatitis Induced by Hovenia Dulcis
Yun Ji Kim, Seung Lok Ryu, Jae Won Shim, Duk Soo Kim, Jung Yeon Shim, Moon Soo Park, Hye Lim Jung
Pediatric Gastroenterology, Hepatology & Nutrition.2012; 15(2): 111. CrossRef

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Treatment with pegylated interferon and ribavirin in a patient with fibrosing cholestatic hepatitis due to recurrent hepatitis C after liver transplantation: Byung Kook Kim, M.D., So Young Kwon, M.D., Soon-Young Ko, M.D., Won Hyeok Choe, M.D., Chang Hong Lee, M.D., He-Seong Han, M.D.1, Seong-Hwan Chang, M.D.2; Korean J Hepatol 2008;14(4):519-524.
Published online December 31, 2008; DOI: https://doi.org/10.3350/kjhep.2008.14.4.519

Abstract
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Fibrosing cholestatic hepatitis (FCH) is the most devastating manifestation of recurrent hepatitis C in transplant recipients with hepatitis C virus (HCV), possibly leading to death or retransplantation. Although FCH was first described as a complication of hepatitis B, this manifestation has been well documented in association with HCV in the setting of liver transplantation, bone marrow transplantation, heart transplantation, and end-stage human immunodeficiency virus infection. We report the clinical course and antiviral response in a patient with FCH due to recurrent hepatitis C after cadaveric liver transplantation who was treated with pegylated interferon α-2a and ribavirin. (Korean J Hepatol 2008;14:519-524)

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Folate-Polyethylene Glycol Conjugated Near-Infrared Fluorescence Probe with High Targeting Affinity and Sensitivity for In Vivo Early Tumor Diagnosis
Fei Liu, Dawei Deng, Xinyang Chen, Zhiyu Qian, Samuel Achilefu, Yueqing Gu
Molecular Imaging and Biology.2010; 12(6): 595. CrossRef

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A case of allopurinol-induced granulomatous hepatitis with ductopenia and cholestasis: Jae Young Yoon , Sun Yang Min , Ju Yee Park , Seung Goun Hong , Sang Jong Park , So Ya Paik , Young Min Park; Korean J Hepatol 2008;14(1):97-101.
Published online March 20, 2008; DOI: https://doi.org/10.3350/kjhep.2008.14.1.97

Abstract
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Allopurinol-induced hypersensitivity syndrome is characterized by an idiosyncratic reaction involving multiple-organs, which usually begins 2 to 6 weeks after starting allopurinol. In rare cases, the adverse reactions to allopurinol are accompanied by a variety of liver injury, such as reactive hepatitis, granulomatous hepatitis, vanishing bile duct syndrome, or fulminant hepatic failure. Here we report a case with granulomatous hepatitis and ductopenia. A 69-year-old man with chronic renal failure, hyperuricemia, and previously normal liver function presented with jaundice, skin rash, and fever 2 weeks after taking allopurinol (200 mg/day). In histopathology, a liver biopsy specimen showed mild spotty necrosis of hepatocytes, marked cholestasis in parenchyma, and some granulomas in the portal area. There were vacuolar degeneration in the interlobular bile ducts and ductopenia in the portal tracts. Pathologic criteria strongly suggested the presence of allopurinol-induced granulomatous hepatitis with ductopenia and cholestasis. The patient fully recovered following the early administration of systemic corticosteroid therapy. (Korean J Hepatol 2008;14:97-101)

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Ji Hye Hwang, Kwang Ho Lee, Dong Woo Nam, Ho Sueb Song
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Chunlai Feng, Hengwei Chen, Xianqin Yuan, Mengqiu Sun, Kexin Chu, Hanqin Liu, Mengjie Rui
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Efficacy and Safety of Chinese Medicinal Herbs for the Treatment of Hyperuricemia: A Systematic Review and Meta‐Analysis
Jianping Lin, Shaoqing Chen, Shuzhen Li, Meili Lu, Yanan Li, Youxin Su, Young-Su Yi
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Neil Gupta, Basile Njei
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Allopurinol Hypersensitivity: A Systematic Review of All Published Cases, 1950–2012
Sheena N. Ramasamy, Cameron S. Korb-Wells, Diluk R. W. Kannangara, Myles W. H. Smith, Nan Wang, Darren M. Roberts, Garry G. Graham, Kenneth M. Williams, Richard O. Day
Drug Safety.2013; 36(10): 953. CrossRef
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Clopidogrel‐Induced Hepatocellular Injury and Cholestatic Jaundice in an Elderly Patient: Case Report and Review of the Literature
Rakesh K. Goyal, Dimple Srivastava, Klaus‐Dieter Lessnau
Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy.2009; 29(5): 608. CrossRef

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A Case of Nonfamilial Benign Recurrent Intrahepatic Cholestasis: Oh Young Kim , Bum Yong Sung , Gyo Don Kowg , Hae Seoung Yoon , Yong Min Shin , Hyun Taek Oh , Mi Kyoung Kim , Hyeong Kweon Kim , Ju Ho Kim , Kwang Ung Ri , Hyun I Shon; Korean J Hepatol 1998;4(2):188-193.

Abstract
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Benign recurrent intrahepatic cholestasis (BRIC) is a rare desease, which usually manifests between the age of 10 and 20. Its main clinical feature is multiple recurrent episodes of cholestasis without extrahepatic bile duct obstruction. We report here a case of nonfamilial benign recurrent intrahepatic cholestasis. The patient has experienced recurrent jaundice with pruritus since childhood. Main bile duct obstrution was excluded by abdominal CT and endoscopic retrograde cholangiopancreatography. Other causes of cholestasis were not found. Hepatic histology revealed bile plug which were mainly concentrated in the centrilobular region, and increased number of mononuclear cells in the portal triad, but hepatic parenchyma showed no inflammation and necrosis. In the last anicteric period, she was healthy and the liver function test and biopsy specimen were normal. (Korean J Hepatol 1998;4:188 - 193)

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Review

Role of PXR and CAR in Cholestasis: Jeong Ill Suh; Korean J Hepatol 2006;12(1):5-15.

Abstract
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Cholestatic liver diseases are characterized by impairments of bile flows and accumulations of biliary constituents such as bile acids and bilirubin. The changes of phase I and II metabolism and the hepatobiliary transport system minimize cholestatic liver injury. These adaptive responses are transcriptionally regulated by several nuclear receptors. Recent studies have revealed that the pregnane X receptor (PXR) and the constitutive androstane receptor (CAR) are key nuclear receptors for regulating many of the adaptive responses noted in cholestasis. PXR and CAR coordinately regulate not only bile acid metabolism and transport, but also bilirubin clearance. PXR and CAR ligands may be useful in the future for the treatment of cholestatic liver disease. (Korean J Hepatol 2006;12:5-15)

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Case Report

A Case of Cholestatic Hepatitis lnduced by Epstein-Barr Virus Infection: Min Jae Park , In Kwon Chung , Young Dae Park , Yun Jin Chung , Ho Chul Lee , Han Jin Cho , Eun Hee Seo , Chang Min Cho , Won Young Tak , Sung Kook Kim , Yong Whan Choi; Korean J Hepatol 2006;12(2):237-242.

Abstract
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Acute viral hepatitis in human can be caused by a large number of viruses with a wide range of clinical manifestations and laboratory findings. EBV is a rare causative agent of an acute hepatitis, during the course of infectious mononucleosis. Hepatic manifestations of EBV are usually mild and resolve without serious complications. EBV is rather uncommonly confirmed as an etiologic agent in acute viral hepatitis of adults and it rarely causes cholestatic hepatitis. We report a case of EBV hepatitis with cholestatic feature that was verified through serum viral marker and liver biopsy. (Korean J Hepatol 2006;12:237-242)