Acute vanishing bile duct syndrome after therapy with cephalosporin, metronidazole, and clotrimazole

ZongHao, Zhao; Bao, Lei; Yu, Xiaolan; Zhu, Chuanlong; Xu, Jing; Yu, Wei; Yin, Ming; Li, Yi; Li, Wenting

doi:10.1097/md.0000000000008009

Cited by 13 publications

(12 citation statements)

References 21 publications

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“…While the classical disease phenotypes characteristic of VBDS exclude EHBD obstruction, the possibility of VBDS affecting the extrahepatic biliary system remains unexplored. Interestingly, factors associated with VBDS share common features with BA including congenital disorders affecting bile duct development, viral infections, immune disorders, and in most cases the need for LTx ( 83 ). Indeed, several of the histologic features of acute VBDS correlate with BA including: parenchymal bilirubinostasis, infiltration of portal tracts by mononuclear cells, macrophages and neutrophils, epithelial degeneration, vacuolization and cholangiocyte pyknosis ( 84 ).…”

Section: Triggers Of Ba: Advances and Mechanismsmentioning

confidence: 99%

Recent developments in etiology and disease modeling of biliary atresia: a narrative review

et al. 2020

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Biliary atresia (BA) is a rare but severe fibroinflammatory disease of the extrahepatic and the intrahepatic bile ducts. Without prompt interventions, BA has fatal outcomes and is the most common indicator for pediatric liver transplantation (LTx). While the mainstay of treatment involves surgically correcting the extrahepatic biliary obstruction via Kasai hepato-portoenterostomy (KHPE), activation of a multitude of biological pathways and yet-to-be-determined etiology in BA continue to foster liver inflammation, cirrhosis and need for LTx. However, important caveats still exist in our understandings of the biliary pathophysiology, the rapidity of liver fibrosis and progression to liver failure, largely due to limited knowledge of the triggers of biliary injury and the inability to accurately model human BA. Although inconclusive, a large body of existing literature points to a potential viral infection in the early peri- or postnatal period as triggers of epithelial injury that perpetuates the downstream biliary disease. Further confounding this issue, are the lack of in-vivo and in-vitro models to efficiently recapitulate the cardinal features of BA, primarily liver fibrosis. To overcome these barriers in BA research, new directions in recent years have enabled (I) identification of additional triggers of biliary injury linked mostly to environmental toxins, (II) development of models to investigate liver fibrogenesis, and (III) translational research using patient-derived organoids. Here, we discuss recent advances that undoubtedly will stimulate future efforts investigating these new and exciting avenues towards mechanistic and drug discovery efforts and disease-preventive measures. The implications of these emerging scientific investigations and disease modeling in severe fibrosing cholangiopathies like BA are enormous and contribute substantially in our understandings of this rare but deadly disease. These findings are also expected to facilitate expeditious identification of translationally targetable pathways and bring us one step closer in treating an infant with BA, a population highly vulnerable to life-long liver related complications.

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Section: Triggers Of Ba: Advances and Mechanismsmentioning

confidence: 99%

Recent developments in etiology and disease modeling of biliary atresia: a narrative review

et al. 2020

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“…13 First described in 1988 in three patients, 14 VBDS is largely idiosyncratic, but has been causally associated with a variety of etiologies, including genetic diseases such as cystic fibrosis and Williams syndrome, 15 neoplasms such as lymphoma, 16–18 immune disorders including graft-versus-host disease, 15,19 viral infections, 20–23 and most commonly, pharmaceuticals. VBDS has been associated with numerous drug classes, including antibiotics, non-steroidal anti-inflammatories, antipsychotics, antiepileptics, antihypertensives, diabetes medications, 13,24–33 and oral chemotherapy drugs such as temozolomide. 30,31…”

Section: Discussionmentioning

confidence: 99%

“…In most instances, the ductopenia in VBDS preferentially affects the smaller interlobular bile ducts rather than the larger bile ducts that are usually destroyed in primary biliary cirrhosis. Defined as the loss of >50% of interlobular ducts, or a bile duct to portal tract ratio of <0.5, 2,14,33–35 patients with VBDS commonly present with jaundice, itching, fatigue, and anorexia. 2,31,32 Laboratory evaluation reveals cholestasis, including profound elevations in ALP and gamma-glutamyl transferase, as well as high serum concentrations of bilirubin, with relatively mild elevations in serum aminotransferases.…”

Section: Discussionmentioning

confidence: 99%

A case report of vanishing bile duct syndrome after exposure to pexidartinib (PLX3397) and paclitaxel

et al. 2019

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Pexidartinib (PLX3397) is a small molecule tyrosine kinase and colony-stimulating factor-1 inhibitor with FDA breakthrough therapy designation for tenosynovial giant-cell tumor, and currently under study in several other tumor types, including breast cancer, non-Hodgkin’s lymphoma, and glioblastoma. Here, we report a case of severe drug-induced liver injury requiring liver transplantation due to vanishing bile duct syndrome (VBDS) after exposure to pexidartinib in the I-SPY 2 Trial, a phase 2 multicenter randomized neoadjuvant chemotherapy trial in patients with Stage II–III breast cancer. We also review the current literature on this rare, idiosyncratic, and potentially life-threatening entity.

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“…Hepatotoxicity related to a few drugs such as amoxicillin/clavulanate, carbamazepine or chlorpromazine seems to carry a high risk of this outcome . Likewise, genetic variants of ABCB4 , which encodes for multidrug resistance protein 3 (MDR3), have been associated with VBDS …”

Section: Clinical and Pathological Phenotypesmentioning

confidence: 99%

“…57 Likewise, genetic variants of ABCB4, which encodes for multidrug resistance protein 3 (MDR3), have been associated with VBDS. 60…”

Section: Drug-induced Autoimmune Hepatitis (Di-aih)mentioning

confidence: 99%

Chronic liver injury induced by drugs and toxins

Ortega‐Alonso

Andrade

2018

J of Digest Diseases

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Drug-induced liver injury (DILI) occurs in a small fraction of individuals exposed to drugs, herbs or dietary supplements and is a relatively rare diagnosis compared with other liver disorders. DILI can be serious, resulting in hospitalization and even life-threatening liver failure, death or need for liver transplantation. Toxic liver damage usually presents as an acute hepatitis viral-like syndrome or as an acute cholestasis that resolves upon drug discontinuation. However, un-resolving chronic outcome after acute DILI can ensue in some subjects, the mechanisms and risk factors for this particular evolution being yet scarcely known. Furthermore, the definition of chronicity after acute DILI is controversial, regarding both the time frame of liver injury persistence and the magnitude of the abnormalities required. Besides this, in some instances the phenotypes and pathological manifestations are those of chronic liver disease at the time of DILI diagnosis. These include non-alcoholic fatty liver disease, vascular lesions, drug-induced autoimmune hepatitis, chronic cholestasis leading to vanishing bile duct syndrome and even cirrhosis, and some drugs such as amiodarone or methotrexate have been frequently implicated in some of these forms of chronic DILI. In addition, all of these DILI phenotypes can be indistinguishable from those related to other etiologies, making the diagnosis particularly challenging. In this manuscript we have critically reviewed the more recent data on chronicity in DILI with a particular focus on the epidemiology, mechanisms and risk factors of atypical chronic DILI phenotypes.

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Acute vanishing bile duct syndrome after therapy with cephalosporin, metronidazole, and clotrimazole

Abstract: VBDS is rare but can be severe. A liver biopsy offers an important evidence for the diagnosis of VBDS, especially for those with a history of susceptible drugs taking.

Cited by 13 publications

References 21 publications

Recent developments in etiology and disease modeling of biliary atresia: a narrative review

Recent developments in etiology and disease modeling of biliary atresia: a narrative review

A case report of vanishing bile duct syndrome after exposure to pexidartinib (PLX3397) and paclitaxel

Chronic liver injury induced by drugs and toxins

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