Vanishing bile duct syndrome in the context of concurrent temozolomide for glioblastoma

Mason, Matthew S.; Adeyi, Oyedele; Fung, Scott; Millar, B

doi:10.1136/bcr-2014-208117

Cited by 9 publications

(5 citation statements)

References 19 publications

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“…Although DILI is an uncommon etiology for the VBDS, several medications have been reported to be related to the development of VBDS after liver injury. These medications include: antifungals or antibiotics like terbinafine, [ 12 ] meropenem, [ 13 ] and azithromycin; [ 11 ] anti-seizure medications such as valproic acid, [ 14 ] carbamazepine, [ 15 ] and lamotrigine; [ 16 ] and NSAIDs such as loxoprofen, diclofenac, and ibuprofen in pediatric cases [ 5 – 8 , 17 ]. Five cases of ibuprofen-induced liver injury with the complication of VBDS have been reported by far and all were children.…”

Section: Discussionmentioning

confidence: 99%

“…However, the patient had a complete recovery within 8 months [ 6 ]. These reports suggested that ibuprofen can cause acute VBDS, and weight-based ursodeoxycholic acid was commonly used for VBDS with supportive care, although steroids, immunosuppressive agents, or plasmapheresis were provided occasionally [ 12 , 18 ]. Similar to the clinical presentations described in children, our case had acute onset of jaundice and VBDS developed approximately at weeks 4–6 from the ibuprofen-induced liver injury.…”

Section: Discussionmentioning

confidence: 99%

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Vanishing bile duct syndrome with hyperlipidemia after ibuprofen therapy in an adult patient: a case report

et al. 2018

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BackgroundNon-steroidal anti-inflammatory drugs (NSAIDs) are frequently prescribed drugs and can cause drug-induced liver injury. Although patients with drug-induced liver injury from NSAIDs often recover spontaneously, 3% of them required hospitalization and those with persistent cholestasis present a diagnostic challenge. Recently, a few cases of children with persistent jaundice reported have been linked to the vanishing bile duct syndrome. However, data on adult patients is limited.Case presentationWe report herein a case of an adult patient who had persistent cholestasis with hyperlipidemia from the VBDS after ibuprofen use. We described a female patient with severe jaundice after taking ibuprofen, although she had no history of liver disease before. The drug-induced liver injury from ibuprofen was identified by clinical features and liver biopsy, which included the Roussel Uclaf Causality Assessment Method scores of 6 and pathological features of cholestasis with stage four drug-induced injury as well as loss of bile duct structures. The clinical course was featuring with persistently high levels of bilirubin associated with hyperlipidemia over the period of one month, although the laboratory abnormalities were slightly improved spontaneously after the cessation of ibuprofen. Her autoantibodies markers including AMA-M2 ASMA, RO-52, LKM, SLA, and anti-glycoprotein-210 were negative. The second liver biopsy was performed on day 213 due to persistent hyperbilirubinemia. Pathological findings were consistent with the diagnosis of vanishing bile duct syndrome.ConclusionsA rare case of ibuprofen-associated vanishing bile duct syndrome in an adult female patient is presented. Clinicians need to be aware of vanishing bile duct syndrome as a serious consequence of ibuprofen use in adult patients, although ibuprofen is considered to be among the safest NSAIDs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Vanishing bile duct syndrome with hyperlipidemia after ibuprofen therapy in an adult patient: a case report

et al. 2018

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“…It is often difficult to assess the exact hepatotoxic role of antineoplastic agents in cancer patients, sometimes critically ill, in whom liver injury is likely to be multifactorial. However, reasonably well documented cases of DILI with bile duct injury have been reported, especially with docetaxel [24], paclitaxel (or nab-paclitaxel) [24] and temozolomide [25,26].…”

Section: Systemic Chemotherapiesmentioning

confidence: 99%

Drug-induced bile duct injury: new agents, new mechanisms

Scoazec

2021

Current Opinion in Gastroenterology

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Purpose of reviewDrug-induced bile duct injury can be caused by a long list of agents. In most cases, damage is because of T-cell-mediated idiosyncratic reactions. Recently, a number of new agents, including not only drugs but also herbal supplements, have been incriminated and new mechanisms of bile duct injury have emerged. This review will focus on these new data. Recent findingsNew members of drug families already known to be responsible for bile duct injury have been incriminated. New players have been identified, such as herbal supplements, like kratom, and recreational drugs, such as ketamine used outside the medical setting. Anticytokine monoclonal antibodies are rarely involved. In contrast, antineoplastic treatments are of growing concern, especially immune checkpoint inhibitors, which induce immune-related adverse effects because of the excessive stimulation of the immune system and its lack of regulation.

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“…Anecdotal beneficial effects of ursodeoxycholic acid (UDCA) have been shown in cholangiopathy related to prochlorperazine [22], chlorpromazine [23] and temozolimide [24]. UDCA is known to stimulate biliary secretion of bile acids and other organic compounds, reduces the hydrophobic bile acid component of bile, inhibits the intrinsic apoptotic pathway and promotes cell survival in hepatocytes, through activation of the epidermal growth factor receptor (EGFR) [68].…”

Section: Therapy and Outcomementioning

confidence: 99%

Drug-induced bile duct injury

Visentin

Lenggenhager

Gai

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Drug-induced liver injury includes a spectrum of pathologies, some related to the mode of injury, some to the cell type primarily damaged. Among these, drug-induced bile duct injury is characterized by the destruction of the biliary epithelium following exposure to a drug. Most of the drugs associated with bile duct injury cause immune-mediated lesions to the epithelium of interlobular ducts. These share common histopathological features with primary biliary cholangitis, such as inflammation and necrosis at the expense of cholangiocytes and, if the insult persists, bile duct loss and biliary cirrhosis. Some drugs selectively target larger ducts. Such injury is often dose-dependent and thought to be the result of intrinsic drug toxicity. The histological changes resemble those seen in primary sclerosing cholangitis. This overview focuses on the clinical and pathological features of bile duct injury associated with drug treatment and on the immunological and biochemical effects that drugs exert on the biliary epithelium. This article is part of a Special Issue entitled: Cholangiocytes in Health and Disease edited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.

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Vanishing bile duct syndrome in the context of concurrent temozolomide for glioblastoma

Cited by 9 publications

References 19 publications

Vanishing bile duct syndrome with hyperlipidemia after ibuprofen therapy in an adult patient: a case report

Vanishing bile duct syndrome with hyperlipidemia after ibuprofen therapy in an adult patient: a case report

Drug-induced bile duct injury: new agents, new mechanisms

Drug-induced bile duct injury

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