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Journal articles on the topic 'Drug-induced cholestasis'

Author: Grafiati

Published: 25 May 2024

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1

Al-Azzawi, Hasan, Ruchi Patel, Gagan Sood, and Sumit Kapoor. "Plasmapheresis for Refractory Pruritus due to Drug-Induced Cholestasis." Case Reports in Gastroenterology 10, no. 3 (January 6, 2017): 814–18. http://dx.doi.org/10.1159/000454674.

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Pruritus can be a distressing symptom seen in various cholestatic disorders. It is treated with medications like bile acid sequestrants. Drug-induced cholestasis usually resolves with withdrawal of the causative medication. We describe a case of refractory pruritus due to drug-induced cholestasis, not improved with withdrawal of the drug, managed effectively with multiple sessions of plasmapheresis.

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2

Erlinger, Serge. "Drug-induced cholestasis." Journal of Hepatology 26 (January 1997): 1–4. http://dx.doi.org/10.1016/s0168-8278(97)82326-4.

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3

Harnois, D. M. "Drug-Induced Cholestasis." Yearbook of Gastroenterology 2011 (January 2011): 269–70. http://dx.doi.org/10.1016/j.ygas.2011.07.048.

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4

Levy, Cynthia, and Keith D. Lindor. "Drug-induced cholestasis." Clinics in Liver Disease 7, no. 2 (May 2003): 311–30. http://dx.doi.org/10.1016/s1089-3261(03)00032-1.

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5

Simon, Francis R. "DRUG-INDUCED CHOLESTASIS." Clinics in Liver Disease 2, no. 3 (August 1998): 483–99. http://dx.doi.org/10.1016/s1089-3261(05)70023-4.

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6

Zimmerman, Hyman J., and James H. Lewis. "Drug-Induced Cholestasis." Medical Toxicology 2, no. 2 (April 1987): 112–60. http://dx.doi.org/10.1007/bf03260010.

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7

Bjornsson, Einar S., and Jon Gunnlaugur Jonasson. "Drug-Induced Cholestasis." Clinics in Liver Disease 17, no. 2 (May 2013): 191–209. http://dx.doi.org/10.1016/j.cld.2012.11.002.

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8

Bhamidimarri, Kalyan Ram, and Eugene Schiff. "Drug-Induced Cholestasis." Clinics in Liver Disease 17, no. 4 (November 2013): 519–31. http://dx.doi.org/10.1016/j.cld.2013.07.015.

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9

Velayudham, Lakshumanan S., and Geoffrey C. Farrell. "Drug-induced cholestasis." Expert Opinion on Drug Safety 2, no. 3 (May 2003): 287–304. http://dx.doi.org/10.1517/14740338.2.3.287.

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10

Padda, Manmeet S., Mayra Sanchez, Abbasi J. Akhtar, and James L. Boyer. "Drug-induced cholestasis." Hepatology 53, no. 4 (April 2011): 1377–87. http://dx.doi.org/10.1002/hep.24229.

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11

Sundaram, Vinay, and Einar S. Björnsson. "Drug-induced cholestasis." Hepatology Communications 1, no. 8 (September 11, 2017): 726–35. http://dx.doi.org/10.1002/hep4.1088.

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12

Pinazo-Bandera, Jose M., Juan Pedro Toro-Ortiz, Raúl J. Andrade, and Miren García-Cortés. "Drug-induced cholestasis: causative agents and challenges in diagnosis and management." Exploration of Digestive Diseases 2, no. 5 (September 18, 2023): 202–22. http://dx.doi.org/10.37349/edd.2023.00027.

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Drug-induced liver injury (DILI) is an adverse reaction to drugs and other xenobiotics that can have serious consequences and jeopardise progress in pharmacological therapy. While DILI is predominantly hepatocellular, a non-negligible percentage of patients who present with cholestatic damage. Mixed damage is typically lumped together with cholestatic damage in the literature. Drug-induced cholestasis is often caused by the use of some non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics (i.e., amoxicillin-clavulanic acid), statins, and anabolic agents, among others. Drug-associated cholestasis tends to have a more chronic course and mostly affects older population. There is also a genetic predisposition to toxic cholestasis caused by some drugs (amoxicillin-clavulanic acid, statins, etc.). Recently, anatomical alterations of the biliary tract induced by drugs (especially immunotherapy drugs) have been described. Bile duct injury is one of the histopathological findings that have prognostic significance in DILI. A correct differential diagnosis with other causes of cholestasis is mandatory to reach an accurate diagnosis. Ursodexycholic acid, corticosteroids, and replacement therapies have been used as a therapeutic arsenal, although more evidence is needed to establish them as a routine therapeutic management in clinical practice. The breakthrough and validation of biomarkers of cholestasis and bile duct injury is an urgent need for drug development and post-marketing phase.

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13

Larrey, Dominique, and Serge Erlinger. "9 Drug-induced cholestasis." Baillière's Clinical Gastroenterology 2, no. 2 (April 1988): 423–52. http://dx.doi.org/10.1016/0950-3528(88)90010-3.

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14

Vitale, Giovanni, Alessandro Mattiaccio, Amalia Conti, Sonia Berardi, Vittoria Vero, Laura Turco, Marco Seri, and Maria Cristina Morelli. "Molecular and Clinical Links between Drug-Induced Cholestasis and Familial Intrahepatic Cholestasis." International Journal of Molecular Sciences 24, no. 6 (March 18, 2023): 5823. http://dx.doi.org/10.3390/ijms24065823.

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Idiosyncratic Drug-Induced Liver Injury (iDILI) represents an actual health challenge, accounting for more than 40% of hepatitis cases in adults over 50 years and more than 50% of acute fulminant hepatic failure cases. In addition, approximately 30% of iDILI are cholestatic (drug-induced cholestasis (DIC)). The liver’s metabolism and clearance of lipophilic drugs depend on their emission into the bile. Therefore, many medications cause cholestasis through their interaction with hepatic transporters. The main canalicular efflux transport proteins include: 1. the bile salt export pump (BSEP) protein (ABCB11); 2. the multidrug resistance protein-2 (MRP2, ABCC2) regulating the bile salts’ independent flow by excretion of glutathione; 3. the multidrug resistance-1 protein (MDR1, ABCB1) that transports organic cations; 4. the multidrug resistance-3 protein (MDR3, ABCB4). Two of the most known proteins involved in bile acids’ (BAs) metabolism and transport are BSEP and MDR3. BSEP inhibition by drugs leads to reduced BAs’ secretion and their retention within hepatocytes, exiting in cholestasis, while mutations in the ABCB4 gene expose the biliary epithelium to the injurious detergent actions of BAs, thus increasing susceptibility to DIC. Herein, we review the leading molecular pathways behind the DIC, the links with the other clinical forms of familial intrahepatic cholestasis, and, finally, the main cholestasis-inducing drugs.

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15

Liu, Xiaoqiang, Boming Xu, Yilin Zeng, Peizhong Chen, and Yubin Wang. "Case report: Severe cholestatic jaundice associated with hyperthyroidism treated with methimazole." Medicine 102, no. 45 (November 10, 2023): e35972. http://dx.doi.org/10.1097/md.0000000000035972.

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Rationale: We present a case of a 43-year-old female patient diagnosed with hyperthyroidism. This study aims to demonstrate the rare association between hyperthyroidism and severe cholestatic jaundice, and the effectiveness of methimazole treatment. Patient concerns: The patient developed severe jaundice, a typically mild symptom in most hyperthyroidism cases. Diagnosis: The severe jaundice was suspected to be a result of cholestasis induced by hyperthyroidism, with other potential causes such as drug-induced or autoimmune liver dysfunction being ruled out. Outcomes: The patient was effectively treated with methimazole. Outcomes: Treatment with methimazole alleviated the severe cholestatic jaundice and restored normal thyroid function. Lessons: The specific mechanism of cholestasis as a secondary complication of hyperthyroidism remains unclear, and there are no specific biochemical markers for cholestasis caused by this hormonal disease. This case underscores the possibility of severe jaundice as a clinical manifestation of hyperthyroidism, and highlights antithyroid drug treatment as an effective strategy for managing severe cholestatic jaundice.

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16

Grieco, Antonio, Luca Miele, Andrea Giorgi, Ignazio M. Civello, and Giovanni Gasbarrini. "Acute Cholestatic Hepatitis Associated with Celecoxib." Annals of Pharmacotherapy 36, no. 12 (December 2002): 1887–89. http://dx.doi.org/10.1345/aph.1c110.

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OBJECTIVE: To report a case of acute cholestatic hepatitis associated with the selective cyclooxygenase-2 inhibitor celecoxib. CASE SUMMARY: A 41-year-old white man was hospitalized for jaundice after 2 doses of celecoxib 200 mg for pain associated with right-knee trauma. Laboratory workup showed hyperbilirubinemia, mildly elevated serum transaminase concentrations, and cholestasis. Abdominal imaging showed no dilation of the biliary tree. Histology showed cholestasis, with bile plugs in dilated bile canaliculi and a mild portal infiltrate that are highly suggestive of drug-induced cholestasis. DISCUSSION: This is the fourth report in the English-language literature describing cholestatic hepatitis temporally related to celecoxib use, the second supported by histologic findings typical of drug-induced cholestasis, and the first in a patient who denied use of alcoholic beverages and was taking no other drugs or herbal products at the time of the reaction. The Naranjo probability scale indicated that celecoxib was a probable cause of acute cholestatic hepatitis in this patient. CONCLUSIONS: Cholestatic hepatitis is a well-recognized adverse effect of several drugs. Although celecoxib is considered to have a very low potential for hepatic toxicity, well-documented reports of adverse reactions can contribute significantly to the definition of more accurate safety profiles for new drugs introduced into clinical practice.

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17

Cataletti, Giovanni, Fabrizio Santagata, Luca Pastorelli, and Pier Maria Battezzati. "Severe azathioprine-induced liver injury 22 months after initiation of treatment." BMJ Case Reports 15, no. 12 (December 2022): e253505. http://dx.doi.org/10.1136/bcr-2022-253505.

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Drug-induced liver injury (DILI) is the leading cause of acute liver failure in high-income countries. Acute cholestasis is one of the most common forms of hepatotoxicity induced by azathioprine. It usually begins during the first year of treatment, with most cases reported during the first month. We describe an uncommon case of DILI that occurred after 22 months of drug administration. A woman in her 50s was hospitalised because of jaundice and asthenia. She had been treated with azathioprine for myasthenia gravis during the last 2 years. Acute cholestatic injury was diagnosed. After ruling out most common causes of cholestasis, azathioprine was withdrawn and subsequent histological findings in liver biopsy were consistent with drug-induced cholestatic liver damage. After discontinuation of azathioprine, biochemical parameters progressively normalised and remarkable clinical improvement was achieved. With this report, we suggest that azathioprine should be considered among the causes of liver injury, despite long treatment duration.

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18

Volynets, Galina V. "FAMILIAL INTRAHEPATIC CHOLESTASIS IN CHILDREN: PROBLEMS AND PROSPECTS." Russian Pediatric Journal 22, no. 6 (December 15, 2019): 388–94. http://dx.doi.org/10.18821/1560-9561-2019-22-6-388-394.

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The review presents various aspects of the clinic and diagnosis of familial intrahepatic cholestasis (FIC) in children, including such forms of liver pathology as progressive FIC (PFIC) types 1-5; PFIC associated with mutations in the MYO5B gene; non-progressive forms of intrahepatic cholestasis (benign recurrent IC, gestational IC, drug-induced cholestasis, hypophospholipid-associated cholelithiasis and liver cancer accompanied by cholestasis). The main methods for the diagnosis and treatment of cholestatic diseases in children are described. The feasibility of using full-exomic sequencing for the accurate diagnosis of HPV in children is shown.

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19

Richardson, C. E. "Drug points: Gabapentin induced cholestasis." BMJ 325, no. 7365 (September 21, 2002): 635. http://dx.doi.org/10.1136/bmj.325.7365.635.

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20

Mohi-ud-din, Raja, and James H. Lewis. "Drug- and chemical-induced cholestasis." Clinics in Liver Disease 8, no. 1 (February 2004): 95–132. http://dx.doi.org/10.1016/s1089-3261(03)00124-7.

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21

Lewis, James H., and Hyman J. Zimmerman. "DRUG- AND CHEMICAL-INDUCED CHOLESTASIS." Clinics in Liver Disease 3, no. 3 (August 1999): 433–64. http://dx.doi.org/10.1016/s1089-3261(05)70079-9.

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22

Köklü, Seyfettin, Osman Yüksel, Levent Filik, Oğuz Üsküdar, Kadri Altundağ, and Emin Altiparmak. "Recurrent Cholestasis Due to Ampicillin." Annals of Pharmacotherapy 37, no. 3 (March 2003): 395–97. http://dx.doi.org/10.1345/aph.1c273.

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OBJECTIVE: To present a single case of ampicillin-induced recurrent cholestasis and a literature review. CASE SUMMARY: A 23-year-old man was hospitalized due to recurrent and self-limited cholestatic symptoms. He had used ampicillin before each cholestatic attack. He became well clinically and biochemically each time after cessation of the drug. One year after his recovery and discontinuance of ampicillin, the patient has had no recurrence of cholestasis. An objective causality assessment revealed that the adverse drug reaction was probable. DISCUSSION: Ampicillin-related hepatotoxicity is very rare, with injury being mainly hepatocellular. To our knowledge, there is only 1 case report in the literature referring to chronic cholestatic-type hepatotoxicity related to ampicillin. CONCLUSIONS: Ampicillin, which is one of the most widely used antibiotics, may cause recurrent cholestatic hepatitis. Clinicians should be aware of this adverse effect, and it should be kept in mind during diagnostic workup of liver injury.

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23

Nakanishi, Yukihiro, and Romil Saxena. "Pathophysiology and Diseases of the Proximal Pathways of the Biliary System." Archives of Pathology & Laboratory Medicine 139, no. 7 (July 1, 2015): 858–66. http://dx.doi.org/10.5858/arpa.2014-0229-ra.

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Context Diseases of the proximal pathways of the biliary system can be divided into those that affect the interlobular bile ducts and those that affect the bile canaliculi. The former include primary biliary cirrhosis, small-duct variant of primary sclerosing cholangitis, graft-versus-host disease, and drug-induced liver injury, whereas the latter include progressive familial intrahepatic cholestasis, benign recurrent intrahepatic cholestasis, intrahepatic cholestasis of pregnancy, and drug-induced liver injury. Objective To summarize the current state of knowledge of diseases of the proximal pathways of the biliary system, with special emphasis on clinical presentation, pathological features, and differential diagnosis. Data Sources Clinicopathological information was extracted from pertinent published literature. Conclusions Care of the patient with cholestasis hinges on identifying the etiology. Diagnostic steps in cholestatic conditions comprise a thorough patient history, abdominal imaging, distinct serological studies, and liver biopsy. Primary biliary cirrhosis is characterized by distinctive serological and histological findings. The small-duct variant of primary sclerosing cholangitis is very rare and difficult to diagnose; imaging of the bile ducts is not helpful. Graft-versus-host disease is characterized by damage and loss of intrahepatic bile ducts. Drugs can cause injury variably at the level of bile canaliculus or the interlobular bile duct. Loss of bile ducts may be seen with primary biliary cirrhosis, primary sclerosing cholangitis, graft-versus-host disease, and drug-induced liver injury. Progressive familial intrahepatic cholestasis and progressive familial intrahepatic cholestasis represent 2 extreme ends of the spectrum of abnormalities in transporters responsible for bile formation. Intrahepatic cholestasis of pregnancy has a variable incidence in different parts of the world and may be due to abnormalities in transporter molecules.

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24

Ostroumova, O. D., E. V. Shikh, N. V. Shikh, T. M. Ostroumova, and Y. A. Isaakyan. "Drug-induced liver injury with cholestasis in the neurologist and psychiatric practice." Neurology, Neuropsychiatry, Psychosomatics 14, no. 1 (February 22, 2022): 14–21. http://dx.doi.org/10.14412/2074-2711-2022-1-14-21.

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Among drug-induced liver injuries (DILI), the cholestatic type is second in frequency (from 20 to 40%), the most common is the hepatocellular variant (up to 78%). For this reason, practitioners of various specialties, including neurologists and psychiatrists, do not monitor cholestasis parameters, and drug-induced liver injury with cholestasis (DILIС) remains unrecognized. The urgency of this problem is great, because the frequency of deaths in DILIС is only slightly lower than t in the hepatocellular type; in addition, it DILIС is much more likely to become persistent increasing the risk of chronic liver injury.Among the drugs used in neurology and psychiatry, the “leaders” in terms of the number of DILIС are antidepressants, both tricyclic (amitriptyline, imipramine) and selective serotonin reuptake inhibitors (SSRIs: paroxetine, sertraline, fluoxetine, citalopram, escitalopram), antidepressants), antipsychotics (chlorpromazine, fluphenazine), anticonvulsants (mainly carbamazepine).If the patient has a history of DILI caused by any of the forementioned medications, the agent should be switched to another drug from the same group with a minimal risk of DILI. If there is a history of DILI associated with antidepressants, it is recommended to choose SSRIs. It is necessary to monitor not only the activity of transaminases and bilirubin, but also the cholestasis parameters (alkaline phosphatase, γ-glutamyl transpeptidase) during treatment.

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25

Wright, Tara M., and Amy M. Vandenberg. "Risperidone- and Quetiapine-Induced Cholestasis." Annals of Pharmacotherapy 41, no. 9 (September 2007): 1518–23. http://dx.doi.org/10.1345/aph.1k145.

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Objective: To describe a case of a patient who developed drug-induced cholestasis after being on risperidone maintenance therapy for 8 years. Case Summary: A 30-year-old male with schizoaffective disorder, bipolar type, and insulin-dependent diabetes mellitus had been stable on risperidone 6 mg at night for 8 years. His other medications included lithium 900 mg twice daily and enalapril 5 mg daily, as well as regular insulin and NPH insulin as needed. The patient developed cholestasis that resolved once risperidone was discontinued. Over the next 11 months, he tolerated trials of ziprasidone and olanzapine. When quetiapine was initiated, the patient developed signs and symptoms of cholestasis within 3 weeks after starting this medication. The signs and symptoms of cholestasis resolved with removal of quetiapine. The Naranjo probability scale indicated that these atypical antipsychotics (risperidone and quetiapine) were the probable cause of cholestasis in this patient. Discussion: It is well known that atypical antipsychotics can cause isolated asymptomatic increases in aminotransferase levels. Liver injury, both the hepatic and cholestatic type, has been described previously, although the incidence with atypical antipsychotics is rare. Conclusions: To our knowledge, this is the first case of cholestasis that developed after years of treatment and reappeared with another antipsychotic agent. Given that liver failure, of either the hepatic or cholestatic type, is a relatively rare phenomenon with atypical antipsychotics, it seems that the most reasonable approach to manage this risk is through education. By educating patients on early warning signs of hepatotoxicity, this rare but potentially fatal consequence could be detected early to allow appropriate intervention.

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26

Pereverzev, A. P., O. D. Ostroumova, and A. I. Kochetkov. "Drug-induced liver damage with cholestasis." Kachestvennaya klinicheskaya praktika, no. 3 (September 27, 2020): 61–74. http://dx.doi.org/10.37489/2588-0519-2020-3-61-74.

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The liver is the main organ responsible for the biotransformation and elimination of drugs, and therefore its function is often impaired by different medications. In this article, the authors inform practical health care professionals about the possible liver damage with cholestasis caused by drugs (DILI). Most often, DILI is caused some antibacterial drugs, steroids, barbiturates and some other drugs. DILI has no pathognomonic clinical manifestations. tte scientific literature describes both an asymptomatic increase of “liver” enzymes and the development of acute liver failure. Important diagnostic methods are the collection of anamnesis (especially the medicinal one), analysis of blood biochemical tests, and data from visual diagnostic methods. If the patient has DILI, it is necessary, whenever possible, to stop intake of a drug. ttere are no specific drugs recommended for pharmacotherapy of DILI but there is some the positive effect of ademetionine and ursodeoxycholic acid. ttere are no specific preventive measures for DILI. Healthcare practitioners are recommended not to use drugs off-label, optimize pharmacotherapy and fight with polypharmacy, monitore biochemical tests regularly etc.

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27

Petrov, Petar D., M. Leonor Fernández-Murga, Mireia López-Riera, M. José Goméz-Lechón, Jose V. Castell, and Ramiro Jover. "Predicting drug-induced cholestasis: preclinical models." Expert Opinion on Drug Metabolism & Toxicology 14, no. 7 (June 20, 2018): 721–38. http://dx.doi.org/10.1080/17425255.2018.1487399.

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28

Pauli-Magnus, Christiane, and Peter J. Meier. "Hepatobiliary transporters and drug-induced cholestasis." Hepatology 44, no. 4 (2006): 778–87. http://dx.doi.org/10.1002/hep.21359.

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29

Sultana, Halima, Michio Komai, and Hitoshi Shirakawa. "The Role of Vitamin K in Cholestatic Liver Disease." Nutrients 13, no. 8 (July 23, 2021): 2515. http://dx.doi.org/10.3390/nu13082515.

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Vitamin K (VK) is a ligand of the pregnane X receptor (PXR), which plays a critical role in the detoxification of xenobiotics and metabolism of bile acids. VK1 may reduce the risk of death in patients with chronic liver failure. VK deficiency is associated with intrahepatic cholestasis, and is already being used as a drug for cholestasis-induced liver fibrosis in China. In Japan, to treat osteoporosis in patients with primary biliary cholangitis, VK2 formulations are prescribed, along with vitamin D3. Animal studies have revealed that after bile duct ligation-induced cholestasis, PXR knockout mice manifested more hepatic damage than wild-type mice. Ligand-mediated activation of PXR improves biochemical parameters. Rifampicin is a well-known human PXR ligand that has been used to treat intractable pruritus in severe cholestasis. In addition to its anti-cholestatic properties, PXR has anti-fibrotic and anti-inflammatory effects. However, because of the scarcity of animal studies, the mechanism of the effect of VK on cholestasis-related liver disease has not yet been revealed. Moreover, the application of VK in cholestasis-related diseases is controversial. Considering this background, the present review focuses on the effect of VK in cholestasis-related diseases, emphasizing its function as a modulator of PXR.

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30

Ming, Jiaxiong, Qianqian Xu, Limin Gao, Yanfang Deng, Jie Yin, Qun Zhou, Qingyi Tong, and Yonghui Zhang. "Kinsenoside Alleviates 17α-Ethinylestradiol-Induced Cholestatic Liver Injury in Rats by Inhibiting Inflammatory Responses and Regulating FXR-Mediated Bile Acid Homeostasis." Pharmaceuticals 14, no. 5 (May 11, 2021): 452. http://dx.doi.org/10.3390/ph14050452.

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Cholestasis is an important predisposing factor of liver diseases, such as hepatocyte necrosis, liver fibrosis and primary biliary cirrhosis. In this study, we aimed to investigate the effects of Kinsenoside (KD), a natural active ingredient of Anoectochilus roxburghii, on estrogen-induced cholestatic liver injury in Sprague-Dawley rats and the underlying mechanism. The rats were randomly divided into six groups: control group, model group, low-dose KD group (50 mg/kg body weight, KD-L), medium-dose KD group (100 mg/kg body weight, KD-M), high-dose KD group (200 mg/kg body weight, KD-H) and ursodeoxycholic acid group (40 mg/kg body weight, UDCA). 17α-Ethinylestradiol (EE) was used to establish an experimental animal model of estrogen-induced cholestasis (EIC). The results demonstrated that KD alleviated liver pathologic damage, serum biochemical status and inhibited hepatocellular microstructure disorder and bile duct hyperplasia in EE-induced cholestatic rats. Mechanically, KD alleviated EE-induced cholestatic liver injury by inhibiting inflammatory responses and regulating bile acid homeostasis. Concretely, KD reduced the expression of IL-1β and IL-6 by inhibiting NF-κB p65 to suppress EE-mediated inflammation in rat liver. KD enhanced the expression of FXR and inhibited EE-mediated reduction of FXR in vitro and in vivo. It was the potential mechanism that KD mitigates cholestasis by increasing efflux and inhibiting uptake of bile acids via FXR-mediated induction of bile salt export pump (BSEP) and reduction of Na+-dependent taurocholate cotransport peptide (NTCP) to maintain bile acid homeostasis. Moreover, KD repressed the bile acid synthesis through reducing the expression of synthetic enzyme (CYP7A1), thereby normalizing the expression of metabolic enzyme (SULT2A1) of bile acid. In conclusion, our results revealed that KD may be an effective drug candidate for the treatment of cholestasis.

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31

Pauli-Magnus, Christiane, Peter Meier, and Bruno Stieger. "Genetic Determinants of Drug-induced Cholestasis and Intrahepatic Cholestasis of Pregnancy." Seminars in Liver Disease 30, no. 02 (April 26, 2010): 147–59. http://dx.doi.org/10.1055/s-0030-1253224.

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32

Chatterjee, Sagnik, and Pieter Annaert. "Drug-induced Cholestasis: Mechanisms, Models, and Markers." Current Drug Metabolism 19, no. 10 (September 14, 2018): 808–18. http://dx.doi.org/10.2174/1389200219666180427165035.

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33

King, Paul, and Bennett Blitzer. "Drug-Induced Cholestasis: Pathogenesis and Clinical Features." Seminars in Liver Disease 10, no. 04 (November 1990): 316–21. http://dx.doi.org/10.1055/s-2008-1040487.

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34

Rocchetti, Nicolás Sebastián, María Florencia Corbacho Re, and Daniel Horacio Bagilet. "A rare cause of drug-induced cholestasis." Medicina Clínica Práctica 2, no. 2 (March 2019): 26–28. http://dx.doi.org/10.1016/j.mcpsp.2019.01.001.

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35

Van Brantegem, Pieter, Sagnik Chatterjee, Tom De Bruyn, Pieter Annaert, and Neel Deferm. "Drug-induced cholestasis assay in primary hepatocytes." MethodsX 7 (2020): 101080. http://dx.doi.org/10.1016/j.mex.2020.101080.

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36

Hashim, Ahmed, Ashley Barnabas, Rosa Miquel, and Kosh Agarwal. "Successful liver transplantation for drug-induced vanishing bile duct syndrome." BMJ Case Reports 13, no. 1 (January 2020): e233052. http://dx.doi.org/10.1136/bcr-2019-233052.

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Drug-induced cholestasis has a wide range of clinical presentations, and in a small number of patients, it can progress to severe ductopenia. A 63-year-old woman was referred to our department with progressive cholestasis and hyperbilirubinaemia following a course of flucloxacillin. Despite the comprehensive laboratory, imaging and genetic investigations, no other cause for the cholestasis was demonstrated. Sequential liver biopsies confirmed the development of vanishing bile duct syndrome. She developed significant cachexia and pruritus that did not respond to medical therapy, and hence she was listed for liver transplantation. She underwent liver transplantation 6 months after the initial drug-induced injury. She has remained well with good graft function at 1-year follow-up. The case highlights an extreme form of drug-induced ductopenia and underscores the need for meticulous hepatology input and consideration of liver transplantation in some patients.

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Skurnik, Yair D., Alexandra Tcherniak, Karl Edlan, and Zev Sthoeger. "Ticlopidine-Induced Cholestatic Hepatitis." Annals of Pharmacotherapy 37, no. 3 (March 2003): 371–75. http://dx.doi.org/10.1345/aph.1a406.

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OBJECTIVE: To report 2 cases of ticlopidine-induced cholestatic hepatitis, investigate its mechanism, and compare the observed main characteristics with those of the published cases. CASE SUMMARIES: Two patients developed prolonged cholestatic hepatitis after receiving ticlopidine following percutaneous coronary angioplasty, with complete remission during the follow-up period. T-cell stimulation by therapeutic concentration of ticlopidine was demonstrated in vitro in the patients, but not in healthy controls. DISCUSSION: Cholestatic hepatitis is a rare complication of the antiplatelet agent ticlopidine; several cases have been reported but few in the English literature. Our patients developed jaundice following treatment with ticlopidine and showed the clinical and laboratory characteristics of cholestatic hepatitis, which resolved after discontinuation of the drug. Hepatitis may develop weeks after discontinuation of the drug and may run a prolonged course, but complete remission was observed in all reported cases. An objective causality assessment revealed that the adverse drug event was probably related to the use of ticlopidine. The mechanisms of this ticlopidine-induced cholestasis are unclear. Immune mechanisms may be involved in the drug's hepatotoxicity, as suggested by the T-cell stimulation study reported here. CONCLUSIONS: Cholestatic hepatitis is a rare adverse effect of ticlopidine that may be immune mediated. Patients receiving the drug should be monitored with liver function tests along with complete blood cell counts. This complication will be observed even less often in the future as ticlopidine is being replaced by the newer antiplatelet agent clopidogrel.

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Li, Wen, Fang Yuan, and Lai-You Wang. "Mechanism, prevention, and treatment of drug-induced cholestasis." World Chinese Journal of Digestology 27, no. 21 (November 8, 2019): 1295–303. http://dx.doi.org/10.11569/wcjd.v27.i21.1295.

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39

Brouwer, Kim L. R. "Mechanistic modeling of drug-induced cholestasis: Clinical relevance." Toxicology Letters 258 (September 2016): S48. http://dx.doi.org/10.1016/j.toxlet.2016.06.1273.

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40

Krell, Herbert, J�rgen Metz, Hartmut Jaeschke, Hartmut H�ke, and Erich Pfaff. "Drug-induced intrahepatic cholestasis: characterization of different pathomechanisms." Archives of Toxicology 60, no. 1-3 (May 1987): 124–30. http://dx.doi.org/10.1007/bf00296964.

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41

Frenette, Anne Julie, Marie-Eve Bédard Dufresne, Valérie Bonhomme, Martin Albert, and David R. Williamson. "Drug-induced hepatic cholestasis in the critically ill." Intensive Care Medicine 37, no. 7 (March 3, 2011): 1225–26. http://dx.doi.org/10.1007/s00134-011-2188-2.

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42

Chang, Chung-Che, Mary Petrelli, Joseph F. Tomashefski, and Arthur J. McCullough. "Severe Intrahepatic Cholestasis Caused by Amiodarone Toxicity After Withdrawal of the Drug." Archives of Pathology & Laboratory Medicine 123, no. 3 (March 1, 1999): 251–56. http://dx.doi.org/10.5858/1999-123-0251-siccba.

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Abstract Cholestasis has been reported as a rare presentation among patients with severe liver injury secondary to amiodarone hepatic toxicity. We report an unusual case of amiodarone-induced cholestatic hepatotoxicity occurring after amiodarone had been discontinued and the initial abnormal liver function findings had improved. The patient, without jaundice at the initial presentation, developed severe jaundice about 4 months after withdrawal of amiodarone. Light and transmission electron microscopic examination of a specimen secured by computed tomographically guided liver biopsy was consistent with amiodarone hepatic toxicity as the cause of intrahepatic cholestasis. An abdominal ultrasound, endoscopic retrograde cholangiography, and dimethyl iminodiacetic acid and computed tomographic scans of the abdomen all failed to demonstrate any other causes for jaundice other than amiodarone toxicity. Thus, amiodarone hepatic toxicity may occur after drug withdrawal even if results of liver function tests improve. Histopathologic examination of a liver biopsy specimen is of value for diagnosis and prognosis. The liver biopsy findings, clinical course, and liver function test results are discussed, and the English-language literature on amiodarone cholestatic hepatotoxicity is reviewed.

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Sukhanov, D. S., E. V. Timofeev, Yu S. Alekseeva, and D. Yu Azovtsev. "Drug-Induced Liver Injury in Tuberculosis: Mechanisms of Development and Diagnostic Methods." Juvenis Scientia 9, no. 1 (2023): 24–42. http://dx.doi.org/10.32415/jscientia_2023_9_1_24-42.

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The review article discusses modern aspects of drug-induced liver injury (DILI) in patients with tuberculosis who are receiving etiotropic therapy. The main mechanisms of DILI, including toxic and idiosyncratic types, are described, as well as their pathogenetic, biochemical, and epidemiological differences. DILI can manifest as various clinicomorphological forms of liver damage, such as steatosis and steatohepatitis, acute and chronic hepatitis, mitochondrial cytopathy, cholestasis, sclerosing cholangitis, vascular injury, and others. The main diagnostic method for DILI is the detection of liver enzymes - transaminases and alkaline phosphatase - based on the degree of elevation and their ratio, which identify two main types of liver injury - hepatocellular and cholestatic - as well as a mixed variant. The article provides a scoring assessment of liver damage in a patient receiving chemotherapy to classify it as drug-induced liver injury.

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Zollner, Gernot, Martin Wagner, and Michael Trauner. "Nuclear receptors as drug targets in cholestasis and drug-induced hepatotoxicity." Pharmacology & Therapeutics 126, no. 3 (June 2010): 228–43. http://dx.doi.org/10.1016/j.pharmthera.2010.03.005.

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45

Vilas-Boas, Vânia, Eva Gijbels, Kaat Leroy, Alanah Pieters, Audrey Baze, Céline Parmentier, and Mathieu Vinken. "Primary Human Hepatocyte Spheroids as Tools to Study the Hepatotoxic Potential of Non-Pharmaceutical Chemicals." International Journal of Molecular Sciences 22, no. 20 (October 12, 2021): 11005. http://dx.doi.org/10.3390/ijms222011005.

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Drug-induced liver injury, including cholestasis, is an important clinical issue and economic burden for pharmaceutical industry and healthcare systems. However, human-relevant in vitro information on the ability of other types of chemicals to induce cholestatic hepatotoxicity is lacking. This work aimed at investigating the cholestatic potential of non-pharmaceutical chemicals using primary human hepatocytes cultured in 3D spheroids. Spheroid cultures were repeatedly (co-) exposed to drugs (cyclosporine-A, bosentan, macitentan) or non-pharmaceutical chemicals (paraquat, tartrazine, triclosan) and a concentrated mixture of bile acids for 4 weeks. Cell viability (adenosine triphosphate content) was checked every week and used to calculate the cholestatic index, an indicator of cholestatic liability. Microarray analysis was performed at specific time-points to verify the deregulation of genes related to cholestasis, steatosis and fibrosis. Despite the evident inter-donor variability, shorter exposures to cyclosporine-A consistently produced cholestatic index values below 0.80 with transcriptomic data partially supporting its cholestatic burden. Bosentan confirmed to be hepatotoxic, while macitentan was not toxic in the tested concentrations. Prolonged exposure to paraquat suggested fibrotic potential, while triclosan markedly deregulated genes involved in different types of hepatotoxicity. These results support the applicability of primary human hepatocyte spheroids to study hepatotoxicity of non-pharmaceutical chemicals in vitro.

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Gubergrits, N. B., N. V. Byelyayeva, A. Ye Klochkov, G. M. Lukashevich, and P. G. Fomenko. "Drug-induced liver injury: from pathogenesis to treatment." Herald of Pancreatic Club 46, no. 1 (March 26, 2020): 72–80. http://dx.doi.org/10.33149/vkp.2020.01.10.

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The article presents data on classification, pathogenesis, clinical picture, diagnosis and differentiated treatment tactics, as well as practical algorithm for recognizing and preventing the development of drug-induced liver injury. Pathogenesis of drug-induced liver injury is analyzed, mechanisms of drug metabolism are explained, metabolism phases are described. Four main mechanisms of the pathological effect of drugs on the liver are identified: direct toxic effect on hepatocytes; toxic effect of drug metabolites; immunoallergic liver injury; idiosyncrasy. Peculiar attention is paid to the pathogenesis of drug-induced cholestasis. Direct hepatotoxic reactions develop according to the cytolytic (hepatocellular, parenchymal), cholestatic or mixed option. The most commonly diagnosed clinical variant of drug-induced liver injury is drug-induced hepatitis. Five forms of hepatitis induced by the use of pharmacological agents are distinguished: drug-induced hepatitis with an isolated increase in transaminases (anti-TB drugs, methyldopa, amiodarone, statins); acute hepatitis with jaundice; pseudo-surgical form of acute hepatitis: abdominal pain, fever, jaundice, enlarged gall bladder (cytostatics, antidepressants, antiarrhythmic drugs); severe forms of acute hepatitis with liver failure; chronic drug hepatitis. International diagnostic criteria, basic data on morphological liver changes are presented. Action of ursodeoxycholic acid is explained. It has a litholytic, anticholestatic, cytoprotective, immunomodulating, anti-inflammatory, antitoxic, hypocholesterolemic effect, modulates apoptosis, has a differentiated effect on the regeneration of hepatocytes.

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Lim, Roxanne, Hassan Choudry, Kim Conner, and Wikrom Karnsakul. "A Challenge for Diagnosing Acute Liver Injury with Concomitant/Sequential Exposure to Multiple Drugs: Can Causality Assessment Scales Be Utilized to Identify the Offending Drug?" Case Reports in Pediatrics 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/156389.

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Drug-induced hepatotoxicity most commonly manifests as an acute hepatitis syndrome and remains the leading cause of drug-induced death/mortality and the primary reason for withdrawal of drugs from the pharmaceutical market. We report a case of acute liver injury in a 12-year-old Hispanic boy, who received a series of five antibiotics (amoxicillin, ceftriaxone, vancomycin, ampicillin/sulbactam, and clindamycin) for cervical lymphadenitis/retropharyngeal cellulitis. Histopathology of the liver biopsy specimen revealed acute cholestatic hepatitis. All known causes of acute liver injury were appropriately excluded and (only) drug-induced liver injury was left as a cause of his cholestasis. Liver-specific causality assessment scales such as Council for the International Organization of Medical Sciences/Roussel Uclaf Causality Assessment Method scoring system (CIOMS/RUCAM), Maria and Victorino scale, and Digestive Disease Week-Japan were applied to seek the most likely offending drug. Although clindamycin is the most likely cause by clinical diagnosis, none of causality assessment scales aid in the diagnosis.

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Pereverzev, A. P., and O. D. Ostroumova. "Antineoplastic drugs and drug-induced liver damage with cholestasis." Medical alphabet 1, no. 19 (November 2, 2020): 47–54. http://dx.doi.org/10.33667/2078-5631-2020-19-47-54.

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The number of cases of drug-induced liver injury (DILI) has been increasing since the 1990s. DILIs cause up to 40,000 deaths each year. One of the leaders in the number of DILIs are antineoplastic drugs ms, such as alkylating agents, antimetabolites, targeted drugs, monoclonal antibodies, etc. One of the most effective and safe strategies for the treatment and prevention of DILI is to use hepatoprotective drugs. Currently, on the market of the Russian Federation, is available novel drug Heptrong® (does not have an International Non-proprietary Name), which has anti-inflammatory, antioxidant activity and the ability to stabilize and reduce the permeability of hepatocyte membranes, suppress the activity 5-lipoxygenase, a decrease in the synthesis of leukotriene B4, interleukin-1, interleukin-6, which are pro-inflammatory cytokines. The drug activates the antitoxic function of the liver, improves its protein- and lipid-synthesizing functions. Heptrong® neutralizes the processes of inflammation in the liver, thereby reducing the severity of the clinical manifestations of drug-induced lesions.

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MASUMOTO, T., M. ISHIKAWA, Y. YAMAUCHI, Y. HIASA, K. YAMAMOTO, H. IUCHI, K. OHKUBO, S. FAZLEAKBAR, K. MICHITAKA, and N. HORIIKE. "Drug-induced hepatitis with severe cholestasis due to voglibose." International Hepatology Communications 5, no. 4-5 (September 1996): 289–96. http://dx.doi.org/10.1016/0928-4346(96)00310-6.

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Gijbels, Eva, Vânia Vilas-Boas, Neel Deferm, Lindsey Devisscher, Hartmut Jaeschke, Pieter Annaert, and Mathieu Vinken. "Mechanisms and in vitro models of drug-induced cholestasis." Archives of Toxicology 93, no. 5 (April 10, 2019): 1169–86. http://dx.doi.org/10.1007/s00204-019-02437-2.

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