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Thematische Bibliographien / Drug-induced cholestasis / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Drug-induced cholestasis“

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Veröffentlicht am 25. Mai 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 (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 (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 (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 (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 (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 (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 (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 (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 (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 (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 cho

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13

Larrey, Dominique, and Serge Erlinger. "9 Drug-induced cholestasis." Baillière's Clinical Gastroenterology 2, no. 2 (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, et al. "Molecular and Clinical Links between Drug-Induced Cholestasis and Familial Intrahepatic Cholestasis." International Journal of Molecular Sciences 24, no. 6 (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) pro

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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 (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 effectivel

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Grieco, Antonio, Luca Miele, Andrea Giorgi, Ignazio M. Civello, and Giovanni Gasbarrini. "Acute Cholestatic Hepatitis Associated with Celecoxib." Annals of Pharmacotherapy 36, no. 12 (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

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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 (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 o

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Volynets, Galina V. "FAMILIAL INTRAHEPATIC CHOLESTASIS IN CHILDREN: PROBLEMS AND PROSPECTS." Russian Pediatric Journal 22, no. 6 (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 fo

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Richardson, C. E. "Drug points: Gabapentin induced cholestasis." BMJ 325, no. 7365 (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 (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 (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 (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 ver

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Nakanishi, Yukihiro, and Romil Saxena. "Pathophysiology and Diseases of the Proximal Pathways of the Biliary System." Archives of Pathology & Laboratory Medicine 139, no. 7 (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

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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 (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 c

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Wright, Tara M., and Amy M. Vandenberg. "Risperidone- and Quetiapine-Induced Cholestasis." Annals of Pharmacotherapy 41, no. 9 (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 a

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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 diag

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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 (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 (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

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Ming, Jiaxiong, Qianqian Xu, Limin Gao та ін. "Kinsenoside Alleviates 17α-Ethinylestradiol-Induced Cholestatic Liver Injury in Rats by Inhibiting Inflammatory Responses and Regulating FXR-Mediated Bile Acid Homeostasis". Pharmaceuticals 14, № 5 (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 ur

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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 (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 (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 (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 (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 (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 w

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Skurnik, Yair D., Alexandra Tcherniak, Karl Edlan, and Zev Sthoeger. "Ticlopidine-Induced Cholestatic Hepatitis." Annals of Pharmacotherapy 37, no. 3 (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 ti

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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 (2019): 1295–303. http://dx.doi.org/10.11569/wcjd.v27.i21.1295.

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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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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 (1987): 124–30. http://dx.doi.org/10.1007/bf00296964.

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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 (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 (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 consist

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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 li

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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 (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, et al. "Primary Human Hepatocyte Spheroids as Tools to Study the Hepatotoxic Potential of Non-Pharmaceutical Chemicals." International Journal of Molecular Sciences 22, no. 20 (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)

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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 (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 p

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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 appro

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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 (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 ac

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MASUMOTO, T., M. ISHIKAWA, Y. YAMAUCHI, et al. "Drug-induced hepatitis with severe cholestasis due to voglibose." International Hepatology Communications 5, no. 4-5 (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, et al. "Mechanisms and in vitro models of drug-induced cholestasis." Archives of Toxicology 93, no. 5 (2019): 1169–86. http://dx.doi.org/10.1007/s00204-019-02437-2.

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