Relevant bibliographies by topics / Drug-induced cholestasis

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Academic literature on the topic 'Drug-induced cholestasis'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Drug-induced cholestasis"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Drug-induced cholestasis"

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Charanek, Ahmad. "The Bile Canaliculus Revisited : Morphological And Functional Alterations Induced By Cholestatic Drugs In HepaRG Cells." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B011/document.

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La cholestase est l'une des manifestations les plus courantes des lésions induitespar des médicaments. Dans 40% des cas elle n’est pas prévisible; une meilleure prédictibilité représente donc un défi majeur. Tout d'abord, nous avons démontré que les cellules hépatiques humaines HepaRG différenciées sont un modèle approprié pour étudier la cholestase induite par les médicaments en comparant la localisation et l’activité des transporteurs d'influx et d'efflux avec les hépatocytes humains primaires. Tous les transporteurs d'efflux et d’influx testés ont été correctement localisés au niveau des membranes canaliculaire (BSEP, MRP2, MDR1 et MDR3) et basolatéral (NTCP, MRP3) et sont fonctionnels. En outre, ces cellules expriment également les enzymes qui métabolisent les acides biliaires (ABs) et ont la capacité de les synthétiser et de les conjuguer avec la taurine, la glycine et le sulfate, à un taux similaire à celui des hépatocytes primaires. Des changements ont été observés sur la répartition des ABs totaux après traitements de cellules HepaRG par un médicament cholestatique, la cyclosporine A (CsA), de manière concentration- dépendante. L'inhibition de l'efflux et de l'influx de taurocholate a été observée après 15 min et 1 h respectivement. Ces premiers effets ont été associés à la dérégulation de la voie des cPKC et l'induction d’un stress du réticulum endoplasmique puis d’un stress oxydant. Nous avons également montré pour la première fois une accumulation intracellulaire d’ABs endogènes avec un médicament cholestatique in vitro. En outre, notre travail apporte des preuves que la motilité des canalicules biliaires (BC) est indispensable à la clairance des ABs. La voie ROCK et le complexe actomyosine sont fortement impliqués. Nous avons fourni la première démonstration que la voie ROCK et les dynamiques des BC sont des cibles majeures des composés cholestatiques. Nos données devraient contribuer à l'élaboration de méthodes de screening pour la prédiction précoce des effets secondaires induits par les médicaments cholestatiques
Cholestasis is one of the most common manifestations of drug-induced liver injury (DILI). Since up to now it is unpredictable in 40% of all cases its accurate prediction represents a major challenge. First, we validated that differentiated HepaRG human liver cells are a suitable in vitro model to study drug-induced cholestasis, by comparing localization of influx and efflux transporters and their functional activity in these cells and primary human hepatocytes. All tested influx and efflux transporters were correctly localized to canalicular (BSEP, MRP2, MDR1, and MDR3) or basolateral (NTCP, MRP3) membrane domains and were functional. In addition, the HepaRG cell line also exhibits bile acids (BAs) metabolizing enzymes and has the capacity to synthesize BAs and to further amidate these BAs with taurine and glycine as well as sulfate, at a rate similar to that of primary hepatocytes. Concentration- dependent changes were observed in total BAs disposition after treatment of HepaRG cells by the cholestatic drug cyclosporine A (CsA). Inhibition of efflux and uptake of taurocholate was evidenced as early as 15 min and 1 h respectively. These early effects were associated with deregulation of cPKC pathway and induction of endoplasmic reticulum stress that preceded generation of oxidative stress. We also showed for the first time intracellular accumulation of endogenous BAs by a cholestatic drug in vitro. In addition, our work brings evidences that motility of bile canaliculi (BC) is essential for BAs clearance where ROCK pathway and actomyosin complex are highly implicated. We provided the first demonstration that ROCK pathway and BC dynamics are major targets of cholestatic compounds. Our data should help in the development of screening methods for early prediction of drug-induced cholestatic side effects
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Burban, Audrey. "Mécanismes impliqués dans la cholestase d'origine médicamenteuse : perturbations de la voie ROCK/MLCK et du profil intracellulaire des acides biliaires." Thesis, Rennes 1, 2017. http://www.theses.fr/2017REN1B018/document.

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La cholestase intrahépatique représente environ 40% des lésions hépatiques induites par les médicaments et se caractérise par une accumulation intracellulaire des acides biliaires (AB). Les mécanismes impliqués sont encore mal connus et sa prédiction reste difficile. Le but de ce travail était de caractériser dans la cholestase d’origine médicamenteuse et de développer des méthodes de screening pour sa prédiction précoce, en utilisant la lignée humaine hépatique HepaRG et les hépatocytes humains. Tout d’abord, nous avons démontré que la motilité des canalicules biliaires (CB) est indispensable à la clairance des AB et requiert une alternance de phosphorylation/déphosphorylation de la chaine légère de la myosine (MLC), contrôlé par la voie Rho-kinase/Myosin Light Chain Kinase (ROCK/MLCK). Nous avons ensuite montré pour la première fois que les médicaments cholestatiques altèrent la voie ROCK/MLCK/MLC et la dynamique des CB. En utilisant la famille des antibiotiques résistant à la pénicillinase, dont fait partie la flucloxacilline, responsable de nombreux cas de cholestase, nous avons observé que la dérégulation de ROCK pouvait se faire par activation de HSP27, associée aux voies de signalisation PKC/P38 et PI3K/AKT. Enfin, nous avons montré une capacité variable des médicaments cholestatiques à moduler les profils des AB. En effet, les médicaments cholestatiques majeurs induisent une accumulation préférentielle des AB hydrophobes toxiques, in vitro, dans les premières 24h, qui résulte d’une inhibition de leur amidation. Au total, l’ensemble du travail a permis de progresser dans la compréhension des mécanismes impliqués dans la cholestase d’origine médicamenteuse et de mettre en évidence de nouveaux biomarqueurs utiles pour sa prédiction
Intrahepatic cholestasis represents around 40% of drug-induced liver injuries and is characterized by intracellular accumulation of bile acids (BA); mechanisms involved and its accurate prediction remains challenging. The aim of the current work was to characterize the mechanisms involved in drug-induced cholestasis and to develop screening methods for its early prediction, using human differentiated HepaRG and primary human hepatocytes. First, we demonstrated that bile canaliculi (BC) motility is essential for BA clearance and requires alternating phosphorylation/dephosphorylation of myosin light chain (MLC) that is controlled by the Rho-kinase/Myosin Light Chain Kinase (ROCK/MLCK) signaling pathway. Then, we showed, for the first time that cholestatic drugs could alter the ROCK/MLCK/MLC pathway and BC dynamics. Using the penicillinase-resistant antibiotics family, including flucloxacillin that is responsible for many cases of cholestasis, we found that deregulation of ROCK could be modulated by HSP27, associated with PKC/P38 and PI3K/AKT signaling pathways. Finally, we evidenced variable potency of cholestatic drugs to modulate BA profiles. Indeed, the well-known cholestatic drugs induced a preferential accumulation of unconjugated toxic hydrophobic BA in vitro within the first 24h that resulted from inhibition of their amidation. Altogether, these data bring new information on the understanding of the mechanisms involved in drug-induced cholestasis and highlight new morphological and molecular predictive biomarkers of drug-induced cholestasis
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Valentin, Loïse. "Développement de modèles de culture en 3D pour l’étude des maladies et des infections hépatiques humaines." Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS442.pdf.

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Les infections et maladies hépatiques sont une cause majeure de morbidité et de mortalité. Elles incluent des infections causées par des pathogènes hépatotropiques, comme le parasite Plasmodium, et des maladies d’origine non infectieuse causées notamment par des traitements médicamenteux, telle que la cholestase. L’hépatocyte humain primaire (PHH) est le type cellulaire de choix pour étudier ces infections et pathologies in vitro, mais il est nécessaire de développer de nouveaux modèles de culture plus proches de la physiologie des cellules in vivo et plus pertinents que les modèles 2D. C’est dans ce contexte que s’inscrit mon projet de thèse visant à développer des systèmes de culture en 3D de cellules hépatiques humaines. Les travaux menés ont conduit à la mise en place d’un modèle 3D sphéroïde scaffold-free de PHH viable et plus fonctionnel que le modèle 2D+. Les résultats montrent également que les sphéroïdes de PHH sont un modèle approprié pour la culture du stade hépatique de Plasmodium et suggèrent une meilleure sensibilité de ce modèle pour la prédiction d’activité de molécules antipaludiques. Dans le but d’améliorer la manipulation des sphéroïdes, la magnétisation des sphéroïdes à l’aide de nanoparticules (NS) a été testée. Les NS n’affectent ni la viabilité, ni les fonctions hépatiques des PHH, ni leur susceptibilité à l’infection par Plasmodium. Enfin, un modèle identique avec des cellules HepaRG a été utilisé pour tester une méthode de détection de la cholestase médicamenteuse à l’aide d’une nouvelle sonde fluorescente. Les résultats suggèrent que cette sonde peut être utilisée dans des modèles sphéroïdes pour l’évaluation de l’activité de molécules cholestatiques
Liver infections and diseases are a major cause of morbidity and mortality. They include infections caused by hepatotropic pathogens, such as the Plasmodium parasite, and diseases of non-infectious origin caused in particular by drug treatments, such as cholestasis. The primary human hepatocyte (PHH) is the cell type of choice to study these infections and pathologies in vitro, but it is essential to develop new culture models closer to the physiology of cells in vivo and more relevant than 2D models. In this context, my thesis project aims to develop 3D culture systems for human liver cells. The work allowed to the establishment of a viable 3D spheroid scaffold-free model of PHH more functional than the 2D+ model. The results also demonstrate that PHH spheroids are an appropriate model for the culture of the liver stage of Plasmodium and would be more sensitive to antimalarial molecules. In order to improve the manipulation of spheroids, the magnetization of spheroids using nanoparticles (NS) was tested. NS do not affect the viability or hepatic functions of PHHs or their susceptibility to Plasmodium infection. Finally, an identical model with HepaRG cells was used to test a method for detecting drug induced cholestasis using a new fluorescent probe. The results proved that this probe can be used in spheroid models for the evaluation of the activity of cholestatic molecules
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Books on the topic "Drug-induced cholestasis"

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Kortgen, Andreas, and Michael Bauer. The effect of acute hepatic failure on drug handling in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0197.

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Impaired hepatic function is a common event in intensive care unit patients and as the liver plays a central role in drug metabolism and excretion this may lead to profound changes in pharmacokinetics. Underlying mechanisms are altered enzyme function of phase I and phase II metabolism, altered transporter protein function together with cholestasis and hepatic perfusion disorders. Moreover, multidrug therapy may lead to induction and inhibition of these enzymes and transporter proteins. In addition, changes in plasma protein binding and volumes of distribution of drugs are common. Altogether, these changes may not only lead to sometimes unpredictable plasma levels of xenobiotics, but also to drug-induced liver injury when hepatocellular accumulation of noxious substances occurs. Concomitant renal dysfunction may further complicate this situation. Pharmacodynamic alterations might also occur. In conclusion, the clinician must carefully evaluate medication given to patients with hepatic failure. Therapeutic drug monitoring should be performed wherever available to guide therapy.
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Iverson, Suzanne Leah. In vitro and in vivo investigations into idiosyncratic drug reactions: the role of reactive metabolites produced by the target tissue in terbinafine-induced cholestatic hepatitis and antipsychotic-induced agranulocytosis. 2002, 2002.

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Iverson, Suzanne Leah. In vitro and in vivo investigations into idiosyncratic drug reactions: The role of reactive metabolites produced by the target tissue in terbinafine-induced cholestatic hepatitis and antipsychotic-induced agranulocytosis. 2002.

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Book chapters on the topic "Drug-induced cholestasis"

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Hamilton, James P., and Jacqueline M. Laurin. "Drug-Induced Cholestasis." In Cholestatic Liver Disease, 21–43. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-118-5_2.

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Björnsson, Einar S. "Drug-Induced Cholestasis." In Clinical Gastroenterology, 13–31. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1013-7_2.

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Gijbels, Eva, and Mathieu Vinken. "Mechanisms of Drug-Induced Cholestasis." In Methods in Molecular Biology, 1–14. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9420-5_1.

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Watkins, J. B., and C. D. Klaassen. "Mechanisms of Drug-Induced Cholestasis." In Handbook of Experimental Pharmacology, 155–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61013-4_7.

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Kullak-Ublick, Gerd A. "Drug-Induced Cholestatic Liver Disease." In Molecular Pathogenesis of Cholestasis, 256–65. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9034-1_19.

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Aithal, Guruprasad P., and Ann K. Daly. "Drug-Induced Cholestasis: Mechanisms and Importance." In Biliary Disease, 117–28. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50168-0_7.

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Ramaiahgari, Sreenivasa C., and Stephen S. Ferguson. "Organotypic 3D HepaRG Liver Model for Assessment of Drug-Induced Cholestasis." In Methods in Molecular Biology, 313–23. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9420-5_20.

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Deferm, Neel, Lysiane Richert, Pieter Van Brantegem, Tom De Vocht, Bing Qi, Peter de Witte, Thomas Bouillon, and Pieter Annaert. "Detection of Drug-Induced Cholestasis Potential in Sandwich-Cultured Human Hepatocytes." In Methods in Molecular Biology, 335–50. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9420-5_22.

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Krell, H. "Increase in Paracellular Permeability as a Pathophysiological Principle of Drug-Induced Intrahepatic Cholestasis in Rats." In Proceedings in Life Sciences, 33–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74247-7_4.

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Kenna, J. Gerry, Simone H. Stahl, and Tobias Noeske. "Strategies for Minimisation of the Cholestatic Liver Injury Liability Posed by Drug-Induced Bile Salt Export Pump (BSEP) Inhibition." In Topics in Medicinal Chemistry, 191–223. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7355_2013_30.

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