Journal articles: 'Toxic hepatitis'

1

Peker, Erdal, Eren Cagan, and Murat Dogan. "Ceftriaxone-induced toxic hepatitis." World Journal of Gastroenterology 15, no. 21 (2009): 2669. http://dx.doi.org/10.3748/wjg.15.2669.

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2

Dierckx, R. I. R., and M. F. J. Vandewoude. "DONEPEZIL-RELATED TOXIC HEPATITIS." Acta Clinica Belgica 63, no. 5 (October 2008): 339–42. http://dx.doi.org/10.1179/acb.2008.066.

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3

Topal, Firdevs, Ersan Özaslan, Sabiye Akbulut, Metin Küçükazman, Osman Yüksel, and Emin Altiparmak. "Methylprednisolone-Induced Toxic Hepatitis." Annals of Pharmacotherapy 40, no. 10 (October 2006): 1868–71. http://dx.doi.org/10.1345/aph.1h171.

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4

Baum, Susan L., and Anthony J. Suruda. "Toxic Hepatitis from Dimethylacetamide." International Journal of Occupational and Environmental Health 3, no. 1 (January 1997): 1–4. http://dx.doi.org/10.1179/oeh.1997.3.1.1.

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5

Lança, Sara, Amanda Alves, Ana Isabel Vieira, José Barata, João de Freitas, and Álvaro de Carvalho. "Chromium-induced toxic hepatitis." European Journal of Internal Medicine 13, no. 8 (December 2002): 518–20. http://dx.doi.org/10.1016/s0953-6205(02)00164-4.

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6

Cicognani, Camilla, Mauro Malavolti, Antonio Maria Morselli-Labate, Claudia Sama, and Luigi Barbara. "Flutamide-induced toxic hepatitis." Digestive Diseases and Sciences 41, no. 11 (November 1996): 2219–21. http://dx.doi.org/10.1007/bf02071403.

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7

Yang, Ha Na, Dong Joon Kim, Young Mook Kim, Byoung Ho Kim, Kyoung Min Sohn, Myung Jin Choi, and Young Hee Choi. "Aloe-induced Toxic Hepatitis." Journal of Korean Medical Science 25, no. 3 (2010): 492. http://dx.doi.org/10.3346/jkms.2010.25.3.492.

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8

Sheikh, Israr, and Joan Culpepper-Morgan. "Sorrel Induced Toxic Hepatitis." American Journal of Gastroenterology 110 (October 2015): S884—S885. http://dx.doi.org/10.14309/00000434-201510001-02117.

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9

Aydın, Mesut. "Toxic hepatitis due to heliz." Van Medical Journal 28, no. 1 (2021): 15–18. http://dx.doi.org/10.5505/vtd.2021.02328.

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10

Ahn, Byung-Min. "Medicinal Herbs and Toxic Hepatitis." Journal of the Korean Medical Association 48, no. 4 (2005): 318. http://dx.doi.org/10.5124/jkma.2005.48.4.318.

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11

Colakoglu, O., E. Tankurt, B. Unsal, F. Ugur, A. Kupelioglu, Z. Buyrac, and Z. Akpinar. "Toxic hepatitis associated with paroxetine." International Journal of Clinical Practice 59, no. 7 (June 17, 2005): 861–62. http://dx.doi.org/10.1111/j.1368-5031.2005.00572.x.

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12

Aunsholt, Niels Aage, and Jørgen Agnholt. "Toxic Hepatitis Due to Femoxetine." Acta Pharmacologica et Toxicologica 58, no. 4 (March 13, 2009): 253–54. http://dx.doi.org/10.1111/j.1600-0773.1986.tb00104.x.

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13

Safrai, A. "Morphological changes in toxic hepatitis." Forensic Science International 169 (June 2007): S10. http://dx.doi.org/10.1016/j.forsciint.2007.04.179.

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14

Tsai, Chu-Lin, Cheng-Chung Fang, Wen-Jone Chen, and Kerry Dierberg. "Hornet Sting-Induced Toxic Hepatitis." Clinical Toxicology 43, no. 2 (February 1, 2005): 127–28. http://dx.doi.org/10.1081/clt-200050386.

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15

Tsai, Chu-Lin, Cheng-Chung Fang, Wen-Jone Chen, and Kerry Dierberg. "Hornet Sting-Induced Toxic Hepatitis." Clinical Toxicology 43, no. 2 (January 2005): 127–28. http://dx.doi.org/10.1081/clt-50386.

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16

AKIN, Mete, Mehmet İŞLER, Altuğ ŞENOL, Gökhan AKSAKAL, Cem KOÇKAR, and Yıldıran SONGÜR. "Paroxetine Induced Toxic Hepatitis: Case Report." Turkiye Klinikleri Journal of Medical Sciences 32, no. 1 (2012): 264–66. http://dx.doi.org/10.5336/medsci.2010-18864.

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17

Mitrovic, Nikola, Ksenija Bojovic, Jasmina Simonovic, Natasa Nikolic, Aleksandar Urosevic, and Dragan Delic. "Severe toxic acute liver injury." Srpski arhiv za celokupno lekarstvo 147, no. 7-8 (2019): 479–83. http://dx.doi.org/10.2298/sarh171124036m.

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Introduction. Toxic liver injury is becoming greater problem in today?s hepatology. Until today more than 900 drugs, toxins and herbs have been identified that can cause different liver injury. There was no significant research of this problem in Serbia so far. The aim of this study is to present the patient with severe form of acute hepatitis, whose etiology is exclusively toxic. Case outline. A 23-year-old male, from Belgrade, previously healthy, got sick with signs and symptoms that correlated with acute hepatitis. Biochemical analyses pointed to severe form of acute hepatitis with impending hepatocellular failure. The diagnosis of toxic liver injury was set. It was caused by the use of number substances and supplements: ecstasy, whey protein, branched-chain amino acid (BCAA), creatine, high doses of vitamin D, glutamine, and multivitamin complex. He was treated with infusion, gastroprotective, and substitution therapy. During hospitalization, the patient?s symptoms disappeared with gradual normalization of biochemical analyses of the liver. When the patient?s condition was satisfying, blind percutaneous liver biopsy was performed, with the following pathohistological findings: lobular hepatitis, with no fibrosis, etiology correlates to toxic. After a month and a half since the disease had begun, the patient fully recovered. Conclusion. Increased number of persons with toxic liver injury is being registered in developed countries worldwide. Similar trend can be noted in Serbia as well. By presenting young previously healthy man with the severe form of toxic acute hepatitis and impending liver failure, we are pointing out the significance of this problem. Multidisciplinary approach is needed to reach the most effective solutions.

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18

Yesil, Bayram, Hale Gokcan, Mahmut Yuksel, Sabite Kacar, Derya Ari, and Meral Akdogan. "Toxic hepatitis and hyponatremia: Case report." Turkish Journal of Gastroenterology 30, Supp1 (May 20, 2019): 51–52. http://dx.doi.org/10.5152/tjg.2019.33.

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19

Okpara, R. A. "Toxic Hepatitis Caused by Herbal Medicine." Journal of the American Board of Family Medicine 13, no. 4 (July 1, 2000): 321. http://dx.doi.org/10.3122/15572625-13-4-321.

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20

Jahn, Stephan, Gernot Zollner, Carolin Lackner, and Rudolf Stauber. "Severe Toxic Hepatitis Associated with Dronedarone." Current Drug Safety 8, no. 3 (August 1, 2013): 201–2. http://dx.doi.org/10.2174/15748863113089990031.

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21

Bae, Sang Hoon, Dong Hyun Kim, Young Seok Bae, Kwang Jae Lee, Dong Wan Kim, Jeoung Bin Yoon, Joon Ho Hong, and Sang Hyun Kim. "Toxic hepatitis associated with Polygoni multiflori." Korean Journal of Hepatology 16, no. 2 (2010): 182. http://dx.doi.org/10.3350/kjhep.2010.16.2.182.

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22

Štimac, Davor, Sandra Milić, Renata Dobrila Dintinjana, Dražen Kovač, and Smiljana Ristić. "Androgenic/Anabolic Steroid-Induced Toxic Hepatitis." Journal of Clinical Gastroenterology 35, no. 4 (October 2002): 350–52. http://dx.doi.org/10.1097/00004836-200210000-00013.

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23

Steele, Malcolm A., Raymond F. Burk, and Roger M. DesPrez. "Toxic Hepatitis with Isoniazid and Rifampin." Chest 99, no. 2 (February 1991): 465–71. http://dx.doi.org/10.1378/chest.99.2.465.

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24

Castells, LI, J. Gámez, C. Cervera, and J. Guardia. "Icteric toxic hepatitis associated with riluzole." Lancet 351, no. 9103 (February 1998): 648. http://dx.doi.org/10.1016/s0140-6736(05)78431-2.

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25

Gallardo-Caballero, Eva, Ma Isabel Lucena, Raúl J. Andrade, Luis Rodrigo, Juan Pérez-Martı́nez, and Elena Garcı́a-Ruiz. "Severe toxic hepatitis related to chlormethiazole." Journal of Hepatology 39, no. 6 (December 2003): 1093. http://dx.doi.org/10.1016/s0168-8278(03)00466-5.

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26

Maev, Igor V., Rafik I. Shaburov, Alexandr I. Pavlov, Alevtina I. Molodova, Aram G. Karakozov, Sergey P. Kazakov, Ekaterina G. Lebedeva, Aleksandr F. Ivolgin, Mikhail N. Eremin, and Olga B. Levchenko. "Treatment of toxic hepatitis in COVID-19 patients." Terapevticheskii arkhiv 94, no. 12 (January 16, 2023): 1413–20. http://dx.doi.org/10.26442/00403660.2022.12.202021.

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Background. The article reflects the clinical significance of the early diagnosis of toxic hepatitis in patients who have undergone a new coronavirus infection with the determination of clinical and laboratory predictors of the response to therapy. A dynamic analysis of the effectiveness of toxic hepatitis therapy in patients of three experimental groups and a control group is presented. Aim. The aim of the present study is to increase the effectiveness of the treatment of toxic hepatitis in patients who have undergone COVID-19. Materials and methods. On the basis of the newly created infection centers of the Central Clinical Hospital RZhD-Medicine and Vishnevsky 3-rd Central Military Clinical Hospital 996 patients with COVID-19, who had clinical and laboratory signs of toxic liver damage (cytolytic and/or cholestatic syndromes) against the background of COVID-19 therapy. Results. On the 14th day from the start of therapy in group 3, there was a significant decrease in the clinical manifestations of jaundice in 163 (72.8%) patients, on the 21st day of treatment, this symptom was stopped in all patients. In groups 1 and 2, the decrease in clinical manifestations of jaundice was significantly lower 122 (55.2%) and 134 (58.8%); p0.05. At the end of therapy, no manifestations of jaundice were observed in all experimental groups, while in the control group, symptom reduction was achieved only in 47 (14.5%) patients. Conclusion. The use of drugs with hepatoprotective effect in the form of monotherapy in groups 1 (UDCA) and 2 (ademethionine) showed a low therapeutic effect with positive dynamics of clinical and laboratory indicators of toxic hepatitis activity. The use of combined treatment in group 3 (UDCA and ademethionine) demonstrated the maximum therapeutic effect, pronounced positive dynamics in the form of normalization of clinical and laboratory indicators of toxic hepatitis activity.

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27

Myazin, R. G., G. L. Snigur, D. N. Emel'yanov, and M. V. Chernyshova. "Pharmacological Correction of Experimental Acute Toxic Hepatitis." Journal of Anatomy and Histopathology 8, no. 1 (April 7, 2019): 49–54. http://dx.doi.org/10.18499/2225-7357-2019-8-1-49-54.

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The aim of study was to develop new methods of treatment of acute toxic hepatitis. To achieve this objective, the authors investigated dynamics of pathological changes in the hepatic tissue under acute intoxication followed by the pharmacological correction with sodium hypochlorite.Material and methods. The study included 45 male rats that were subjected to the experimental simulation of acute toxic hepatosis. Group 1 included intact animals; group 2 included animals that were intragastrically administered allyl alcohol resulting in acute toxic hepatosis; group 3 included rats with acute toxic hepatosis caused by allyl alcohol introduction that was corrected by sodium hypochlorite; group 4 included animals with acute toxic hepatosis corrected by essentiale N; group 5 included animals with acute toxic hepatosis corrected by the combined application of sodium hypochlorite and essentiale N. On the 6th day the animals were removed from the experiment with the followed histological examination of the hepatic tissue.Results. The introduction of allyl alcohol was accompanied by significant changes in hepatocytes expressed by dystrophic, necrotic processes and circulatory disorders of the hepatic lobules. Pharmacological correction by sodium hypochlorite, essential H, or their combination did not result in the complete histological recovery of hepatocytes; however, the degree of fatty degeneration decreased significantly under the influence of sodium hypochlorite or its combination with essentiale N.Conclusions. The application of sodium hypochlorite as a monotherapy or in combination with essential N in acute toxic hepatitis has allowed to relieve the severity of fatty liver disease. 0.03% solution of sodium hypochlorite can be effective as both - an independent method for treating acute toxic hepatitis, and in combination with other hepatoprotectors.

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28

Chatterjee, S., J. Pal, and N. Biswas. "Nimesulide-induced hepatitis and toxic epidermal necrolysis." Journal of Postgraduate Medicine 54, no. 2 (2008): 150. http://dx.doi.org/10.4103/0022-3859.40786.

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29

Choi, Tae Sung, Kuck Hyeun Woo, Jin Seok Kim, Wan Seup Park, Jung Ho Ham, Sang Je Jung, and Jae Young Yu. "Toxic Hepatitis Induced by Occupational Dimethylacetamide Exposure." Korean Journal of Occupational and Environmental Medicine 13, no. 2 (2001): 164. http://dx.doi.org/10.35371/kjoem.2001.13.2.164.

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30

KAPLAN, Mustafa, Muhammet Yener AKPINAR, Orhan COŞKUN, Adem AKSOY, and Volkan GÖKBULUT. "Didrogesterone-Induced Toxic Hepatitis: A Case Report." Ahi Evran Medical Journal 4, no. 1 (April 23, 2020): 21–23. http://dx.doi.org/10.46332/aemj.626178.

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31

GOZUKUCUK, Ramazan, Ilker ABCI, and Mustafa GUCLU. "Albendazole-induced toxic hepatitis: A case report." Turkish Journal of Gastroenterology 24, no. 1 (February 1, 2009): 82–84. http://dx.doi.org/10.4318/tjg.2013.0426.

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32

Ahn, Byung-Min. "Do Natural Health Products Cause Toxic Hepatitis?" Journal of the Korean Medical Association 48, no. 5 (2005): 448. http://dx.doi.org/10.5124/jkma.2005.48.5.448.

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33

Dyachkova, S. Yu, and A. V. Turovsky. "EXPERIMENTAL APPROACHES TO IMMUNOPHARMACOTHERAPY FOR TOXIC HEPATITIS." Pharmacy & Pharmacology 2, no. 6(7) (September 14, 2015): 80. http://dx.doi.org/10.19163/2307-9266-2014-2-6(7)-80-83.

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34

Malaguarnera, Giulia. "Toxic hepatitis in occupational exposure to solvents." World Journal of Gastroenterology 18, no. 22 (2012): 2756. http://dx.doi.org/10.3748/wjg.v18.i22.2756.

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35

Agca, Erhan, Ali Akcay, and Halis Simsek. "Ursodeoxycholic Acid for Terbinafine-Induced Toxic Hepatitis." Annals of Pharmacotherapy 38, no. 6 (June 2004): 1088–89. http://dx.doi.org/10.1345/aph.1d420.

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36

Kim, Seon Jung, Bon Wook Koo, Jin Ho Bae, and Seung Woon Lim. "Amiodarone Induced Toxic Hepatitis - A case report -." Korean Journal of Anesthesiology 53, no. 4 (2008): 528. http://dx.doi.org/10.4097/kjae.2007.53.4.528.

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37

Fong, S. Y. Y., K. L. Au Yeung, J. M. Y. Tosh, and Y. K. Wing. "Clozapine-induced toxic hepatitis with skin rash." Journal of Psychopharmacology 19, no. 1 (January 2005): 107. http://dx.doi.org/10.1177/0269881105047287.

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38

Gracheva, O. A., A. E. Pugatina, M. G. Zukhrabov, D. R. Amirov, and B. F. Tamimdarov. "Experimental model of toxic hepatitis on rabbits." IOP Conference Series: Earth and Environmental Science 315 (August 23, 2019): 072021. http://dx.doi.org/10.1088/1755-1315/315/7/072021.

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39

Kleefstra, Nanne, Sebastiaan T. Houweling, and Henk J. G. Bilo. "Hepatitis yes, but toxic effect of chromium?" European Journal of Internal Medicine 14, no. 2 (March 2003): 136–37. http://dx.doi.org/10.1016/s0953-6205(03)00025-6.

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40

Futuh, Ashraf Abul, Waleed Hamed, Abdel Ghany Soliman, Salwa El-Hadad, Mahmoud Omar, and Sayed El-Hendawy. "Toxic hepatitis induced by androgenic/anabolic steroids." Journal of Hepatology 36 (April 2002): 196–97. http://dx.doi.org/10.1016/s0168-8278(02)80696-1.

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41

BaŞ, Vedat, Tulay Erkan, Salim CalİŞkan, Lale Sever, Ozgur Kasapcopur, Gulsen Ozbay, and Nil Arİsoy. "Toxic hepatitis due to enalapril in childhood." Pediatrics International 45, no. 6 (December 2003): 755–57. http://dx.doi.org/10.1111/j.1442-200x.2003.01817.x.

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42

Ishak, Kamal G., and Hyman J. Zimmerman. "11 Drug-induced and toxic granulomatous hepatitis." Baillière's Clinical Gastroenterology 2, no. 2 (April 1988): 463–80. http://dx.doi.org/10.1016/0950-3528(88)90012-7.

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43

Rizzioli, Emanuela, Elena Incasa, Susanna Gamberini, Sandra Savelli, Arnaldo Zangirolami, Marilena Tampieri, and Roberto Manfredini. "Acute toxic hepatitis after amiodarone intravenous loading." American Journal of Emergency Medicine 25, no. 9 (November 2007): 1082.e1–1082.e4. http://dx.doi.org/10.1016/j.ajem.2007.02.045.

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44

Skuratov, A. G., A. N. Lyzikov, E. V. Voropayev, S. L. Achinovich, and B. B. Osipov. "EXPERIMENTAL MODELING OF TOXIC HEPATIC INJURY." Health and Ecology Issues, no. 4 (December 28, 2011): 27–33. http://dx.doi.org/10.51523/2708-6011.2011-8-4-4.

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Objective: to perfect in experiment models of acute and chronic toxic injuries of liver, to evaluate possibilities of their application to study the processes of liver regeneration and its correction. Materials and methods: white male rats Vistar; intraperitoneal injection of 50 % solution of carbon tetrachloride made on olive oil; intragastric introduction of acetaminophen; morphological and morphometrical methods. Results. The models of toxic hepatitis and hepatic cirrhosis were received in experiment. Hepatic cirrhosis is postnecrotic and mainly multilobular. Conclusion. The carbon tetrachloride model of toxic hepatitis and cirrhosis can be used for reproduction of this pathology in experiment. However it is not optimal as the sensitivity of rats to carbon tetrachloride differs and the changes in liver have reversible character after the preparation cancellation.

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45

Maklakova, Irina, Dmitry Grebnev, Victoria Vakhrusheva, and Ilya Gavrilov. "Pathogenetic substantiation of the combined transplantation use of multipotent mesenchymal stromal cells and hepatic stellate cells to restore the liver morphofunctional state after acute toxic hepatitis in the old body." BIO Web of Conferences 22 (2020): 01009. http://dx.doi.org/10.1051/bioconf/20202201009.

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The purpose of this study was to study the cotransplantation influence of multipotent mesenchymal stromal (MMSC) and hepatic stellate (HSC) cells on liver regeneration of old laboratory animals in conditions of its toxic damage. Acute toxic hepatitis was caused by single intraperitoneal CC14 injection at a dose of 50 μg/kg. The introduction of MMSC and HSC was carried out at doses of 4 million cl/kg and 9 million cl/kg respectively 1 hour after toxic hepatitis modelling. The morphofunctional liver state of old laboratory mice was evaluated on the 1st, 3rd, 7th day after combined injection of MMSC and HSC in laboratory animals with toxic hepatitis. As a result of the study, it was obtained that MMSC and HSC cotransplantation leads to cellular and intracellular liver regeneration activation in old mice with acute toxic hepatitis. Also, the introduction of these cell types leads to decreased liver mutagenesis, inhibition of programmed cellular hepatocytes death. Thus, the conducted studies indicate the ability of combined MMSC and HSC transplantation to restore the morphofunctional liver state of the old organism under the conditions of its toxic damage.

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46

Kovacevic, Zoran, Goran Davidovic, Jelena Vuckovic-Filipovic, Mirjana A. Janicijevic-Petrovic, Katarina Janicijevic, and Andrijana Popovic. "A Toxic Hepatitis Caused the Kombucha Tea – Case Report." Open Access Macedonian Journal of Medical Sciences 2, no. 1 (March 15, 2014): 128–31. http://dx.doi.org/10.3889/oamjms.2014.023.

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Background: Toxic hepatitis may clinically manifest as other diseases of the liver, where it must always be considered in differential diagnoses of unexplained liver damage, such as poisoning with kombucha tea.Case report: 47-year old female patient was hospitalized and has consumed daily ounces of kombucha tea. During hospitalization patient was diagnosed with toxic hepatitis and treated with intravenous solutions of hepatic protective and ursodeoxycholic-acid (effective therapy). Conclusion: Examinations showed that kombucha tea has potential to revert the CCl4-induced hepatic toxicity, but used in overdose can induce toxicity himself.

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47

Peredelcu Rodica, Gonciar Veaceslav, Scutari Corina, and Cazacu Vasile. "THE INFLUENCE OF COPTISINE BISULFATE ON THE EVOLUTION OF ACUTE TOXIC HEPATITIS." World Science 2, no. 8(36) (August 30, 2016): 42–46. http://dx.doi.org/10.31435/rsglobal_ws/30082018/6065.

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In the experiments made on white rats was studied the influence of coptisine bisulfate, alkaloid extracted from Chelidonium majus, in the following doses: 10 mg/kg and 20 mg/kg on acute toxic hepatitis cause by carbon tetrachloride. It was established that the researched substance reduced hepatic cytolysis and cholestasis through reestablishment of the transaminases activity and lactate dehydrogenase, while lowering the alkaline phosphatase/alanine aminotransferase ratio and modulated the deflection of the metabolic parameters of acute toxic hepatitis. Coptisine bisulfate corrected the carbon tetrachloride caused hypoproteinemia when administered for 7 days and normalized the albumin level at 14th day of treatment of acute toxic hepatitis.

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48

Safonova, O. A., T. N. Popova, and L. Saidi. "Citrate influence on oxidative status of rats tissues under experimental toxic hepatitis." Biomeditsinskaya Khimiya 56, no. 4 (2010): 490–98. http://dx.doi.org/10.18097/pbmc20105604490.

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The effect of citrate free-radical oxidation intensity and aconitate hydratase, superoxide dismutase and catalase activities in liver and blood serum of rats with experimental toxic hepatitis has been investigated. Citrate administration to rats with hepatitis decreased biochemiluminescence parameters and conjugated diene content in rats tissues, increased under conditions of CCl4-induced liver damage. At the same time aconitase activity, decreased at the pathology, increases. The superoxide dismutase and catalase activities increased in at experimental toxic hepatitis, tended towards control values after citrate administration.

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49

Vokhmintseva, L. V., N. N. Mayanskaya, S. S. Rymar′, P. A. Zheleznyi, A. P. Nadeyev, and V. V. Vanyunina. "Peculiarities of functional neutrophil activity in rats having periodontitis in thesetting of toxic hepatitis." Bulletin of Siberian Medicine 6, no. 2 (June 30, 2007): 11–16. http://dx.doi.org/10.20538/1682-0363-2007-2-11-16.

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Experimental toxic hepatitis was induced by single administration of Acetaminophen ( paracetamol) in a dose of 1000 mg per 1 kg of body mass in Wistar rats. Inflammation pathology was modeled by wounding the upper maxilla gingiva in toxic hepatitis rats on the 6-th day. Intact rats were controls. On the 1-st and 7-th day, ratio of neutrophil-macrophag was determined in smears of the upper maxillas gingival, oxygen-dependent functional activity of neutrophils was assessed based upon HST-test, functional activity reserves were assessed by the stimulation index. On the 7-th and 13-th day, alaninaminotransferase and aspartataminotransferase activity, level of general and indirect bilirubin, general blood protein were assessed in blood serum of these rats. Toxic hepatitis was established to be accomplished by increased biocidity of phagocytes, decreased functional reserves of neutrophils and their migration into the parodontium. In experimental inflammation, suppurative processes in parodontium tissues are revealed in toxic hepatitis rats by 1.5 times less than in controls due to lower biocide activity of phagocyte cells and increased migration of macrophages.

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50

Lim, Jae Gyun, Jeong Ho Kim, Chang Youl Lee, Sang In Lee, and Yang Sup Kim. "Amanita virosainduced toxic hepatitis: report of three cases." Yonsei Medical Journal 41, no. 3 (2000): 416. http://dx.doi.org/10.3349/ymj.2000.41.3.416.

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Journal articles on the topic 'Toxic hepatitis'

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