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Journal articles on the topic 'Hepatic injury'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Stracieri, Luis Donizeti da Silva, and Sandro Scarpelini. "Hepatic injury." Acta Cirurgica Brasileira 21, suppl 1 (2006): 85–88. http://dx.doi.org/10.1590/s0102-86502006000700019.

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Hepatic trauma occurs in approximately 5% of all admissions in emergency rooms. The anatomic location and the size of the liver make the organ even more susceptible to trauma and frequently in penetrating injuries. The American Association for the Surgery of Trauma established a detailed classification system that provides for uniform comparisons of hepatic injury. Diagnosis of hepatic injury can be sometimes easy; however the use diagnostic modalities as diagnostic peritoneal lavage, ultrasound and computed tomography allow faster and more accurate diagnosis. Nonoperative management of the he

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2

Pillai, Akshita S., Girish Kumar, and Anil K. Pillai. "Hepatic Trauma Interventions." Seminars in Interventional Radiology 38, no. 01 (2021): 096–0104. http://dx.doi.org/10.1055/s-0041-1724014.

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AbstractThe liver is the second most commonly involved solid organ (after spleen) to be injured in blunt abdominal trauma, but liver injury is the most common cause of death in such trauma. In patients with significant blunt abdominal injury, the liver is involved approximately 35 to 45% of the time. Its large size also makes it a vulnerable organ, commonly injured in penetrating trauma. Other than its position and size, the liver is surrounded by fragile parenchyma and its location under the diaphragm makes it vulnerable to shear forces during deceleration injuries. The liver is also a vascul

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3

Kuboki, Satoshi, Nozomu Sakai, Johannes Tschöp, Michael J. Edwards, Alex B. Lentsch, and Charles C. Caldwell. "Distinct contributions of CD4+ T cell subsets in hepatic ischemia/reperfusion injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 5 (2009): G1054—G1059. http://dx.doi.org/10.1152/ajpgi.90464.2008.

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Helper T cells are known to mediate hepatic ischemia/reperfusion (I/R) injury. However, the precise mechanisms and subsets of CD4+ T cells that contribute to this injury are still controversial. Therefore, we sought to determine the contributions of different CD4+ T cell subsets during hepatic I/R injury. Wild-type, OT-II, or T cell receptor (TCR)-δ-deficient mice were subjected to 90 min of partial hepatic ischemia followed by 8 h of reperfusion. Additionally, wild-type mice were pretreated with anti-CD1d, -NK1.1, or -IL-2R-α antibodies before I/R injury. OT-II mice had diminished liver injur

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4

Herrera, Jorge L. "Hepatic medication injury." Current Opinion in Critical Care 3, no. 2 (1997): 153–58. http://dx.doi.org/10.1097/00075198-199704000-00012.

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5

Harada, Naoaki, Kenji Okajima, Shigeki Kushimoto, Hirotaka Isobe, and Keiichi Tanaka. "Antithrombin Reduces Ischemia/Reperfusion Injury of Rat Liver by Increasing the Hepatic Level of Prostacyclin." Blood 93, no. 1 (1999): 157–64. http://dx.doi.org/10.1182/blood.v93.1.157.401k08_157_164.

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We investigated whether antithrombin (AT) can reduce ischemia/reperfusion (I/R)-induced injury of rat liver by promoting prostacyclin release from endothelial cells. Although intravenous administration of AT (250 U/kg) markedly reduced hepatic injury, neither dansyl-Glu-Gly-Arg-chloromethyl ketone-treated factor Xa (DEGR-Xa), a selective inhibitor of thrombin generation, nor Trp49-modified AT, which lacks affinity for heparin, had any effect. Hepatic levels of 6-keto-PGF1, a stable prostacyclin (PGI2) metabolite, were increased significantly after I/R of the rat liver. AT significantly increa

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6

SOUZA LIMA, MARCOS A. "Ranitidine and Hepatic Injury." Annals of Internal Medicine 105, no. 1 (1986): 140. http://dx.doi.org/10.7326/0003-4819-105-1-140_1.

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7

Noreña, I., A. Varón, C. Dennis, and R. Dennis. "Hepatic injury following colonoscopy." Endoscopy 45, S 02 (2013): E247. http://dx.doi.org/10.1055/s-0033-1344354.

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8

Tabak, Fehmi, Ali Mert, Resat Ozaras, et al. "Losartan-Induced Hepatic Injury." Journal of Clinical Gastroenterology 34, no. 5 (2002): 585–86. http://dx.doi.org/10.1097/00004836-200205000-00022.

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9

Siemaszko, Olga, and Hamish A. McLure. "Repeat anaesthesia: hepatic injury." Anaesthesia & Intensive Care Medicine 5, no. 2 (2004): 52–54. http://dx.doi.org/10.1383/anes.5.2.52.28692.

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10

FARRELL, GEOFFREY C. "Drug-induced hepatic injury." Journal of Gastroenterology and Hepatology 12, no. 9-10 (1997): S242—S250. http://dx.doi.org/10.1111/j.1440-1746.1997.tb00507.x.

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11

STRICKER, BRUNO H. CH, A. P. ROELAND BLOK, and FRANS B. BRONKHORST. "Glafenine-associated hepatic injury." Liver 6, no. 2 (2008): 63–72. http://dx.doi.org/10.1111/j.1600-0676.1986.tb00270.x.

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12

Koek, G. H., B. H. Ch Stricker, A. P. R. Blok, S. W. Schalm, and V. J. Desmet. "Flucloxacillin-associated hepatic injury." Liver 14, no. 5 (2008): 225–29. http://dx.doi.org/10.1111/j.1600-0676.1994.tb00079.x.

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13

Stricker, B. H. Ch, A. P. R. Blok, F. B. Bronkhorst, G. E. Van Parys, and V. J. Desmet. "Ketoconazole-associated hepatic injury." Journal of Hepatology 3, no. 3 (1986): 399–406. http://dx.doi.org/10.1016/s0168-8278(86)80495-0.

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14

De Herder, W. W., P. Schröder, A. Purnode, A. C. M. Van Vliet, and B. H. Ch Stricker. "Pirprofen-associated hepatic injury." Journal of Hepatology 4, no. 1 (1987): 127–32. http://dx.doi.org/10.1016/s0168-8278(87)80019-3.

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15

Bascom, John U., Peter Gosling, and Bashir A. Zikria. "Hepatic ischemia-reperfusion injury." American Journal of Surgery 184, no. 1 (2002): 84. http://dx.doi.org/10.1016/s0002-9610(01)00838-8.

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16

Fujimoto, Yoshinori, Motoyuki Ohhira, Naoyuki Miyokawa, Shigeru Kitamori, and Yutaka Kohgo. "Acarbose-induced hepatic injury." Lancet 351, no. 9099 (1998): 340. http://dx.doi.org/10.1016/s0140-6736(05)78337-9.

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17

van 't Wout, Jan W., Werner A. Herrmann, Richard A. de Vries, and Bruno H. Ch Stricker. "Terbinafine-associated hepatic injury." Journal of Hepatology 21, no. 1 (1994): 115–17. http://dx.doi.org/10.1016/s0168-8278(94)80146-0.

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18

Serracino-Inglott, Ferdinand, Nagy A. Habib, and Robert T. Mathie. "Hepatic ischemia-reperfusion injury." American Journal of Surgery 181, no. 2 (2001): 160–66. http://dx.doi.org/10.1016/s0002-9610(00)00573-0.

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19

de Beer, C. D., and J. W. Sear. "Repeat anaesthesia: hepatic injury." Anaesthesia & Intensive Care Medicine 8, no. 2 (2007): 41–43. http://dx.doi.org/10.1016/j.mpaic.2006.12.003.

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20

Lopez, Annette M., and Robert G. Hendrickson. "Toxin-Induced Hepatic Injury." Emergency Medicine Clinics of North America 32, no. 1 (2014): 103–25. http://dx.doi.org/10.1016/j.emc.2013.09.005.

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21

Nehra, Archna, Florabel Mullick, Kamal G. Ishak, and Hyman J. Zimmerman. "Pemoline-associated hepatic injury." Gastroenterology 99, no. 5 (1990): 1517–19. http://dx.doi.org/10.1016/0016-5085(90)91186-a.

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22

Nathan, Naveen. "Rhabdomyolysis and Hepatic Injury." Anesthesia & Analgesia 136, no. 5 (2023): 841. http://dx.doi.org/10.1213/ane.0000000000006482.

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23

Harbrecht, Brian G., Howard R. Doyle, Keith D. Clancy, Ricard N. Townsend, Timothy R. Billiar, and Andrew B. Peitzman. "The Impact of Liver Dysfunction on Outcome in Patients with Multiple Injuries." American Surgeon 67, no. 2 (2001): 122–26. http://dx.doi.org/10.1177/000313480106700205.

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Multiple organ dysfunction syndrome (MODS) is the leading cause of late deaths after traumatic injury. The relative importance of dysfunction of individual organ systems in determining outcome from MODS has not been clearly defined. Some studies have suggested that hepatic dysfunction associated with MODS increases mortality, whereas others have suggested that it contributes little to outcome in trauma patients. To clarify the role of the hepatic dysfunction after traumatic injury we retrospectively reviewed all trauma patients with an Injury Severity Score ≥14 admitted from January 1, 1994 th

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24

Zhou, Jiangqiao, Tao Qiu, Tianyu Wang, et al. "USP4 deficiency exacerbates hepatic ischaemia/reperfusion injury via TAK1 signalling." Clinical Science 133, no. 2 (2019): 335–49. http://dx.doi.org/10.1042/cs20180959.

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Abstract Ubiquitin-specific peptidase 4 (USP4) protein is a type of deubiquitination enzyme that is correlated with many important biological processes. However, the function of USP4 in hepatic ischaemia/reperfusion (I/R) injury remains unknown. The aim of the present study was to explore the role of USP4 in hepatic I/R injury. USP4 gene knockout mice and primary hepatocytes were used to construct hepatic I/R models. The effect of USP4 on hepatic I/R injury was examined via pathological and molecular analyses. Our results indicated that USP4 was significantly up-regulated in liver of mice subj

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25

Harada, Naoaki, Kenji Okajima, Shigeki Kushimoto, Hirotaka Isobe, and Keiichi Tanaka. "Antithrombin Reduces Ischemia/Reperfusion Injury of Rat Liver by Increasing the Hepatic Level of Prostacyclin." Blood 93, no. 1 (1999): 157–64. http://dx.doi.org/10.1182/blood.v93.1.157.

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Abstract We investigated whether antithrombin (AT) can reduce ischemia/reperfusion (I/R)-induced injury of rat liver by promoting prostacyclin release from endothelial cells. Although intravenous administration of AT (250 U/kg) markedly reduced hepatic injury, neither dansyl-Glu-Gly-Arg-chloromethyl ketone-treated factor Xa (DEGR-Xa), a selective inhibitor of thrombin generation, nor Trp49-modified AT, which lacks affinity for heparin, had any effect. Hepatic levels of 6-keto-PGF1, a stable prostacyclin (PGI2) metabolite, were increased significantly after I/R of the rat liver. AT significant

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26

Kogure, Takayuki, Stefan Costinean, Irene Yan, Chiara Braconi, Carlo Croce, and Tushar Patel. "Hepatic miR-29ab1 expression modulates chronic hepatic injury." Journal of Cellular and Molecular Medicine 16, no. 11 (2012): 2647–54. http://dx.doi.org/10.1111/j.1582-4934.2012.01578.x.

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27

BEHRENDS, M., R. HIROSE, S. CHOI, and C. NIEMANN. "Normothermia during partial hepatic ischemia increases hepatic injury." Journal of Gastrointestinal Surgery 9, no. 4 (2005): 554–55. http://dx.doi.org/10.1016/j.gassur.2005.01.090.

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28

Zhang, Sen, Sijing Rao, Meiwen Yang, Chen Ma, Fengfang Hong, and Shulong Yang. "Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury." International Journal of Molecular Sciences 23, no. 4 (2022): 2357. http://dx.doi.org/10.3390/ijms23042357.

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Hepatic ischemia-reperfusion injury is a major cause of post-operative hepatic dysfunction and liver failure after transplantation. Mitochondrial pathways can be either beneficial or detrimental to hepatic cell apoptosis during hepatic ischemia/reperfusion injury, depending on multiple factors. Hepatic ischemia/reperfusion injury may be induced by opened mitochondrial permeability transition pore, released apoptosis-related proteins, up-regulated B-cell lymphoma-2 gene family proteins, unbalanced mitochondrial dynamics, and endoplasmic reticulum stress, which are integral parts of mitochondria

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29

Qiu, Tao, Tianyu Wang, Jiangqiao Zhou, et al. "DUSP12 protects against hepatic ischemia–reperfusion injury dependent on ASK1-JNK/p38 pathway in vitro and in vivo." Clinical Science 134, no. 17 (2020): 2279–94. http://dx.doi.org/10.1042/cs20191272.

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Abstract Hepatic ischemia–reperfusion (I/R) injury is an important risk factor resulting in liver failure during liver surgery. However, there is still lack of effective therapeutic methods to treat hepatic I/R injury. DUSP12 is a member of the dual specific phosphatase (DUSP) family. Some DUSPs have been identified as being involved in the regulation of hepatic I/R injury. However, the role of DUSP12 during hepatic I/R injury is still unclear. In the present study, we observed a significant decrease in DUSP12 expression in a hepatic I/R injury mouse model in vivo and in hypoxia/reoxygenation

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30

Hakim, HA Nazmul, Kazi Mazharul Islam, Md Aminul Islam, ANM Nure Azam, Md Tuhin Talukder, and Mohammad Mahmud Sarder. "Outcome and management strategy of traumatic liver injury in a tertiary hospital in Bangladesh." Journal of Surgical Sciences 22, no. 1 (2020): 36–42. http://dx.doi.org/10.3329/jss.v22i1.44013.

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Background: Liver remains the second most common injured organ in both blunt and penetrating trauma of the abdomen. Management of blunt or penetrating injury to the liver remains a significant challenge to trauma surgeons. Unstable patients require immediate laparotomy. Selective patients can be managed without surgery and with careful monitoring. Mortality is mainly due to damage to major hepatic blood vessels, massive parenchymal and biliary injury. Associated non-hepatic injuries contribute greatly to the overall mortality. With improved understanding of the major causes of mortality from h

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31

Harada, Naoaki, Shigeki Kushimoto, Mitsuhiro Uchiba, and Kenji Okajima. "Role of Microthrombus Formation in the Development of Ischemia/Reperfusion-induced Liver Injury in Rats." Thrombosis and Haemostasis 88, no. 09 (2002): 473–80. http://dx.doi.org/10.1055/s-0037-1613240.

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SummaryAlthough tumor necrosis factor-α (TNF-α) has been shown to play a critical role in the pathologic process leading to ischemia/reperfusion (I/R)-induced liver injury in rats by activating neutrophils, it is not clear whether or not microthrombus formation induced by TNF-α contributes to the liver injury. In the present study, we investigated the role of microthrombus formation in I/R-induced liver injury in rats. Hepatic tissue levels of TNF-α were significantly increased after reperfusion, and these were higher in animals subjected to 120 min-hepatic I/R than in those subjected to 60 mi

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32

Kim, SJ, HS Oh, YS Cha, MY Kim, and H. Kim. "Evaluation of hepatic injury in acute carbon monoxide-poisoned patients in emergency department." Human & Experimental Toxicology 39, no. 7 (2020): 883–89. http://dx.doi.org/10.1177/0960327120909521.

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Introduction: The affinity of hemoglobin for carbon monoxide (CO) is 250 times higher than that for oxygen. Therefore, exposure to CO leads to a reduction in oxygen delivery to tissues, resulting in cellular hypoxia and affects whole body. Hepatic dysfunction in critically ill patients is related to poor outcome, but few studies have been conducted on this subject that occurs after CO poisoning. This study aims to conduct a study of hepatic injury in CO-poisoned patients in emergency department (ED). Methods: This retrospective observational study collected data from patients who were diagnose

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33

Xu, Dongwei, Jianjun Zhu, Seogsong Jeong, et al. "Rictor Deficiency Aggravates Hepatic Ischemia/Reperfusion Injury in Mice by Suppressing Autophagy and Regulating MAPK Signaling." Cellular Physiology and Biochemistry 45, no. 6 (2018): 2199–212. http://dx.doi.org/10.1159/000488165.

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Background/Aims: The role of Rictor in hepatic ischemia/reperfusion (I/R) injury remains unknown. Here, we comprehensively examined the role of Rictor in hepatic I/R injury. Methods: We studied the expression of Rictor during hepatic I/R injury. The regulatory effects of Rictor on inflammatory responses, cytokine and chemokine release, apoptotic and anti-apoptotic responses, and autophagy induction during hepatic I/R injury were identified via the shRNA-mediated knockdown of Rictor. Subsequently, we collected the liver and blood samples of these mice to evaluate liver injury, mRNA and protein

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34

Long, Yunxiang, Yingmu Tong, Yang Wu, et al. "Interaction between Acute Hepatic Injury and Early Coagulation Dysfunction on Mortality in Patients with Acute Myocardial Infarction." Journal of Clinical Medicine 12, no. 4 (2023): 1534. http://dx.doi.org/10.3390/jcm12041534.

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Background: In acute myocardial infarction (AMI), acute hepatic injury is an independent risk factor for prognosis and is associated with complex coagulation dynamics. This study aims to determine the interaction between acute hepatic injury and coagulation dysfunction on outcomes in AMI patients. Methods: The Medical Information Mart for Intensive Care (MIMIC-III) database was used to identify AMI patients who underwent liver function testing within 24 h of admission. After ruling out previous hepatic injury, patients were divided into the hepatic injury group and the nonhepatic injury group

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35

Maeda, Koki, Naohisa Kuriyama, Daisuke Noguchi, et al. "Xa inhibitor edoxaban ameliorates hepatic ischemia-reperfusion injury via PAR-2–ERK 1/2 pathway." PLOS ONE 19, no. 5 (2024): e0292628. http://dx.doi.org/10.1371/journal.pone.0292628.

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Hepatic ischemia-reperfusion injury causes liver damage during surgery. In hepatic ischemia-reperfusion injury, the blood coagulation cascade is activated, causing microcirculatory incompetence and cellular injury. Coagulation factor Xa (FXa)- protease-activated receptor (PAR)-2 signaling activates inflammatory reactions and the cytoprotective effect of FXa inhibitor in several organs. However, no studies have elucidated the significance of FXa inhibition on hepatic ischemia-reperfusion injury. The present study elucidated the treatment effect of an FXa inhibitor, edoxaban, on hepatic ischemia

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36

Makin, A. J., R. D. Hughes, and R. Williams. "Systemic and hepatic hemodynamic changes in acute liver injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 3 (1997): G617—G625. http://dx.doi.org/10.1152/ajpgi.1997.272.3.g617.

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Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subs

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37

SEIFALIAN, Alexander M., Hamid EL-DESOKY, David T. DELPY, and Brian R. DAVIDSON. "Effects of hepatic ischaemia/reperfusion injury in a rabbit model of Indocyanine Green clearance." Clinical Science 102, no. 5 (2002): 579–86. http://dx.doi.org/10.1042/cs1020579.

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Hepatic ischaemia/reperfusion (I/R) injury is a major cause of primary non-function of the graft after liver transplantation. The ability to assess the severity of ischaemic injury would be of prognostic value and allow the possibility of therapeutic interventions. Currently there is no reliable clinical method for assessing the severity of hepatic ischaemic injury. The hepatic handling of Indocyanine Green as a technique for monitoring the severity of I/R injury has been investigated in the present study. A rabbit model of lobar ischaemia was used. At laparotomy, left lobe hepatic ischaemia w

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38

Wang, Wei, Xiaoyan Hu, Zhiping Xia та ін. "Mild Hypothermia Attenuates Hepatic Ischemia–Reperfusion Injury through Regulating the JAK2/STAT3-CPT1a-Dependent Fatty Acid β-Oxidation". Oxidative Medicine and Cellular Longevity 2020 (20 березня 2020): 1–16. http://dx.doi.org/10.1155/2020/5849794.

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Hepatic ischemia–reperfusion (IR) injury is a clinical issue that can result in poor outcome and lacks effective therapies at present. Mild hypothermia (32–35°C) is a physiotherapy that has been reported to significantly alleviate IR injury, while its protective effects are attributed to multiple mechanisms, one of which may be the regulation of fatty acid β-oxidation (FAO). The aim of the present study was to investigate the role and underlying mechanisms of FAO in the protective effects of mild hypothermia. We used male mice to establish the experimental models as previously described. In br

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39

Lin, Jung-Chun, Yi-Jen Peng, Shih-Yu Wang та ін. "Sympathetic Nervous System Control of Carbon Tetrachloride-Induced Oxidative Stress in Liver throughα-Adrenergic Signaling". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/3190617.

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In addition to being the primary organ involved in redox cycling, the liver is one of the most highly innervated tissues in mammals. The interaction between hepatocytes and sympathetic, parasympathetic, and peptidergic nerve fibers through a variety of neurotransmitters and signaling pathways is recognized as being important in the regulation of hepatocyte function, liver regeneration, and hepatic fibrosis. However, less is known regarding the role of the sympathetic nervous system (SNS) in modulating the hepatic response to oxidative stress. Our aim was to investigate the role of the SNS in h

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40

Jiang, Jun, Jishu Wei, Junli Wu, et al. "Partial Portal Vein Arterialization Attenuates Acute Bile Duct Injury Induced by Hepatic Dearterialization in a Rat Model." BioMed Research International 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/7427246.

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Hepatic infarcts or abscesses occur after hepatic artery interruption. We explored the mechanisms of hepatic deprivation-induced acute liver injury and determine whether partial portal vein arterialization attenuated this injury in rats. Male Sprague-Dawley rats underwent either complete hepatic arterial deprivation or partial portal vein arterialization, or both. Hepatic ischemia was evaluated using biochemical analysis, light microscopy, and transmission electron microscopy. Hepatic ATP levels, the expression of hypoxia- and inflammation-associated genes and proteins, and the expression of b

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41

Hsieh, Po-Chow, Yu-Ling Ho, Guan-Jhong Huang, et al. "Hepatoprotective Effect of the Aqueous Extract of Flemingia macrophylla on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats Through Anti-Oxidative Activities." American Journal of Chinese Medicine 39, no. 02 (2011): 349–65. http://dx.doi.org/10.1142/s0192415x11008877.

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This study investigated the protective effect of the aqueous extract of Flemingia macrophylla (AFM) against hepatic injury induced by CCl4. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected as biomarkers in the blood to indicate hepatic injury. Product of lipid peroxidation (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and reduced glutathione (GSH) contents were evaluated for oxidative stress in hepatic injury. Moreover, histopathological observation was assayed for the degree of hepatic injury. After oral administration of

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42

Koneru, Meghana, Bidya Dhar Sahu, Salma Mukhtar Mir, et al. "Capsaicin, the pungent principle of peppers, ameliorates alcohol-induced acute liver injury in mice via modulation of matrix metalloproteinases." Canadian Journal of Physiology and Pharmacology 96, no. 4 (2018): 419–27. http://dx.doi.org/10.1139/cjpp-2017-0473.

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Alcohol, the most common cause for hepatic injury, may further deteriorate the hepatic tissue when left unattended. Capsaicin, the pungent principle of chilli peppers, possesses antioxidant and anti-inflammatory properties and is a proven dietary antioxidant in various ailments. However, its role in alcohol-induced hepatic injury is unclear. In this study, we investigated the effects of capsaicin on the hepatic tissue of mice treated with alcohol. Acute liver injury was induced in mice by oral gavage of 5 doses of 10 mL/kg of 50% ethyl alcohol at an interval of 12 h. The tissue antioxidant lev

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43

Katayama, Toshiya, and Kazuya Ooi. "Preventing Acarbose-induced Hepatic Injury." Iryo Yakugaku (Japanese Journal of Pharmaceutical Health Care and Sciences) 29, no. 3 (2003): 300–304. http://dx.doi.org/10.5649/jjphcs.29.300.

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44

&NA;. "Hepatic injury linked to natalizumab." Reactions Weekly &NA;, no. 1207 (2008): 2. http://dx.doi.org/10.2165/00128415-200812070-00003.

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45

WAHI, P. N., H. D. TANDON, and T. P. BHARADWAJ. "ACUTE CARBON TETRACHLORIDE HEPATIC INJURY." Acta Pathologica Microbiologica Scandinavica 37, no. 4 (2009): 305–14. http://dx.doi.org/10.1111/j.1699-0463.1955.tb00952.x.

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46

WAHI, P. N., H. D. TANDON, and T. P. BHARADWAJ. "ACUTE CARBON TETRACHLORIDE HEPATIC INJURY." Acta Pathologica Microbiologica Scandinavica 37, no. 4 (2009): 315–21. http://dx.doi.org/10.1111/j.1699-0463.1955.tb00953.x.

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47

Andrade, Raúl J., MaIsabel Lucena, and Fermin Santalla. "Hepatic Injury Associated with Losartan." Annals of Pharmacotherapy 32, no. 12 (1998): 1371. http://dx.doi.org/10.1345/aph.18087a.

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48

Chan, C. H. "Dantrolene sodium and hepatic injury." Neurology 40, no. 9 (1990): 1427. http://dx.doi.org/10.1212/wnl.40.9.1427.

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49

Wu, Na, Guang-Ming Cai, and Qun He. "Oxidative stress and hepatic injury." World Chinese Journal of Digestology 16, no. 29 (2008): 3310. http://dx.doi.org/10.11569/wcjd.v16.i29.3310.

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Kaplowitz, Neil. "Avoiding hepatic injury from drugs." Gastroenterology 117, no. 4 (1999): 759. http://dx.doi.org/10.1016/s0016-5085(99)70329-x.

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