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1 RUCAM in retrospectively-identified cases of drug induced liver injury.
2 lead the list of non-acetaminophen causes of drug-induced liver injury.
3 an important role in the protection against drug-induced liver injury.
4 e RUCAM is problematic for future studies of drug-induced liver injury.
5 fy the key publications of 2006 dealing with drug-induced liver injury.
6 engineering because of the high frequency of drug-induced liver injury.
7 disruption, and increased susceptibility to drug-induced liver injury.
8 tion of K8/18 is to protect hepatocytes from drug-induced liver injury.
9 based instruments for assessing causality in drug-induced liver injury.
10 amic behaviour in the biological response to drug-induced liver injury.
11 ies have evaluated the incidence of ALF from drug-induced liver injury.
12 y revealed signs of immune-mediated toxic or drug-induced liver injury.
13 cells in human leukocyte antigen-associated, drug-induced liver injury.
14 biopsy samples from patients suffering from drug-induced liver injury.
15 elevance for understanding the regulation of drug-induced liver injury.
16 offer better specificity in ruling out late drug-induced liver injury.
17 city (22.2 and 82.1%) for prediction of late drug-induced liver injury.
18 her sensitive nor specific for prediction of drug-induced liver injury.
19 iction of early and 22.2% and 63.7% for late drug-induced liver injury.
20 drug metabolism, drug-drug interaction, and drug-induced liver injury.
21 lates what is believed to occur during human drug-induced liver injury.
22 as sensitive and informative biomarkers for drug-induced liver injury.
24 8 patients included, and 21 (7.3%) developed drug-induced liver injury (57.1% "early" at 2 wk and 42.
25 ug-related serious adverse events (potential drug-induced liver injury and depression or lipodystroph
26 -induced liver injury group compared with no drug-induced liver injury and late drug-induced liver in
27 entification of a subgroup who develop early drug-induced liver injury and may offer better specifici
28 ophen (APAP) overdose is a frequent cause of drug-induced liver injury and the most frequent cause of
29 sts that many cases of serious idiosyncratic drug-induced liver injury are mediated by the adaptive i
32 prospective study of patients with suspected drug-induced liver injury; clinical information and biol
33 29%), indeterminate ALF (23%), idiosyncratic drug-induced liver injury DILI (22%), acute hepatitis B
39 ic health concern in the United States, with drug-induced liver injury (DILI) being the single most c
40 hilia has been associated with incidences of drug-induced liver injury (DILI) for more than 50 years,
64 nd important data published on idiosyncratic drug-induced liver injury (DILI) over the past 2 years i
69 Hy's Law, which states that hepatocellular drug-induced liver injury (DILI) with jaundice indicates
70 lay an important role in the pathogenesis of drug-induced liver injury (DILI), but supporting data ar
71 patients, but statins rarely lead to serious drug-induced liver injury (DILI), chronic liver disease,
75 e associated with positive rechallenge after drug-induced liver injury (DILI): antimicrobials; and ce
76 adults with nevirapine hypersensitivity (15 drug-induced liver injury [DILI], 33 SJS/TEN, 20 hyperse
82 individuals with HIV infection in the early drug-induced liver injury group compared with no drug-in
83 d with no drug-induced liver injury and late drug-induced liver injury groups (33% vs. 7.1% vs. 0%; P
85 ty to discuss challenges in the diagnosis of drug-induced liver injury in an era of increasing awaren
87 th it several reminders of the importance of drug-induced liver injury in the clinical trial as well
95 important element in assessing causality in drug-induced liver injury is whether the implicated agen
96 important feature of the normal response to drug-induced liver injury may be the increased expressio
97 However, the complexity of idiosyncratic drug-induced liver injury means that no current single-c
98 rospective study of subjects enrolled in the Drug Induced Liver Injury Network (DILIN) from 2004 to 2
99 d 2012 in a prospective registry by the U.S. Drug Induced Liver Injury Network, 22 were attributed to
100 ses of patients with DILI (the United States Drug Induced Liver Injury Network, DILIGEN, and the Span
109 terile inflammation (SI) is a key process in drug-induced liver injury, nonalcoholic steatohepatitis,
111 rt represents the second documented cases of drug-induced liver injury related to varenicline therapy
116 in the world and accounts for most cases of drug induced liver injury resulting in acute liver failu
117 ng clinical evaluation and stopping rules of drug-induced liver injury signals, including Hy's Law ca
118 idrug and autoAbs has been observed in other drug-induced liver injury that is presumed to be immune
119 Conclusion: Telithromycin is a rare cause of drug-induced liver injury that may have a distinctive cl
120 al for chronic injury to develop after acute drug-induced liver injury was analyzed in a large Swedis
121 vents reporting and experience in evaluating drug-induced liver injury was formed, including members
124 clinical features, and outcomes of cases of drug-induced liver injury with histologically proven bil
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