ライフサイエンスコーパス: DILI

1 DILI also occurred in 1 of 9480 patients taking diclofen

2 DILI associated with SJS/TEN is rare and associated with

3 DILI had a primary role in 68 (64%), a contributory role

4 DILI is an uncommon indication for hospitalization carry

5 DILI is caused by a wide array of medications, herbal su

6 DILI leads directly or indirectly to fatality in 7.6% of

7 DILI may be attenuated or exacerbated by pathogens depen

8 DILI was caused by a single prescription medication in 7

9 DILI was caused by a single prescription medication in 7

10 DILI with cirrhosis yielded the highest in-hospital and

11 Two most common causes for 60 DILI cases with latency >365 days were nitrofurantoin (2

12 ring n = 354 drugs, an algorithm to assign a DILI score was developed.

13 te liver failure (controls) collected from a DILI Biobank in Germany.

14 For these purposes, a DILI ontology (DILIo) was developed by using the Unified

15 ased on daily dose, lipophilicity, and RM, a DILI score algorithm was developed that provides a scale

16 Acetaminophen DILI yielded lower risks of mortality (HR 0.24, 95 % CI:

17 At 6 months after DILI onset, 18.9% of the 598 evaluable subjects had pers

18 ularly when fatalities occur >26 weeks after DILI onset.

19 N-acetylcysteine may be protective against DILI while taking antituberculosis medication.

20 ap of histologic findings exists for AIH and DILI, sufficient differences exist so that pathologists

21 relationship between hepatic metabolism and DILI of prescription medications.

22 amoxicillin-clavulanate as outpatients, and DILI occurred in 1 of 2350 (43 of 100,000; 95% CI, 24-70

23 ationship between calculated DILI scores and DILI risk was obtained when applied to three independent

24 ght network investigators and categorized as DILI having a primary, a contributory, or no role in the

25 prospective study used two methods to assess DILI causality: a structured expert opinion process and

26 e molecular features important for assessing DILI risk.

27 eliable, and reproducible means of assessing DILI causality is still needed.

28 When applied at DILI recognition, the nR criteria for Hy's Law provides

29 We analyzed data collected at DILI recognition and at the time of peak levels of alani

30 f DILI can help with predicting and avoiding DILI in clinical practice and provide the foundation for

31 Because DILI is a diagnosis of exclusion, selected elements of t

32 46 nevirapine-induced rash plus 3 with both DILI and SJS phenotype) and 155 age-, sex- and ethnicity

33 splantation (P < 0.001), and death caused by DILI (P = 0.004) but not alanine aminotransferase (ALT)

34 ore, a clear relationship between calculated DILI scores and DILI risk was obtained when applied to t

35 he single largest class of agents that cause DILI.

36 assessing the likelihood of an agent causing DILI and written criteria for improving the reliability,

37 ibiotics remain the most common drug causing DILI in the United States and Europe.

38 >1000 drugs for their likelihood of causing DILI in humans, of which >700 drugs were classified into

39 patients with clinically well-characterized DILI [n = 35, including 19 hepatocellular injury (HC) an

40 Chronic DILI may occur, but development of clinically important

41 nt were independent risk factors for chronic DILI (C-statistic = 0.71).

42 no-DILI drugs in comparison with the 2-class DILI model.

43 e developed and compared 2-class and 3-class DILI prediction models using the machine learning algori

44 quantitative assessment of risk of clinical DILI.

45 exposure thresholds associated with clinical DILI.

46 -approved drugs by extracting all clinically DILI-related histopathologic descriptions for 1082 liver

47 Conclusion: DILI is an uncommon cause of ALF that evolves slowly, af

48 a foundation for future studies correlating DILI pathology with its causality and outcome.

49 llance is the most useful tool for detecting DILI, and prompt discontinuation of the drug responsible

50 We identified patients who developed DILI in association with SJS/TEN from a registry of DILI

51 may still be the better method of diagnosing DILI compared with an objective tool such as the Roussel

52 ients (10%) with pre-existing liver disease, DILI appeared to be more severe than in those without (d

53 During DILI, oncotic necrosis with concomitant release and reco

54 tic regression analyses the algorithm (i.e., DILI score model) defined the relative contribution of d

55 not only had a higher resolution to estimate DILI risk but also showed an improved capability to diff

56 Although an infrequent event, DILI from antidepressant drugs may be irreversible, and

57 stically to promote sex bias in experimental DILI by reducing Tregs.

58 terms were "liver injury," "liver failure," "DILI," "hepatitis," "hepatotoxicity," "cholestasis," and

59 ailure (28% versus 9%, P = 0.004), and fatal DILI (23% versus 4%, P = 0.001), but not jaundice (46% v

60 ver failure, liver transplantation, or fatal DILI.

61 ver failure, liver transplantation, or fatal DILI.

62 from patients who have experienced bone fide DILI.

63 66,399 markers in 51 cases of flucloxacillin DILI and 282 controls matched for sex and ancestry.

64 nsights into the mechanism of flucloxacillin DILI and have the potential to substantially improve dia

65 interesting example is flucloxacillin (FLUX)-DILI, which is associated with the HLA-B*57:01 allele.

66 At present, the mechanism of FLUX-DILI is not understood, but the HLA association suggests

67 Causality assessment for DILI and SJS/TEN was carried out with the Roussel Uclaf

68 veloping truly predictive new biomarkers for DILI.

69 ption has been proposed as a risk factor for DILI from medications, but there is insufficient evidenc

70 lar target but differ in their potential for DILI.

71 an appropriate means of estimating risk for DILI compared with dose alone.

72 There is an unmet need to predict risk for DILI more reliably, and lipophilicity might be a contrib

73 s to be associated with significant risk for DILI; however, the RO2 failed to estimate grades of DILI

74 Mortality from DILI is significantly higher in individuals with pre-exi

75 Liver samples from DILI patients contained more activated JNK, predominantl

76 Proposed scales for grading DILI severity and assessing the likelihood of an agent c

77 bjects were deemed by expert opinion to have DILI; 81.1% were considered highly likely, 15.0% probabl

78 tivity was generally correlated across human DILI concern categories.

79 a affirm that severe manifestations of human DILI are multifactorial, highly associated with combinat

80 ere highly associated with more severe human DILI, more restrictive product safety labeling related t

81 rs contribute to the susceptibility to human DILI and its severity that are either compound- and/or p

82 Idiosyncratic DILI was shown to have an important dose-dependency and

83 daily dose of medications and idiosyncratic DILI, we conducted a study with two aims.

84 l prescription medications and idiosyncratic DILI.

85 ionship between daily dose and idiosyncratic DILI.

86 Furthermore, idiosyncratic DILI is not a single disease entity but rather a spectru

87 We describe here cases of idiosyncratic DILI ALF enrolled during a 10.5-year period.

88 inical models for the study of idiosyncratic DILI and its pathogenesis is poorly understood.

89 isk factors, and mechanisms of idiosyncratic DILI.

90 iated any genetic factors with idiosyncratic DILI.

91 factoring RM into the RO2 to highly improve DILI prediction.

92 he most robust increase in plasma miR-122 in DILI and it correlated with the highest ALT levels.

93 d and gender-based susceptibility factors in DILI development.

94 n approach for evaluating liver histology in DILI and demonstrate numerous associations between patho

95 tigators, and clinicians with an interest in DILI.

96 cellular) cholestasis were more prevalent in DILI (CS) (P < 0.02).

97 Transplant-free survival in DILI ALF is determined by the degree of liver dysfunctio

98 current nomenclature and terminology used in DILI research.

99 d with the exosome-rich fraction, whereas in DILI/APAP injury these miRNAs were present in the protei

100 sociation between azithromycin and increased DILI in patients with chronic liver disease.

101 xiclav (amoxicillin-clavulanic acid) induced DILI.

102 3%), idiosyncratic drug-induced liver injury DILI (22%), acute hepatitis B virus infection (12%), aut

103 Drug-induced liver injury (DILI) accounts for 20-40% of all instances of clinical h

104 ogy and function, drug-induced liver injury (DILI) and liver diseases are difficult to study using cu

105 the incidence of drug-induced liver injury (DILI) and risk factors for adverse outcomes.

106 he association of drug-induced liver injury (DILI) and Stevens-Johnson syndrome (SJS) or toxic epider

107 ited States, with drug-induced liver injury (DILI) being the single most common reason for regulatory

108 ith incidences of drug-induced liver injury (DILI) for more than 50 years, although its role in this

109 Distinguishing drug-induced liver injury (DILI) from idiopathic autoimmune hepatitis (AIH) can be

110 he role of JNK in drug-induced liver injury (DILI) in liver tissue from patients and in mice with gen

111 the incidence of drug-induced liver injury (DILI) in the general population.

112 Drug-induced liver injury (DILI) is a challenging problem in drug development and c

113 Drug-induced liver injury (DILI) is a leading cause of drug failure in clinical tri

114 Drug-induced liver injury (DILI) is a main cause of drug withdrawal.

115 Drug-induced liver injury (DILI) is a major health issue, as it remains difficult t

116 Drug-induced liver injury (DILI) is a major public health concern, and improving it

117 Drug-induced liver injury (DILI) is a major safety concern in drug development.

118 Idiosyncratic drug-induced liver injury (DILI) is a rare disease that develops independently of d

119 Idiosyncratic drug-induced liver injury (DILI) is a rare disorder that is not related directly to

120 Idiosyncratic drug-induced liver injury (DILI) is among the most common causes of acute liver fai

121 Idiosyncratic drug-induced liver injury (DILI) is an important but relatively infrequent cause of

122 Drug-induced liver injury (DILI) is an important cause of acute liver failure, with

123 Drug-induced liver injury (DILI) is an important cause of death and indication for

124 Drug-induced liver injury (DILI) is an important cause of serious liver disease.

125 Drug-induced liver injury (DILI) is considered to be a diagnosis of exclusion.

126 and management of drug-induced liver injury (DILI) is hindered by the limited utility of traditional

127 Drug-induced liver injury (DILI) is largely a diagnosis of exclusion and is therefo

128 Drug-induced liver injury (DILI) is of major interest to hepatologists and clinicia

129 Idiosyncratic drug-induced liver injury (DILI) is traditionally thought not to be dose-related.

130 Drug-induced liver injury (DILI) limits the development and application of many the

131 Drug-induced liver injury (DILI) may present any morphologic characteristic of acut

132 on idiosyncratic drug-induced liver injury (DILI) over the past 2 years in the peer-reviewed literat

133 Drug-induced liver injury (DILI) presents a significant challenge to drug developme

134 Drug-induced liver injury (DILI) remains a leading cause of drug withdrawal from hu

135 URPOSE OF REVIEW: Drug-induced liver injury (DILI) remains an important disease in clinical practice.

136 Idiosyncratic drug induced liver injury (DILI) remains poorly understood.

137 Immune-mediated, drug-induced liver injury (DILI) triggered by drug haptens is more prevalent in wom

138 at hepatocellular drug-induced liver injury (DILI) with jaundice indicates a serious reaction, is use

139 (acetaminophen, APAP)-induced liver injury (DILI), and Toll-like receptor (TLR) 9+4 ligand-induced i

140 e pathogenesis of drug-induced liver injury (DILI), but supporting data are limited.

141 y lead to serious drug-induced liver injury (DILI), chronic liver disease, or acute liver failure.

142 lure (ALF) due to drug-induced liver injury (DILI), though uncommon, is a concern for both clinicians

143 t drugs can cause drug-induced liver injury (DILI).

144 mainly caused by drug-induced liver injury (DILI).

145 rechallenge after drug-induced liver injury (DILI): antimicrobials; and central nervous system, cardi

146 ersensitivity (15 drug-induced liver injury [DILI], 33 SJS/TEN, 20 hypersensitivity syndrome, and 46

147 ibitory properties of 24 Most-DILI-, 28 Less-DILI-, and 20 No-DILI-concern drugs were investigated.

148 ified into three categories (most-DILI, less-DILI, and no-DILI).

149 d provide a pharmaceutical strategy to limit DILI and improve drug safety.

150 eir role in a mouse model of immune-mediated DILI.

151 To model DILI, we immunized BALB/c, BALB/cBy, IL-6-deficient, and

152 ificant hepatic metabolism should cause more DILI than those without it.

153 -LTKB), the inhibitory properties of 24 Most-DILI-, 28 Less-DILI-, and 20 No-DILI-concern drugs were

154 were classified into three categories (most-DILI, less-DILI, and no-DILI).

155 an improved capability to differentiate most-DILI drugs from no-DILI drugs in comparison with the 2-c

156 s of 24 Most-DILI-, 28 Less-DILI-, and 20 No-DILI-concern drugs were investigated.

157 ree categories (most-DILI, less-DILI, and no-DILI).

158 ity to differentiate most-DILI drugs from no-DILI drugs in comparison with the 2-class DILI model.

159 Nonetheless, DILI is challenging to investigate because of its rarity

160 resentations spanned many different areas of DILI, and included novel data concerning mechanisms of h

161 of the blood transcriptome for biomarkers of DILI.

162 ranscriptome might provide new biomarkers of DILI.

163 ing analyses are under way to study cases of DILI attributed to a single medication.

164 ntribute similarly in many clinical cases of DILI.

165 e ultimate aim of preventing future cases of DILI.

166 tent with events that occur in many cases of DILI.

167 al agent flucloxacillin is a common cause of DILI, but the genetic basis for susceptibility remains u

168 drugs and are also the most common cause of DILI.

169 The most common causes of DILI were acetaminophen (35.0 %) and anti-tuberculous dr

170 f mechanisms and clinical characteristics of DILI.

171 We describe our experience of DILI occurring in association with SJS/TEN including the

172 patic DNA accumulation is a novel feature of DILI pathogenesis.

173 c accuracy, but the histological features of DILI and their relationship to biochemical parameters an

174 s descriptors of histopathologic features of DILI.

175 lism are associated with higher frequency of DILI.

176 owever, the RO2 failed to estimate grades of DILI severity.

177 ion-based study in Iceland, the incidence of DILI was the highest reported to date.

178 es of patients with short vs long latency of DILI.

179 Defining lexemes of DILI histopathology would allow the development of advan

180 the diagnosis, prediction and management of DILI will be reviewed.

181 e sensitive to more severe manifestations of DILI than drugs that only have a single liability factor

182 MicroRNAs are a potential marker of DILI.

183 specifically related to known mechanisms of DILI (like mitochondrial and BSEP inhibition), and, alon

184 unction protein, is an essential mediator of DILI by showing that mice deficient in Cx32 are protecte

185 rgo liver transplantation within 6 months of DILI onset and nearly 1 in 5 of the remaining patients h

186 Within 6 months of DILI onset, 30 patients received liver transplants (4.5%

187 d diagnostic criteria regarding the onset of DILI, evolution of liver injury, risk factors, and manda

188 We assessed incidences and outcomes of DILI including associated factors for mortality.

189 The pathogenesis of DILI is not fully understood.

190 s into the mechanisms of the pathogenesis of DILI.

191 establishing the diagnosis and prognosis of DILI were reviewed.

192 The crude annual incidence rate of DILI was 19.1 (95% confidence interval [CI], 15.4-23.3)

193 At recognition of DILI, the R- and nR-based models identified patients who

194 association with SJS/TEN from a registry of DILI patients from a single center.

195 d the incidence and the quantitative risk of DILI in a population-based cohort.

196 The role of DILI in these fatalities is poorly characterized, partic

197 de crucial insights into the mechanism(s) of DILI with the ultimate aim of preventing future cases of

198 rovides a scale of assessing the severity of DILI risk in humans associated with oral medications.

199 or other etiologies, causes, and severity of DILI.

200 ics of pathophysiology and susceptibility of DILI can help with predicting and avoiding DILI in clini

201 of the pathophysiology and susceptibility of DILI.

202 Hepatocellular type of DILI is more common in younger patients, whereas cholest

203 cell-cell interactions in specific types of DILI.

204 e, will harmonize and accelerate research on DILI.

205 estasis yielded an AUC of 0.91 in predicting DILI (CS) versus AIH.

206 teristic curve (AUROC) of 0.90 in predicting DILI (HC) versus AIH.

207 the rule-of-two performed best in predicting DILI in seven therapeutic categories.

208 to have definite, highly likely, or probable DILI.

209 ts with definite, highly likely, or probable DILI.

210 in liver pathways, predicting human-relevant DILI using in vitro human liver models is crucial.

211 Second, we examined serious DILI cases reported to the Swedish Adverse Drug Reaction

212 inically important liver injury after severe DILI is rare.

213 se individuals who are susceptible to severe DILI.

214 ver Injury Network, DILIGEN, and the Spanish DILI registry) are important tools for clinical and gene

215 ts with DILI (805 episodes) from the Spanish DILI registry, from April 1994 through August 2012.

216 l networks enrolling patients with suspected DILI according to standardized methodologies are needed.

217 n in 2003 to recruit patients with suspected DILI and create a repository of biological samples for a

218 hould be excluded in patients with suspected DILI by HCV RNA testing.

219 es obtained from 249 patients with suspected DILI enrolled in the prospective, observational study co

220 data on eligible individuals with suspected DILI in 2004, following them for 6 months or longer.

221 Patients with suspected DILI were enrolled based on predefined criteria and foll

222 Among 1257 enrolled subjects with suspected DILI, the causality was assessed in 1091 patients, and 8

223 Among 250 patients with suspected DILI, the expert opinion adjudication process scored 78

224 laboratory data from patients with suspected DILI.

225 Of 598 eligible Swedish DILI cases, 9% belonged to the < or =10 mg/day group, 14

226 (death or liver transplantation) of Swedish DILI cases (2%, 9.4%, and 13.2% in < or =10, 11-49, and

227 , liver diseases, drug targets and long-term DILI.

228 but were more severe in AIH (P < 0.05) than DILI (HC).

229 ammation scores were more severe in AIH than DILI (CS) (P </= 0.05).

230 The DILI score model was also functional with drug pairs def

231 ly, for drug pairs where the RO2 failed, the DILI score correctly identified toxic drugs.

232 Standardization of the DILI nomenclature and methods to assess causality, along

233 's LiverTox database to demonstrate that the DILI score correlated with the severity of clinical outc

234 umbers may provide a therapeutic approach to DILI.

235 ility factors that predispose individuals to DILI.

236 The most common drugs leading to DILI in the United States are antibiotics, central nervo

237 mpound-specific primary mechanisms linked to DILI include: cytotoxicity, reactive metabolite formatio

238 Patient susceptibility to DILI is multifactorial, making these reactions difficult

239 ential hallmarks to differentiate AIH versus DILI.

240 cytopenia were independently associated with DILI fatalities.

241 rt or long latencies are not associated with DILI mortality.

242 eosinophilia has often been associated with DILI, although its role remains unclear.

243 an 100 different agents were associated with DILI; antimicrobials (45.5%) and central nervous system

244 and a stronger independent association with DILI fatalities within 26 weeks compared to the original

245 cted data from 96 individuals diagnosed with DILI in Iceland from 2010 through 2011 (54 women; median

246 We collected data from 771 patients with DILI (805 episodes) from the Spanish DILI registry, from

247 We studied liver sections from patients with DILI (due to acetaminophen, phenprocoumon, nonsteroidal

248 Multicenter databases of patients with DILI (the United States Drug Induced Liver Injury Networ

249 outcomes of a large cohort of patients with DILI enrolled in an ongoing multicenter prospective stud

250 Among 748 consecutive patients with DILI from 1997 to March 2015, 36 (4.8%) had associated f

251 ducting a prospective study of patients with DILI in the United States.

252 Of the 771 patients with DILI, 32 developed ALF.

253 a model for predicting ALF in patients with DILI.

254 on-based study of hospitalized patients with DILI.

255 ransfer from naive female mice to those with DILI reduced hepatitis severity and hepatic IL-6.