Amoxicillin–Clavulanate-Induced Liver Injury
Background and Aims Amoxicillin–clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs. Methods Subjects with suspected...
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| Published in | Digestive diseases and sciences Vol. 61; no. 8; pp. 2406 - 2416 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Springer US
01.08.2016
Springer Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background and Aims
Amoxicillin–clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs.
Methods
Subjects with suspected DILI were enrolled prospectively, and cases were adjudicated as previously described. Clinical variables and outcomes of patients with AC-DILI were compared to the overall DILIN cohort and to DILI caused by other antimicrobials.
Results
One hundred and seventeen subjects with AC-DILI were identified from the cohort (
n
= 1038) representing 11 % of all cases and 24 % of those due to antimicrobial agents (
n
= 479). Those with AC-DILI were older (60 vs. 48 years,
P
< 0.001). AC-DILI was more frequent in men than women (62 vs. 39 %) compared to the overall cohort (40 vs. 60 %,
P
< 0.001). The mean time to symptom onset was 31 days. The Tb, ALT, and ALP were 7 mg/dL, 478, and 325 U/L at onset. Nearly all liver biopsies showed prominent cholestatic features. Resolution of AC-DILI, defined by return of Tb to <2.5 mg/dL, occurred on average 55 days after the peak value. Three female subjects required liver transplantation, and none died due to DILI.
Conclusion
AC-DILI causes a moderately severe, mixed hepatocellular–cholestatic injury, particularly in older men, unlike DILI in general, which predominates in women. Although often protracted, eventual apparent recovery is typical, particularly for men and usually in women, but three women required liver transplantation. |
|---|---|
| AbstractList | Background and Aims
Amoxicillin–clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs.
Methods
Subjects with suspected DILI were enrolled prospectively, and cases were adjudicated as previously described. Clinical variables and outcomes of patients with AC-DILI were compared to the overall DILIN cohort and to DILI caused by other antimicrobials.
Results
One hundred and seventeen subjects with AC-DILI were identified from the cohort (
n
= 1038) representing 11 % of all cases and 24 % of those due to antimicrobial agents (
n
= 479). Those with AC-DILI were older (60 vs. 48 years,
P
< 0.001). AC-DILI was more frequent in men than women (62 vs. 39 %) compared to the overall cohort (40 vs. 60 %,
P
< 0.001). The mean time to symptom onset was 31 days. The Tb, ALT, and ALP were 7 mg/dL, 478, and 325 U/L at onset. Nearly all liver biopsies showed prominent cholestatic features. Resolution of AC-DILI, defined by return of Tb to <2.5 mg/dL, occurred on average 55 days after the peak value. Three female subjects required liver transplantation, and none died due to DILI.
Conclusion
AC-DILI causes a moderately severe, mixed hepatocellular–cholestatic injury, particularly in older men, unlike DILI in general, which predominates in women. Although often protracted, eventual apparent recovery is typical, particularly for men and usually in women, but three women required liver transplantation. Amoxicillin-clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs. Subjects with suspected DILI were enrolled prospectively, and cases were adjudicated as previously described. Clinical variables and outcomes of patients with AC-DILI were compared to the overall DILIN cohort and to DILI caused by other antimicrobials. One hundred and seventeen subjects with AC-DILI were identified from the cohort (n = 1038) representing 11 % of all cases and 24 % of those due to antimicrobial agents (n = 479). Those with AC-DILI were older (60 vs. 48 years, P < 0.001). AC-DILI was more frequent in men than women (62 vs. 39 %) compared to the overall cohort (40 vs. 60 %, P < 0.001). The mean time to symptom onset was 31 days. The Tb, ALT, and ALP were 7 mg/dL, 478, and 325 U/L at onset. Nearly all liver biopsies showed prominent cholestatic features. Resolution of AC-DILI, defined by return of Tb to <2.5 mg/dL, occurred on average 55 days after the peak value. Three female subjects required liver transplantation, and none died due to DILI. AC-DILI causes a moderately severe, mixed hepatocellular-cholestatic injury, particularly in older men, unlike DILI in general, which predominates in women. Although often protracted, eventual apparent recovery is typical, particularly for men and usually in women, but three women required liver transplantation. Amoxicillin-clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs.BACKGROUND AND AIMSAmoxicillin-clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs.Subjects with suspected DILI were enrolled prospectively, and cases were adjudicated as previously described. Clinical variables and outcomes of patients with AC-DILI were compared to the overall DILIN cohort and to DILI caused by other antimicrobials.METHODSSubjects with suspected DILI were enrolled prospectively, and cases were adjudicated as previously described. Clinical variables and outcomes of patients with AC-DILI were compared to the overall DILIN cohort and to DILI caused by other antimicrobials.One hundred and seventeen subjects with AC-DILI were identified from the cohort (n = 1038) representing 11 % of all cases and 24 % of those due to antimicrobial agents (n = 479). Those with AC-DILI were older (60 vs. 48 years, P < 0.001). AC-DILI was more frequent in men than women (62 vs. 39 %) compared to the overall cohort (40 vs. 60 %, P < 0.001). The mean time to symptom onset was 31 days. The Tb, ALT, and ALP were 7 mg/dL, 478, and 325 U/L at onset. Nearly all liver biopsies showed prominent cholestatic features. Resolution of AC-DILI, defined by return of Tb to <2.5 mg/dL, occurred on average 55 days after the peak value. Three female subjects required liver transplantation, and none died due to DILI.RESULTSOne hundred and seventeen subjects with AC-DILI were identified from the cohort (n = 1038) representing 11 % of all cases and 24 % of those due to antimicrobial agents (n = 479). Those with AC-DILI were older (60 vs. 48 years, P < 0.001). AC-DILI was more frequent in men than women (62 vs. 39 %) compared to the overall cohort (40 vs. 60 %, P < 0.001). The mean time to symptom onset was 31 days. The Tb, ALT, and ALP were 7 mg/dL, 478, and 325 U/L at onset. Nearly all liver biopsies showed prominent cholestatic features. Resolution of AC-DILI, defined by return of Tb to <2.5 mg/dL, occurred on average 55 days after the peak value. Three female subjects required liver transplantation, and none died due to DILI.AC-DILI causes a moderately severe, mixed hepatocellular-cholestatic injury, particularly in older men, unlike DILI in general, which predominates in women. Although often protracted, eventual apparent recovery is typical, particularly for men and usually in women, but three women required liver transplantation.CONCLUSIONAC-DILI causes a moderately severe, mixed hepatocellular-cholestatic injury, particularly in older men, unlike DILI in general, which predominates in women. Although often protracted, eventual apparent recovery is typical, particularly for men and usually in women, but three women required liver transplantation. Amoxicillin-clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs. Subjects with suspected DILI were enrolled prospectively, and cases were adjudicated as previously described. Clinical variables and outcomes of patients with AC-DILI were compared to the overall DILIN cohort and to DILI caused by other antimicrobials. One hundred and seventeen subjects with AC-DILI were identified from the cohort (n = 1038) representing 11 % of all cases and 24 % of those due to antimicrobial agents (n = 479). Those with AC-DILI were older (60 vs. 48 years, P < 0.001). AC-DILI was more frequent in men than women (62 vs. 39 %) compared to the overall cohort (40 vs. 60 %, P < 0.001). The mean time to symptom onset was 31 days. The Tb, ALT, and ALP were 7 mg/dL, 478, and 325 U/L at onset. Nearly all liver biopsies showed prominent cholestatic features. Resolution of AC-DILI, defined by return of Tb to <2.5 mg/dL, occurred on average 55 days after the peak value. Three female subjects required liver transplantation, and none died due to DILI. AC-DILI causes a moderately severe, mixed hepatocellular-cholestatic injury, particularly in older men, unlike DILI in general, which predominates in women. Although often protracted, eventual apparent recovery is typical, particularly for men and usually in women, but three women required liver transplantation. Background and Aims Amoxicillin-clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined a large cohort of AC-DILI cases and compared features of AC-DILI to those of other drugs. Methods Subjects with suspected DILI were enrolled prospectively, and cases were adjudicated as previously described. Clinical variables and outcomes of patients with AC-DILI were compared to the overall DILIN cohort and to DILI caused by other antimicrobials. Results One hundred and seventeen subjects with AC-DILI were identified from the cohort (n = 1038) representing 11 % of all cases and 24 % of those due to antimicrobial agents (n = 479). Those with AC-DILI were older (60 vs. 48 years, P < 0.001). AC-DILI was more frequent in men than women (62 vs. 39 %) compared to the overall cohort (40 vs. 60 %, P < 0.001). The mean time to symptom onset was 31 days. The Tb, ALT, and ALP were 7 mg/dL, 478, and 325 U/L at onset. Nearly all liver biopsies showed prominent cholestatic features. Resolution of AC-DILI, defined by return of Tb to <2.5 mg/dL, occurred on average 55 days after the peak value. Three female subjects required liver transplantation, and none died due to DILI. Conclusion AC-DILI causes a moderately severe, mixed hepatocellular-cholestatic injury, particularly in older men, unlike DILI in general, which predominates in women. Although often protracted, eventual apparent recovery is typical, particularly for men and usually in women, but three women required liver transplantation. |
| Audience | Professional Academic |
| Author | Ghabril, Marwan Gu, Jiezhun Kleiner, David E. deLemos, Andrew S. Fontana, Robert J. Barnhart, Huiman X. Bonkovsky, Herbert L. Rockey, Don C. |
| AuthorAffiliation | 3 Department of Medicine, Medical University of South Carolina, Charleston, SC, USA 7 Department of Medicine, Wake Forest Baptist Medical Center, Winston Salem, NC, USA 6 Laboratory of Pathology, National Cancer Institute, Bethesda, MD, USA 5 Department of Medicine, University of Michigan School of Medicine, Ann Arbor, MI, USA 1 Department of Medicine, Carolinas Medical Center, 1025 Morehead Medical Drive, Suite 600, Charlotte, NC 28204, USA 2 Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA 4 Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, USA |
| AuthorAffiliation_xml | – name: 3 Department of Medicine, Medical University of South Carolina, Charleston, SC, USA – name: 5 Department of Medicine, University of Michigan School of Medicine, Ann Arbor, MI, USA – name: 1 Department of Medicine, Carolinas Medical Center, 1025 Morehead Medical Drive, Suite 600, Charlotte, NC 28204, USA – name: 4 Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, USA – name: 2 Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA – name: 6 Laboratory of Pathology, National Cancer Institute, Bethesda, MD, USA – name: 7 Department of Medicine, Wake Forest Baptist Medical Center, Winston Salem, NC, USA |
| Author_xml | – sequence: 1 givenname: Andrew S. orcidid: 0000-0003-1232-7986 surname: deLemos fullname: deLemos, Andrew S. email: Andrew.deLemos@carolinashealthcare.org organization: Department of Medicine, Carolinas Medical Center – sequence: 2 givenname: Marwan surname: Ghabril fullname: Ghabril, Marwan organization: Department of Medicine, Indiana University School of Medicine – sequence: 3 givenname: Don C. surname: Rockey fullname: Rockey, Don C. organization: Department of Medicine, Medical University of South Carolina – sequence: 4 givenname: Jiezhun surname: Gu fullname: Gu, Jiezhun organization: Duke Clinical Research Institute, Duke University Medical Center – sequence: 5 givenname: Huiman X. surname: Barnhart fullname: Barnhart, Huiman X. organization: Duke Clinical Research Institute, Duke University Medical Center – sequence: 6 givenname: Robert J. surname: Fontana fullname: Fontana, Robert J. organization: Department of Medicine, University of Michigan School of Medicine – sequence: 7 givenname: David E. surname: Kleiner fullname: Kleiner, David E. organization: Laboratory of Pathology, National Cancer Institute – sequence: 8 givenname: Herbert L. surname: Bonkovsky fullname: Bonkovsky, Herbert L. organization: Department of Medicine, Wake Forest Baptist Medical Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27003146$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Springer Science+Business Media New York 2016 COPYRIGHT 2016 Springer |
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| Keywords | Augmentin Allergy Drug-induced liver injury Clavulanic acid Liver toxicity Amoxicillin |
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| References | Garcia RodriguezLAStrickerBHZimmermanHJRisk of acute liver injury associated with the combination of amoxicillin and clavulanic acidArch Intern Med1996156132713321:CAS:528:DyaK28XksVOktbo%3D10.1001/archinte.156.12.13278651842 AndradeRJLucenaMIFernandezMCPelaezGPachkoriaKGarcia-RuizEDrug-induced liver injury: an analysis of 461 incidences submitted to the Spanish registry over a 10-year periodGastroenterology200512951252110.1016/j.gastro.2005.05.00616083708 FoureauDMWallingTLMaddukuriVComparative analysis of portal hepatic infiltrating leukocytes in acute drug-induced liver injury, idiopathic autoimmune and viral hepatitisClin Exp Immunol201518040511:CAS:528:DC%2BC2MXjvFyksbY%3D10.1111/cei.12558254184874367092 JakabSSWestABMeighanDMBrownRSJrHaleWBMycophenolate mofetil for drug-induced vanishing bile duct syndromeWorld J Gastroenterol200713608760891:CAS:528:DC%2BD1cXit1Srug%3D%3D10.3748/wjg.13.6087180231054250896 FontanaRJWatkinsPBBonkovskyHLChalasaniNDavernTSerranoJDrug-Induced Liver Injury Network (DILIN) prospective study: rationale, design and conductDrug Saf20093255681:CAS:528:DC%2BD1MXjslaltb8%3D10.2165/00002018-200932010-00005191328053637941 FontanaRJPathogenesis of idiosyncratic drug-induced liver injury and clinical perspectivesGastroenterology20141469149281:CAS:528:DC%2BC2cXkslSrsb0%3D10.1053/j.gastro.2013.12.03224389305 FontanaRJShakilAOGreensonJKBoydILeeWMAcute liver failure due to amoxicillin and amoxicillin/clavulanateDig Dis Sci2005501785179010.1007/s10620-005-2938-516187174 LarreyDVialTMicaleffABabanyGMorichau-BeauchantMMichelHHepatitis associated with amoxycillin-clavulanic acid combination report of 15 casesGut1992333683711:STN:280:DyaK383jsValtA%3D%3D10.1136/gut.33.3.36815686571373830 Lewis JH, Zimmerman HJ. Drug- and chemical-induced cholestasis. Clin Liver Dis. 1999;3:433–464, vii. StephensCLopez-NevotMARuiz-CabelloFUlzurrunESorianoGRomero-GomezMHLA alleles influence the clinical signature of amoxicillin–clavulanate hepatotoxicityPLoS One20138e681111:CAS:528:DC%2BC3sXhtFOmtb7N10.1371/journal.pone.0068111238745143706603 RockeyDCSeeffLBRochonJFrestonJChalasaniNBonaciniMCausality assessment in drug-induced liver injury using a structured expert opinion process: comparison to the Roussel-Uclaf causality assessment methodHepatology2010512117212610.1002/hep.23577205129993249230 LucenaMIMolokhiaMShenYUrbanTJAithalGPAndradeRJSusceptibility to amoxicillin–clavulanate–induced liver injury is influenced by multiple HLA class I and II allelesGastroenterology20111413383471:CAS:528:DC%2BC3MXosVGnsLg%3D10.1053/j.gastro.2011.04.001215703973129430 FontanaRJHayashiPHBarnhartHKleinerDEReddyKRChalasaniNPersistent liver biochemistry abnormalities are more common in older patients and those with cholestatic drug induced liver injuryAm J Gastroenterol2015110145014591:CAS:528:DC%2BC2MXhs1OqurvO10.1038/ajg.2015.28326346867 O’DonohueJOienKADonaldsonPUnderhillJClareMMacSweenRNCo-amoxiclav jaundice: clinical and histological features and HLA class II associationGut20004771772010.1136/gut.47.5.717110345911728095 KleinerDEThe pathology of drug-induced liver injurySemin Liver Dis20092936437210.1055/s-0029-124000519826970 Chalasani N, Fontana RJ, Bonkovsky HL, et al. Causes, clinical features, and outcomes from a prospective study of drug-induced liver injury in the United States. Gastroenterology. 2008;135:1924–1934, 1934 e1921–1924. UrbanTJShenYStolzAChalasaniNFontanaRJRochonJLimited contribution of common genetic variants to risk for liver injury due to a variety of drugsPharmacogenet Genomics2012227847951:CAS:528:DC%2BC38XhsVKgsrrP10.1097/FPC.0b013e3283589a76229684313636716 de HaanFStricker BH [Liver damage associated with the combination drug amoxicillin-clavulanic acid (Augmentin)]Ned Tijdschr Geneeskd1997141129813019380177 LucenaMIAndradeRJFernandezMCPachkoriaKPelaezGDuranJADeterminants of the clinical expression of amoxicillin–clavulanate hepatotoxicity: a prospective series from SpainHepatology2006448508561:CAS:528:DC%2BD28XhtFyqsr%2FF10.1002/hep.2132417006920 HautekeeteMLHorsmansYVan WaeyenbergeCDemanetCHenrionJVerbistLHLA association of amoxicillin–clavulanate–induced hepatitisGastroenterology1999117118111861:STN:280:DC%2BD3c%2FgsF2hsg%3D%3D10.1016/S0016-5085(99)70404-X10535882 AlqahtaniSAKleinerDEGhabrilMIdentification and characterization of cefazolin-induced liver injuryClin Gastroenterol Hepatol20151313281336.e21:CAS:528:DC%2BC2MXivFWlur0%3D10.1016/j.cgh.2014.11.03625528012 Bjornsson ES, Bergmann OM, Bjornsson HK, Kvaran RB, Olafsson S. Incidence, presentation, and outcomes in patients with drug-induced liver injury in the general population of Iceland. Gastroenterology. 2013;144:1419–1425, 1425 e1411–1413; quiz e1419–e1420. ThomsonJAFairleyCKUgoniAMForbesABPurcellPMDesmondPVRisk factors for the development of amoxycillin-clavulanic acid associated jaundiceMed J Aust19951626386401:STN:280:DyaK2Mzis12ruw%3D%3D7603374 Mohi-ud-din R, Lewis JH. Drug- and chemical-induced cholestasis. Clin Liver Dis. 2004;8:95–132, vii. LimauroDLChan-TompkinsNHCarterRWBrodmerkelGJJrAgrawalRMAmoxicillin/clavulanate-associated hepatic failure with progression to Stevens–Johnson syndromeAnn Pharmacother1999335605641:STN:280:DyaK1M3ps1ejuw%3D%3D10.1345/aph.1810410369618 ReddyKRBrillantPSchiffERAmoxicillin–clavulanate potassium-associated cholestasisGastroenterology198996113511411:STN:280:DyaL1M7ntFyntA%3D%3D10.1016/0016-5085(89)91633-82925057 DalyAKDonaldsonPTBhatnagarPShenYPe’erIFloratosAHLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillinNat Genet2009418168191:CAS:528:DC%2BD1MXms1alu7o%3D10.1038/ng.37919483685 RJ Fontana (4121_CR4) 2014; 146 MI Lucena (4121_CR15) 2006; 44 RJ Andrade (4121_CR2) 2005; 129 DL Limauro (4121_CR10) 1999; 33 MI Lucena (4121_CR20) 2011; 141 TJ Urban (4121_CR23) 2012; 22 LA Garcia Rodriguez (4121_CR27) 1996; 156 JA Thomson (4121_CR25) 1995; 162 RJ Fontana (4121_CR11) 2009; 32 DC Rockey (4121_CR13) 2010; 51 J O’Donohue (4121_CR26) 2000; 47 C Stephens (4121_CR21) 2013; 8 4121_CR6 4121_CR5 F de Haan (4121_CR24) 1997; 141 4121_CR3 SS Jakab (4121_CR7) 2007; 13 4121_CR1 RJ Fontana (4121_CR9) 2005; 50 DM Foureau (4121_CR19) 2015; 180 SA Alqahtani (4121_CR14) 2015; 13 D Larrey (4121_CR18) 1992; 33 ML Hautekeete (4121_CR17) 1999; 117 KR Reddy (4121_CR16) 1989; 96 RJ Fontana (4121_CR12) 2015; 110 AK Daly (4121_CR22) 2009; 41 DE Kleiner (4121_CR8) 2009; 29 |
| References_xml | – reference: FontanaRJHayashiPHBarnhartHKleinerDEReddyKRChalasaniNPersistent liver biochemistry abnormalities are more common in older patients and those with cholestatic drug induced liver injuryAm J Gastroenterol2015110145014591:CAS:528:DC%2BC2MXhs1OqurvO10.1038/ajg.2015.28326346867 – reference: JakabSSWestABMeighanDMBrownRSJrHaleWBMycophenolate mofetil for drug-induced vanishing bile duct syndromeWorld J Gastroenterol200713608760891:CAS:528:DC%2BD1cXit1Srug%3D%3D10.3748/wjg.13.6087180231054250896 – reference: ThomsonJAFairleyCKUgoniAMForbesABPurcellPMDesmondPVRisk factors for the development of amoxycillin-clavulanic acid associated jaundiceMed J Aust19951626386401:STN:280:DyaK2Mzis12ruw%3D%3D7603374 – reference: RockeyDCSeeffLBRochonJFrestonJChalasaniNBonaciniMCausality assessment in drug-induced liver injury using a structured expert opinion process: comparison to the Roussel-Uclaf causality assessment methodHepatology2010512117212610.1002/hep.23577205129993249230 – reference: Lewis JH, Zimmerman HJ. Drug- and chemical-induced cholestasis. Clin Liver Dis. 1999;3:433–464, vii. – reference: Mohi-ud-din R, Lewis JH. Drug- and chemical-induced cholestasis. Clin Liver Dis. 2004;8:95–132, vii. – reference: AlqahtaniSAKleinerDEGhabrilMIdentification and characterization of cefazolin-induced liver injuryClin Gastroenterol Hepatol20151313281336.e21:CAS:528:DC%2BC2MXivFWlur0%3D10.1016/j.cgh.2014.11.03625528012 – reference: FontanaRJShakilAOGreensonJKBoydILeeWMAcute liver failure due to amoxicillin and amoxicillin/clavulanateDig Dis Sci2005501785179010.1007/s10620-005-2938-516187174 – reference: KleinerDEThe pathology of drug-induced liver injurySemin Liver Dis20092936437210.1055/s-0029-124000519826970 – reference: LarreyDVialTMicaleffABabanyGMorichau-BeauchantMMichelHHepatitis associated with amoxycillin-clavulanic acid combination report of 15 casesGut1992333683711:STN:280:DyaK383jsValtA%3D%3D10.1136/gut.33.3.36815686571373830 – reference: DalyAKDonaldsonPTBhatnagarPShenYPe’erIFloratosAHLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillinNat Genet2009418168191:CAS:528:DC%2BD1MXms1alu7o%3D10.1038/ng.37919483685 – reference: StephensCLopez-NevotMARuiz-CabelloFUlzurrunESorianoGRomero-GomezMHLA alleles influence the clinical signature of amoxicillin–clavulanate hepatotoxicityPLoS One20138e681111:CAS:528:DC%2BC3sXhtFOmtb7N10.1371/journal.pone.0068111238745143706603 – reference: LimauroDLChan-TompkinsNHCarterRWBrodmerkelGJJrAgrawalRMAmoxicillin/clavulanate-associated hepatic failure with progression to Stevens–Johnson syndromeAnn Pharmacother1999335605641:STN:280:DyaK1M3ps1ejuw%3D%3D10.1345/aph.1810410369618 – reference: HautekeeteMLHorsmansYVan WaeyenbergeCDemanetCHenrionJVerbistLHLA association of amoxicillin–clavulanate–induced hepatitisGastroenterology1999117118111861:STN:280:DC%2BD3c%2FgsF2hsg%3D%3D10.1016/S0016-5085(99)70404-X10535882 – reference: de HaanFStricker BH [Liver damage associated with the combination drug amoxicillin-clavulanic acid (Augmentin)]Ned Tijdschr Geneeskd1997141129813019380177 – reference: FontanaRJPathogenesis of idiosyncratic drug-induced liver injury and clinical perspectivesGastroenterology20141469149281:CAS:528:DC%2BC2cXkslSrsb0%3D10.1053/j.gastro.2013.12.03224389305 – reference: Garcia RodriguezLAStrickerBHZimmermanHJRisk of acute liver injury associated with the combination of amoxicillin and clavulanic acidArch Intern Med1996156132713321:CAS:528:DyaK28XksVOktbo%3D10.1001/archinte.156.12.13278651842 – reference: LucenaMIMolokhiaMShenYUrbanTJAithalGPAndradeRJSusceptibility to amoxicillin–clavulanate–induced liver injury is influenced by multiple HLA class I and II allelesGastroenterology20111413383471:CAS:528:DC%2BC3MXosVGnsLg%3D10.1053/j.gastro.2011.04.001215703973129430 – reference: FontanaRJWatkinsPBBonkovskyHLChalasaniNDavernTSerranoJDrug-Induced Liver Injury Network (DILIN) prospective study: rationale, design and conductDrug Saf20093255681:CAS:528:DC%2BD1MXjslaltb8%3D10.2165/00002018-200932010-00005191328053637941 – reference: O’DonohueJOienKADonaldsonPUnderhillJClareMMacSweenRNCo-amoxiclav jaundice: clinical and histological features and HLA class II associationGut20004771772010.1136/gut.47.5.717110345911728095 – reference: FoureauDMWallingTLMaddukuriVComparative analysis of portal hepatic infiltrating leukocytes in acute drug-induced liver injury, idiopathic autoimmune and viral hepatitisClin Exp Immunol201518040511:CAS:528:DC%2BC2MXjvFyksbY%3D10.1111/cei.12558254184874367092 – reference: ReddyKRBrillantPSchiffERAmoxicillin–clavulanate potassium-associated cholestasisGastroenterology198996113511411:STN:280:DyaL1M7ntFyntA%3D%3D10.1016/0016-5085(89)91633-82925057 – reference: Chalasani N, Fontana RJ, Bonkovsky HL, et al. Causes, clinical features, and outcomes from a prospective study of drug-induced liver injury in the United States. Gastroenterology. 2008;135:1924–1934, 1934 e1921–1924. – reference: LucenaMIAndradeRJFernandezMCPachkoriaKPelaezGDuranJADeterminants of the clinical expression of amoxicillin–clavulanate hepatotoxicity: a prospective series from SpainHepatology2006448508561:CAS:528:DC%2BD28XhtFyqsr%2FF10.1002/hep.2132417006920 – reference: AndradeRJLucenaMIFernandezMCPelaezGPachkoriaKGarcia-RuizEDrug-induced liver injury: an analysis of 461 incidences submitted to the Spanish registry over a 10-year periodGastroenterology200512951252110.1016/j.gastro.2005.05.00616083708 – reference: UrbanTJShenYStolzAChalasaniNFontanaRJRochonJLimited contribution of common genetic variants to risk for liver injury due to a variety of drugsPharmacogenet Genomics2012227847951:CAS:528:DC%2BC38XhsVKgsrrP10.1097/FPC.0b013e3283589a76229684313636716 – reference: Bjornsson ES, Bergmann OM, Bjornsson HK, Kvaran RB, Olafsson S. Incidence, presentation, and outcomes in patients with drug-induced liver injury in the general population of Iceland. 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| Snippet | Background and Aims
Amoxicillin–clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN)... Amoxicillin-clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN) registry. Here, we examined... Background and Aims Amoxicillin-clavulanate (AC) is the most frequent cause of idiosyncratic drug-induced injury (DILI) in the US DILI Network (DILIN)... |
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| SubjectTerms | Age Factors Alanine Transaminase - blood Alkaline Phosphatase - blood Amoxicillin Amoxicillin-Potassium Clavulanate Combination - adverse effects Anti-Bacterial Agents - adverse effects Anti-infective agents beta-Lactamase Inhibitors - adverse effects Bilirubin - blood Biochemistry Black or African American Chemical and Drug Induced Liver Injury - blood Chemical and Drug Induced Liver Injury - epidemiology Chemical and Drug Induced Liver Injury - etiology Chemical and Drug Induced Liver Injury - pathology Cholestasis - blood Cholestasis - chemically induced Cholestasis - epidemiology Cholestasis - pathology Clavulanate Cohort Studies Ethnicity - statistics & numerical data Female Gastroenterology Hepatology Hispanic or Latino Humans Jaundice Jaundice, Obstructive - blood Jaundice, Obstructive - chemically induced Jaundice, Obstructive - epidemiology Jaundice, Obstructive - pathology Liver Liver - pathology Male Medical colleges Medicine Medicine & Public Health Middle Aged Oncology Original Article Pneumoviridae Prospective Studies Registries Sex Distribution Time Factors Transplant Surgery Transplantation of organs, tissues, etc United States - epidemiology White People |
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| Title | Amoxicillin–Clavulanate-Induced Liver Injury |
| URI | https://link.springer.com/article/10.1007/s10620-016-4121-6 https://www.ncbi.nlm.nih.gov/pubmed/27003146 https://www.proquest.com/docview/1811244612 https://www.proquest.com/docview/1804859776 https://www.proquest.com/docview/1942217644 https://pubmed.ncbi.nlm.nih.gov/PMC4945382 |
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