Genetic and immune predictors for hypersensitivity syndrome to antiepileptic drugs

Neuman, Manuela G.; Cohen, Lawrence B.; Nanau, Radu M.; Hwang, Paul A.

doi:10.1016/j.trsl.2012.01.004

Cited by 29 publications

(15 citation statements)

References 71 publications

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“…The modulation of cytokine production by LTG, TPM and LEV has been subject to small exploratory studies, but not systematically in-vitro or in-vivo (Neuman et al, 2012;Kim et al, 2010;Koçer et al, 2009). Systematic investigation of the modulation of cytokine production by AEDs would clarify whether AEDs with mood stabilizing properties differ from AEDs without clear mood stabilizing effects.…”

Section: Introductionmentioning

confidence: 99%

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Himmerich¹,

Bartsch²,

Hamer³

et al. 2013

Journal of Psychiatric Research

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Section: Introductionmentioning

confidence: 99%

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Himmerich¹,

Bartsch²,

Hamer³

et al. 2013

Journal of Psychiatric Research

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“…In other reports levels of SJS and TEN cytokines were considerably greater in patient serum than healthy individuals' [12].…”

Section: Introductionmentioning

confidence: 68%

MicroRNA and gene signature of severe cutaneous drug hypersensitivity reactions reveal the role of miR-483- 5p/miR-28-5p in inflammation by targeting Granulysin gene

Elbakkoush¹,

Khaleel²,

Liu³

2017

Trop. J. Pharm Res

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“…In inflammation-based liver injury, the excess of proinflammatory cytokines and the reduction of regulatory cytokines cause general cell death within the liver rather than targeting the liver cells that express damaged motifs [110, 111]. Inducing expression of inflammatory cytokines IL-1 α and the use of anti-TNF- α antibodies increase the susceptibility to DILI [108].…”

Section: Mechanisms For Idiosyncratic Hepatotoxicitymentioning

confidence: 99%

Idiosyncratic Drug-Induced Liver Injury (IDILI): Potential Mechanisms and Predictive Assays

Roth

Lee

2017

BioMed Research International

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Idiosyncratic drug-induced liver injury (IDILI) is a significant source of drug recall and acute liver failure (ALF) in the United States. While current drug development processes emphasize general toxicity and drug metabolizing enzyme- (DME-) mediated toxicity, it has been challenging to develop comprehensive models for assessing complete idiosyncratic potential. In this review, we describe the enzymes and proteins that contain polymorphisms believed to contribute to IDILI, including ones that affect phase I and phase II metabolism, antioxidant enzymes, drug transporters, inflammation, and human leukocyte antigen (HLA). We then describe the various assays that have been developed to detect individual reactions focusing on each of the mechanisms described in the background. Finally, we examine current trends in developing comprehensive models for examining these mechanisms. There is an urgent need to develop a panel of multiparametric assays for diagnosing individual toxicity potential.

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Genetic and immune predictors for hypersensitivity syndrome to antiepileptic drugs

Cited by 29 publications

References 71 publications

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

MicroRNA and gene signature of severe cutaneous drug hypersensitivity reactions reveal the role of miR-483- 5p/miR-28-5p in inflammation by targeting Granulysin gene

Idiosyncratic Drug-Induced Liver Injury (IDILI): Potential Mechanisms and Predictive Assays

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