2009
DOI: 10.2486/indhealth.47.479
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Effects of Genetic Polymorphisms of N-Acetyltransferase on Trichloroethylene-Induced Hypersensitivity Dermatitis among Exposed Workers

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Cited by 20 publications
(23 citation statements)
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“…N-acetyltransferase is an important metabolic enzyme in the conjugation pathway of TCE metabolism. 11 NAT includes two isoenzymes, NAT1 and NAT2, which are encoded by two separate genes and exhibit multiple genetic polymorphisms. A previous investigation indicated that slow or intermediate NAT2 acetylators are at increased risk of HS-induced skin disorders, compared with tolerant TCE workers.…”
Section: Polymorphisms In Tumor Necrosis Factor (Tnf)-a and N-acetyltmentioning
confidence: 99%
See 1 more Smart Citation
“…N-acetyltransferase is an important metabolic enzyme in the conjugation pathway of TCE metabolism. 11 NAT includes two isoenzymes, NAT1 and NAT2, which are encoded by two separate genes and exhibit multiple genetic polymorphisms. A previous investigation indicated that slow or intermediate NAT2 acetylators are at increased risk of HS-induced skin disorders, compared with tolerant TCE workers.…”
Section: Polymorphisms In Tumor Necrosis Factor (Tnf)-a and N-acetyltmentioning
confidence: 99%
“…3,7 When we analyzed TCE-induced skin disorders in the published work, many patients have the latter manifestation, characterized by an onset of the reaction, clinical features and laboratory data that are quite similar to those of drug-induced hypersensitivity syndrome (DIHS), 8,9 also referred to as drug rash with eosinophilia and systemic symptoms (DRESS). 10 In fact, Dai et al 11 recently observed that only three of 111 TCErelated generalized skin reaction patients had SJS ⁄ TEN, and the remainder had HS; the authors categorized the other patients as 75 with exfoliative dermatitis and 33 with erythema multiforme, but these are included in HS, as described below. Thus, this review of TCE-induced skin disorders discusses primarily the hypersensitivity syndrome type, and reviews similarities between TCE-induced HS and DIHS.…”
Section: Introductionmentioning
confidence: 99%
“…At present, biomarker researches about OMLDT mainly focused on three aspects: gene polymorphism [3][4][5][6][7], serum proteomics [8][9][10][11][12] and TCE metabolites [13]. Haishan Li, et al [3] identified genetic susceptible biomarkers associated with OMLDT in genes located in the human leukocyte antigen (HLA) region.…”
Section: Introductionmentioning
confidence: 99%
“…This special issue of Industrial Health, "Individual Susceptibility to Occupational Hazard", deals with the individual variability in the effects of various occupational factors including nine articles which refer to chemical [15][16][17][18] , psychosocial [19][20][21] , biological 22,23) and physical factors 24) . The articles regarding chemical factors include a systematic review by Julvez and Grandjean on neurodevelopmental toxicity 15) .…”
mentioning
confidence: 99%
“…Miura 17) presents a review on the individual susceptibility to cadmium toxicity, suggesting that if workers are exposed to industrial materials that have a inhibitory mechanism similar to that of DL-propargylglycine , an inhibitor of the cystathionine pathway (cystathionase inhibitor), free cadmium ions accumulate in the body due to the absence of metallothionein, resulting in serious renal dysfunction. In their original article, Zheng et al 18) report the genetic polymorphisms of N-acetyltransferase (NATs) are related to trichloroethylene -induced hypersensitivity dermatitis. They suggest that slow metabolic phenotype of NAT2 maybe one of risk factor for the dermatitis and combined slow acetylator phenotypes of NAT1 and NAT2 further increase such risk.…”
mentioning
confidence: 99%