Acetylator phenotype in Iraqi patients with allergic contact dermatitis

Najim, Rafid A.; Al-waizt, Makram; Al-Razzuqi, Rafi Abdul Majeed

doi:10.5144/0256-4947.2005.473

Cited by 14 publications

(9 citation statements)

References 6 publications

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“…Hence, it would be misleading to attribute the increased risk exclusively either to the NAT1 or the NAT2 locus. Alternatively, both alleles may be linked to an unknown susceptibility factor. These findings, namely an increased risk of contact allergy for the ‘rapid’ NAT2 polymorphism, were corroborated in studies from Turkey (66) and Iraq (65), although the results of the latter study are compromised by a small sample size and an unconventional, non‐standardized patch test technique. Finally, a recently published study on NAT1 and NAT2 genotypes in 147 PPD‐sensitized individuals and 200 controls with no known history of sensitization to PPD or allergic contact dermatitis did not confirm the theory of an increased risk conferred by the rapid acetylator status (67). There was no significant difference between cases and controls with regard to rapid or slow acetylator genotypes of both NAT1 and NAT2 .…”

Section: Polymorphisms In Contact Allergymentioning

confidence: 55%

“…These findings, namely an increased risk of contact allergy for the ‘rapid’ NAT2 polymorphism, were corroborated in studies from Turkey (66) and Iraq (65), although the results of the latter study are compromised by a small sample size and an unconventional, non‐standardized patch test technique.…”

Section: Polymorphisms In Contact Allergymentioning

confidence: 74%

“…Following the scheme of immunological steps in contact allergy (Table 4), our group (58–62) and others (63–75) set about studying a number of potentially relevant polymorphisms in contact allergic patients. A polymorphism is a genetic variation located in specific DNA sequences found in >1% of the population.…”

Section: Polymorphisms In Contact Allergymentioning

confidence: 99%

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Genetic factors in contact allergy-review and future goals

et al. 2010

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The genetics of contact allergy are still only partly understood, despite decades of research; this might be a consequence of inadequately defined phenotypes used in the past. A recommendation is to study an extreme phenotype, namely, polysensitization (sensitization to three or more unrelated allergens). Another approach to unravel the genetics of contact allergy is the study of candidate genes. In this review, we summarize studies on the associations between genetic variation (e.g. single-nucleotide polymorphisms) in certain candidate genes and contact allergy. Polymorphisms and mutations affecting the following proteins were studied: (i) filaggrin; (ii) N-acetyltransferase (NAT) 1 and 2; (iii) glutathione-S-transferase (GST) M and T; (iv) manganese superoxide dismutase; (v) angiotensin-converting enzyme (ACE); (vi) tumour necrosis factor (TNF); and (vii) interleukin-16 (IL-16). The polymorphisms of NAT1, NAT2, GSTM, GSTT, ACE, TNF and IL-16 were shown to be associated with an increased risk of contact allergy. In one of our studies, the increased risk conferred by the TNF and IL-16 polymorphisms was confined to polysensitized individuals. Other relevant candidate genes may be identified by studying diseases related to contact allergy in terms of clinical symptoms, a more general pathology (inflammation), and possibly an overlapping genetic background, such as irritant contact dermatitis.

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Section: Polymorphisms In Contact Allergymentioning

confidence: 55%

Section: Polymorphisms In Contact Allergymentioning

confidence: 74%

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Genetic factors in contact allergy-review and future goals

et al. 2010

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“…The slow acetylator phenotype associated with NAT2*5b/2*6a was significantly less common in the disease group. Smaller studies on the effects of SNPs in NAT2 supported the notion that a rapid acetylator phenotype may increase the risk of CS to PPD . Even though N‐acetylation is generally regarded as a detoxifying reaction, it may also result in transformation of para‐substituted aryl compounds or their intermediates into stronger haptens, which may explain the reported increased risk of sensitization in ‘rapid’ acetylators.…”

Section: Genetic Markersmentioning

confidence: 97%

Current knowledge on biomarkers for contact sensitization and allergic contact dermatitis

et al. 2017

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Abstract:Contact sensitization is common and affects up to 20% of the general population. The clinical manifestation of contact sensitization is allergic contact dermatitis. This is a clinical expression which is sometimes difficult to distinguish from other types of dermatitis, e.g. irritant and atopic dermatitis. Several studies have examined the pathogenesis and severity of allergic contact dermatitis by measuring the absence or presence of various biomarkers.In this review article, we provide a non-systematic overview of biomarkers which have been studied in allergic contact dermatitis. These include genetic variations and mutations, inflammatory mediators, alarmins, proteases, immunoproteomics, lipids, natural moisturizing factors, tight junctions, and antimicrobial peptides. We conclude that despite the enormous amount of data, convincing specific biomarkers for allergic contact dermatitis are yet to be described.

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“…These include a compromised skin barrier through mutations in fi laggrin (de Jongh et al 2008, Novak et al 2008, Thyssen et al 2008, and altered metabolism of the enzymes N -acetyltransferase 1 and 2 ( NAT1 and NAT2 ). These enzymes have an important role in the detoxifi cation and bioactivation of chemicals through N -acetylation and N-O -acetylation (Najim et al 2005, Schnuch et al 1998, Nacak et al 2006). Furthermore, the cellular defense against electrophiles is reduced in individuals with polymorphisms in AREs, Nrf2 , and Keap1 (Wang et al 2007, Li et al 2005) and glutathione S-transferase mu 1 and glutathione S-transferase theta 1 (Westphal et al 2000).…”

Section: Toward a Mechanistically Based Integrated Testing Strategymentioning

confidence: 98%

Anchoring molecular mechanisms to the adverse outcome pathway for skin sensitization: Analysis of existing data

Veen

Soeteman‐Hernández

Ezendam

et al. 2014

Critical Reviews in Toxicology

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Allergic contact dermatitis (ACD) is a hypersensitivity immune response induced by small protein-reactive chemicals. Currently, the murine local lymph node assay (LLNA) provides hazard identification and quantitative estimation of sensitizing potency. Given the complexity of ACD, a single alternative method cannot replace the LLNA, but it is necessary to combine methods through an integrated testing strategy (ITS). In the development of an ITS, information regarding mechanisms and molecular processes involved in skin sensitization is crucial. The recently published adverse outcome pathway (AOP) for skin sensitization captures mechanistic knowledge into key events that lead to ACD. To understand the molecular processes in ACD, a systematic review of murine in vivo studies was performed and an ACD molecular map was constructed. In addition, comparing the molecular map to the limited human in vivo toxicogenomic data available suggests that certain processes are similarly triggered in mice and humans, but additional human data will be needed to confirm these findings and identify differences. To gain insight in the molecular mechanisms represented by various human in vitro systems, the map was compared to in vitro toxicogenomic data. This analysis allows for comparison of emerging in vitro methods on a molecular basis, in addition to mathematical predictive value. Finally, a survey of the current in silico, in chemico, and in vitro methods was used to indicate which AOP key event is modeled by each method. By anchoring emerging classification methods to the AOP and the ACD molecular map, complementing methods can be identified, which provides a cornerstone for the development of a testing strategy that accurately reflects the key events in skin sensitization.

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Acetylator phenotype in Iraqi patients with allergic contact dermatitis

Cited by 14 publications

References 6 publications

Genetic factors in contact allergy-review and future goals

Genetic factors in contact allergy-review and future goals

Current knowledge on biomarkers for contact sensitization and allergic contact dermatitis

Anchoring molecular mechanisms to the adverse outcome pathway for skin sensitization: Analysis of existing data

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