Department of Dermato-Allergology, National Allergy Research Centre, Copenhagen University Hospital Gentofte, Hellerup, 2900, Denmark.
Contact Dermatitis. 2014 Jul;71(1):49-53. doi: 10.1111/cod.12228. Epub 2014 Mar 27.
On skin contact, nickel accumulates in the stratum corneum, where it is probably bound to proteins and amino acids. One probable contributor is filaggrin, which binds nickel avidly. Filaggrin gene (FLG) null mutations lead to a complete lack of filaggrin production from the affected allele, and have been associated with an increased risk of nickel contact sensitization in German and Danish adults.
To investigate whether the experimental nickel elicitation threshold level differed between heterozygous FLG mutation and non-mutation carriers.
Thirteen nickel-sensitized female patients, seven heterozygous mutation carriers and six non-mutation carriers (genotyped for R501X, 2282del4, or R2447X), were patch tested and performed a repeated open application test (ROAT) with a nickel sulfate dilution series. Logistic threshold dose-response analyses were used to test for differences between the two groups.
No difference was found in the dose-response relationship between FLG mutation and non-mutation carriers.
On the basis of this small patient study, it appears that the elicitation threshold level for nickel is independent of FLG null mutation single-allele carrier status.
镍在皮肤接触时会积聚在角质层中，在那里它可能与蛋白质和氨基酸结合。一种可能的贡献物是角蛋白丝聚合蛋白，它能强烈地结合镍。角蛋白丝聚合蛋白基因（FLG）的纯合突变导致受影响等位基因完全缺乏角蛋白丝聚合蛋白的产生，并且与德国和丹麦成年人镍接触致敏的风险增加有关。
研究实验性镍激发阈值水平在杂合 FLG 突变体和非突变携带者之间是否存在差异。
对 13 名镍致敏的女性患者（7 名杂合突变携带者和 6 名非突变携带者（针对 R501X、2282del4 或 R2447X 进行基因分型）进行斑贴试验和重复开放应用试验（ROAT），使用硫酸镍稀释系列。使用逻辑阈值剂量-反应分析来检验两组之间的差异。
在 FLG 突变和非突变携带者之间的剂量-反应关系中未发现差异。
基于这项小型患者研究，镍的激发阈值似乎独立于 FLG 纯合突变单等位基因携带者状态。
