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Войти в исследования Contact dermatitis · 2025
Genetic Insights Into Allergic Contact Dermatitis: Reassessing the Role of LCE3C_LCE3B Deletion.
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Ben Lamine Zeineb, Moussa Amen, Bouhoula Marwa, Gerisha Razene, Sabbagh Sarra, Kacem Imen, Aloui Asma, Chatti Souheil, Brahem Aicha, Zemni Ramzi, Ben Hadj Slama Foued
Аннотация
BACKGROUND: Allergic contact dermatitis (ACD) is a multifactorial inflammatory skin disorder. Polysensitisation, defined as hypersensitivity to ≥ 3 unrelated allergens, reflects a more severe clinical form. The LCE3C_LCE3B deletion, implicated in skin barrier dysfunction, has a yet unclear role in the susceptibility to ACD and polysensitisation.
OBJECTIVE: This study aims to evaluate the association between LCE3C_LCE3B deletion and susceptibility to ACD and polysensitisation in the Tunisian population.
METHODS: A case-control study included 94 confirmed ACD patients and 125 age- and sex-matched controls without immune-related diseases. Patch testing followed the European Baseline Series. LCE3C_LCE3B genotyping was performed using conventional three-primer PCR after DNA extraction by the salting-out method.
RESULTS: Polysensitisation was observed in 33% of ACD cases. Genotyping of the LCE3C_LCE3B deletion did not reveal statistically significant differences in allelic or genotypic frequencies between ACD cases and controls. Furthermore, no statistically significant association was found between the LCE3C_LCE3B del and polysensitisation. Similarly, no significant associations were observed between the LCE3C_LCE3B deletion and sensitisation to metals, including nickel, cobalt and chromium.
CONCLUSION: No significant association was found between the LCE3C_LCE3B deletion and either ACD or polysensitisation. Larger studies are needed to clarify the genetic contribution to these conditions.
OBJECTIVE: This study aims to evaluate the association between LCE3C_LCE3B deletion and susceptibility to ACD and polysensitisation in the Tunisian population.
METHODS: A case-control study included 94 confirmed ACD patients and 125 age- and sex-matched controls without immune-related diseases. Patch testing followed the European Baseline Series. LCE3C_LCE3B genotyping was performed using conventional three-primer PCR after DNA extraction by the salting-out method.
RESULTS: Polysensitisation was observed in 33% of ACD cases. Genotyping of the LCE3C_LCE3B deletion did not reveal statistically significant differences in allelic or genotypic frequencies between ACD cases and controls. Furthermore, no statistically significant association was found between the LCE3C_LCE3B del and polysensitisation. Similarly, no significant associations were observed between the LCE3C_LCE3B deletion and sensitisation to metals, including nickel, cobalt and chromium.
CONCLUSION: No significant association was found between the LCE3C_LCE3B deletion and either ACD or polysensitisation. Larger studies are needed to clarify the genetic contribution to these conditions.