http://orcid.org/0000-0001-5994-1997
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ABSTRACT
Background: Alopecia areata (AA) is a non-scarring hair loss with a polymorphous presentation ranging from patchy lesions to involvement of the entire scalp. The disease is the consequence of an autoimmune attack on hair bulbs that results in a premature transition of hair follicles to catagen and telogen. Thus the Wnt/β-catenin signaling pathway that regulates the hair cycling might be involved in the pathogenesis of AA. Genetic variations in the components of Wnt/β-catenin could greatly alter their adaptive mechanisms against an immunologic attack.
Objectives: Our aim was to investigate the association between AA and genetic polymorphisms in the TCF7L2 gene, one of the most important components of the Wnt/β-catenin pathway.
Methods: This is a case-control study of 145 patients with AA and 152 healthy controls. Genotyping of the TCF7L2 gene (rs7903146) was performed via the ARMS—PCR method (amplification refractory mutation system- polymerase chain reaction). The allele and genotype distribution was compared between the two groups.
Results: The frequency of the T allele (0.38 vs. 0.28, odds ratio = 1.56, 95% CI = 1.09–2.17, p = 0.013) and TT + CT genotypes (0.68 vs. 0.53, odds ratio = 1.88, 95% CI = 1.17–3.02, p = 0.008) were significantly higher in AA patients.
Conclusions: This study indicates that the TCF7L2 gene variant is associated with AA. Its contribution to disease pathogenesis could either be through a hair cycling defect or dendritic cell dysregulation.
Acknowledgments
We wish to present our special thanks to Dr. Azin Ayatollahi for her contributions that greatly assisted the research.
Disclosure of interest
The authors have no conflict of interest to declare.