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Meta-Analysis
. 2024 Feb 23;103(8):e37300.
doi: 10.1097/MD.0000000000037300.

Interleukin gene polymorphisms and alopecia areata: A systematic review and meta-analysis

Zasia Hossain Tishe  1 , Sanjana Shawkat  1 , Meherun Nessa Popy  1 , Ashfaq Ahmed  1 , Sadia Biswas Mumu  1 , Mohd Nazmul Hasan Apu  2 , Md Shaki Mostaid  1
Affiliations
Meta-Analysis

Interleukin gene polymorphisms and alopecia areata: A systematic review and meta-analysis

Zasia Hossain Tishe et al. Medicine (Baltimore). .

Abstract

Background: Alopecia areata (AA) is an autoimmune disease which results in non-scarring hair loss on the scalp or any surface with hair. Several genetic polymorphisms of the interleukin genes have been linked with this disease but the results are inconsistent. This systematic review and meta-analysis were done to find the association between rs3118470, rs2275913, rs3212227, and rs10889677 of the IL2RA, IL17A, IL12B, and IL23R genes, respectively, of the interleukin family with alopecia areata.

Methods: A comprehensive search for relevant research articles was conducted in Pubmed, Google Scholar, and Embase databases. Our search yielded 8 relevant articles with 1940 cases and 1788 controls. The odds ratio with 95% confidence intervals was calculated using fixed effect and random effect models. Heterogeneity was determined using the Q-test and I2 test. Publication bias was determined and funnel plots were used to adjust the odds ratio.

Results: We found a significant risk effect for rs3118470 of the IL2RA gene with alopecia areata in the dominant model (CC + CT vs TT; OR = 1.54, 95% confidence interval = 1.05-2.26, P < .05, I2 = 69.03%) and homozygous model (CC vs TT; OR = 2.00, 95% confidence interval = 1.07-3.71, P < .05, I2 = 72.84%). For the other single nucleotide polymorphisms, we could not find any statistically significant association with the disease.

Conclusion: Our analysis showed that mutation of rs3118470 of IL2RA gene possesses a significant risk effect for alopecia areata. Future studies with larger sample sizes and ethnic backgrounds are warranted to confirm our findings.

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Conflict of interest statement

The authors have no funding and conflicts of interest to disclose.

Figures

Figure 1.
Figure 1.
Flowchart showing the selection of included studies. The initial search results were 999 articles (PubMed = 19; Google Scholar = 966; Embase = 14). After a thorough screening, data from 8 articles were collected.
Figure 2.
Figure 2.
Forest plots of rs3118470 (IL2RA) with AA risk in 5 genetic models. A: Allelic Model (A vs G); B: Dominant Model (AA + AG vs GG); C: Recessive Model (AA vs AG + GG); D: Heterozygous Model (AG vs GG); E: Homozygous Model (AA vs GG).
Figure 3.
Figure 3.
Forest plots of rs2275913 (IL17A) with AA risk in 5 genetic models. A: Allelic Model (A vs G); B: Dominant Model (AA + AG vs GG); C: Recessive Model (AA vs AG + GG); D: Heterozygous Model (AG vs GG); E: Homozygous Model (AA vs GG).
Figure 4.
Figure 4.
Forest plots rs3212227 (IL12B) of with AA risk in 5 genetic models. A: Allelic model (C vs A); B: Dominant model (CC + CA vs AA); C: Recessive model (CC vs CA + AA); D: Heterozygous model (CA vs AA) and E: Homozygous model (CC vs AA).
Figure 5.
Figure 5.
Forest plots of rs10889677 (IL23R) with AA risk in 5 genetic models. A: Allelic model (A vs C); B: Dominant model (AA + AC vs CC); C: Recessive model (AA vs AC + CC); D: Heterozygous model (AC vs CC) and E: Homozygous model (AA vs CC).
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