Clinical and Histopathological Features of Itch in Patients with Alopecia Areata

Yamakoshi, Takako; Andoh, Tsugunobu; Makino, Teruhiko; Kuraishi, Yasushi; Shimizu, Tadamichi

doi:10.2340/00015555-1613

Cited by 5 publications

(2 citation statements)

References 13 publications

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“…The causal genes were analyzed by GO enrichment and were mainly clustered in phosphatidylethanolamine biosynthetic process, endothelial cell morphogenesis, lipoxygenase pathway, ventricular trabecula myocardium morphogenesis, pericardium development, engulfment of apoptotic cell, and acetylgalactosaminyltransferase activity. The above ndings suggest the involvement of lipoxygenases, bioactive peptides, endothelial cell development, and apoptosis in the pathogenesis of AA, which is consistent with previous studies [23][24][25][26]. KEGG pathway analysis revealed that the four causal genes were signi cantly enriched in the pathways of linoleic acid, ferroptosis, arachidonic acid metabolism, and adhesion junction, suggesting that these signaling pathways may play important roles in AA.…”

Section: Discussionsupporting

confidence: 90%

Identifying causal genes in alopecia areata using integrative analysis of differential expression and Mendelian randomization

Zhao,

He,

Zhang

et al. 2024

Preprint

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Background Compared with sporadic patients with Alopecia areata (AA), the familial cases have a poorer prognosis. At present, the genetic basis of AA still needs further study to improve treatment and prognosis. The aim of this study is to identify the causal genes related to AA. Methods We first used bioinformatics analysis to screen the differentially expressed genes (DEGs) related to AA, and then analyzed large-scale eQTL data and AA GWAS summary data using Mendelian randomization (MR). The enrichment analysis of causal gene functions and pathways as well as immune cell infiltration analysis were also performed, and finally the screened causal genes were analyzed and validated in the experimental group of AA and the normal control group. Results Differential expressed gene (DEG) analysis identified 429 up-regulated and 423 down-regulated genes. Among DEGs, MR screened out four intersecting genes, GIMAP6 and AA (IVW OR: 1.868; 95% CI: 1.175–2.970, p = 0.008), ALOX15 and AA (IVW OR: 1.616; 95% CI: 1.167–2.239, p = 0.004), GALNT6 and AA (IVW OR: 0.710; 95% CI: 0.533–0.945, p = 0.019), HEG1 and AA (IVW OR: 0.648; 95% CI: 0.431–0.975, p = 0.037). Indicating that all four intersecting genes have a causal relationship with AA, they are the four causal genes most related to AA. Among them, genes GIMAP6 and ALOX15 are risk factors for AA, while genes GALNT6 and HEG1 are protective factors for AA. Finally, validation analysis was conducted on the four causal genes between the AA experimental group and the normal control group, and significant differences were found in the GALNT6 and HEG1 genes in the validation group. Conclusion In this study, we identified four causal genes for AA and found that genes GIMAP6 and ALOX15 are risk factors for AA and genes GALNT6 and HEG1 are protective factors for AA. Our data analysis showed significant differences between the GALNT6 and HEG1 genes in the validation group. This study will provide new research directions for the pathogenesis and clinical diagnosis and treatment of AA.

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Section: Discussionsupporting

confidence: 90%

Identifying causal genes in alopecia areata using integrative analysis of differential expression and Mendelian randomization

Zhao,

He,

Zhang

et al. 2024

Preprint

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show abstract

“…Although striking, intense pruritus prior to onset of hair loss is occasionally seen in AA and may be associated with the marked inflammation. 5 Biopsy demonstrated a combination of typical AA/AU findings in conjunction with unusual/uncommon features ( Figs 2 and 3 , Table I ). In particular, the density and mixed nature of the infiltrate, perifollicular fibrosis, follicular destruction, and intrafollicular neutrophils are unusual/uncommon in AA/AU.…”

Section: Discussionmentioning

confidence: 96%

Alopecia universalis with unusual histopathologic features after vaccination with ChAdOx1 nCoV-19 (AZD1222)

Ho¹,

McNish²,

McDonald³

et al. 2022

JAAD Case Reports

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Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing

Suárez‐Fariñas¹,

Ungar²,

Noda³

et al. 2015

Journal of Allergy and Clinical Immunology

192

225

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Clinical and Histopathological Features of Itch in Patients with Alopecia Areata

Cited by 5 publications

References 13 publications

Identifying causal genes in alopecia areata using integrative analysis of differential expression and Mendelian randomization

Identifying causal genes in alopecia areata using integrative analysis of differential expression and Mendelian randomization

Alopecia universalis with unusual histopathologic features after vaccination with ChAdOx1 nCoV-19 (AZD1222)

Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing

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