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<p>Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease, and certain genetic and environmental factors play an important role in the disease process. The immune system plays a significant role in the progression of HS, with tumor necrosis factor (TNF)-α being one of the key cytokines. In recent years, <i>TNF</i> gene polymorphisms have been investigated due to their possible relationship with HS. In this study, we aim to compare the role of the − 376 G &gt; A, -238 G &gt; A, and − 308 G &gt; A single nucleotide polymorphisms (SNPs) in the promoter region of the <i>TNF</i> gene between patients with HS and healthy controls, and to investigate the association between these SNPs and disease susceptibility, as well as disease severity. DNA was isolated from 87 patients with HS and 89 healthy controls. Patients were subgrouped based on the Hurley staging system. Genetic variants within the promoter region of the <i>TNF</i> gene, specifically − 376G &gt; A (rs1800750), -308G &gt; A (rs1800629), and − 238G &gt; A (rs361525) SNPs, were identified via Sanger sequencing. Sequence data were analyzed using SeqScape Software v2.7 and Sequencing Analysis Software v5.1. Among the patients, 4.6% (<i>n</i> = 4) were classified as Hurley stage I, 63.2% (<i>n</i> = 55) as Hurley stage II, and 32.2% (<i>n</i> = 28) as Hurley stage III. The genotypic variants of the − 376 G &gt; A, -238 G &gt; A, and − 308 G &gt; A SNPs in the promoter region of the <i>TNF</i> gene did not differ statistically between patients with HS and controls (<i>P</i> = 0.24, <i>P</i> = 0.84, and <i>P</i> = 0.19, respectively). Additionally, no statistically significant difference was observed between the patient and control groups for the GGG/GAG/GGA/AGA haplotypes (<i>P</i> = 0.23). When comparing HS severity and the presence of SNPs in the <i>TNF</i> gene, no significant association was found between these genotypic variants and HS severity (<i>P</i> = 0.59, <i>P</i> = 0.71, and <i>P</i> = 0.22, respectively). In conclusion, the <i>TNF</i> − 376 (rs1800750 G &gt; A), -308 (rs1800629 G &gt; A), and − 238 (rs361525 G &gt; A) variants were found not to be associated with susceptibility to or severity of HS.</p>

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Tumour necrosis factor gene polymorphisms in patients with hidradenitis suppurativa: a case-control study

  • 期刊论文

  • 发表日期：

    2026年7月11日

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  • Beril Yel,
  • Hatice Gundogan,
  • Ceren Damla Durmaz,
  • Erdem Karabulut,
  • Neslihan Akdogan

摘要

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease, and certain genetic and environmental factors play an important role in the disease process. The immune system plays a significant role in the progression of HS, with tumor necrosis factor (TNF)-α being one of the key cytokines. In recent years, TNF gene polymorphisms have been investigated due to their possible relationship with HS. In this study, we aim to compare the role of the − 376 G > A, -238 G > A, and − 308 G > A single nucleotide polymorphisms (SNPs) in the promoter region of the TNF gene between patients with HS and healthy controls, and to investigate the association between these SNPs and disease susceptibility, as well as disease severity. DNA was isolated from 87 patients with HS and 89 healthy controls. Patients were subgrouped based on the Hurley staging system. Genetic variants within the promoter region of the TNF gene, specifically − 376G > A (rs1800750), -308G > A (rs1800629), and − 238G > A (rs361525) SNPs, were identified via Sanger sequencing. Sequence data were analyzed using SeqScape Software v2.7 and Sequencing Analysis Software v5.1. Among the patients, 4.6% (n = 4) were classified as Hurley stage I, 63.2% (n = 55) as Hurley stage II, and 32.2% (n = 28) as Hurley stage III. The genotypic variants of the − 376 G > A, -238 G > A, and − 308 G > A SNPs in the promoter region of the TNF gene did not differ statistically between patients with HS and controls (P = 0.24, P = 0.84, and P = 0.19, respectively). Additionally, no statistically significant difference was observed between the patient and control groups for the GGG/GAG/GGA/AGA haplotypes (P = 0.23). When comparing HS severity and the presence of SNPs in the TNF gene, no significant association was found between these genotypic variants and HS severity (P = 0.59, P = 0.71, and P = 0.22, respectively). In conclusion, the TNF − 376 (rs1800750 G > A), -308 (rs1800629 G > A), and − 238 (rs361525 G > A) variants were found not to be associated with susceptibility to or severity of HS.