Scholarlink

<p>Hidradenitis suppurativa (HS) is a painful inflammatory disorder of follicular biology. Androgens are believed to play a role in HS pathogenesis; however, the mechanism remains unclear. The high frequency of polycystic ovary disease (PCOS) in HS suggests the influence of testosterone as a driver of disease. In order to assess the impact of PCOS on HS severity, we conducted a retrospective chart review of 55 female patients with HS-PCOS and 57 female HS-controls. Demographic information and disease severity (as measured by HS-physician global assessment, numerical rating scale-pain score, erythrocyte sedimentation rate, c-reactive protein, interleukin-6, testosterone levels, hemoglobin A1C, and treatment protocols) were recorded. Testosterone levels in the HS-PCOS cohort were statistically higher than controls (<i>p</i> &lt; 0.05). Binomial logistic regressions showed no statistical differences in age, sex, race, HS severity, and inflammatory markers when comparing the HS-PCOS cohort with HS-controls. Additionally, there were no significant differences in the range and frequency of HS therapies in these groups. Study limitations include small sample size and cross-sectional design. We report that patients with HS-PCOS have neither increased HS disease severity nor require more aggressive treatments than HS-controls.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Polycystic ovary syndrome diagnosis does not predict increased hidradenitis suppurativa severity

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月3日

查看全文
  • Sarah Romanelli,
  • Zahidul Islam,
  • McCall E. Torpey,
  • Aarthi Parvathaneni,
  • Khyla T. Hill,
  • Hansen Tai,
  • Peter Y. Ch’en,
  • Avigdor Nosrati,
  • Michelle Toker,
  • H. Dean Hosgood,
  • Kristina L. Campton,
  • Steven R. Cohen

摘要

Hidradenitis suppurativa (HS) is a painful inflammatory disorder of follicular biology. Androgens are believed to play a role in HS pathogenesis; however, the mechanism remains unclear. The high frequency of polycystic ovary disease (PCOS) in HS suggests the influence of testosterone as a driver of disease. In order to assess the impact of PCOS on HS severity, we conducted a retrospective chart review of 55 female patients with HS-PCOS and 57 female HS-controls. Demographic information and disease severity (as measured by HS-physician global assessment, numerical rating scale-pain score, erythrocyte sedimentation rate, c-reactive protein, interleukin-6, testosterone levels, hemoglobin A1C, and treatment protocols) were recorded. Testosterone levels in the HS-PCOS cohort were statistically higher than controls (p < 0.05). Binomial logistic regressions showed no statistical differences in age, sex, race, HS severity, and inflammatory markers when comparing the HS-PCOS cohort with HS-controls. Additionally, there were no significant differences in the range and frequency of HS therapies in these groups. Study limitations include small sample size and cross-sectional design. We report that patients with HS-PCOS have neither increased HS disease severity nor require more aggressive treatments than HS-controls.