Scholarlink

Background <p>Pretibial myxoedema (PTM), a rare extrathyroidal manifestation of Graves’ disease (GD), is characterized by dermal glycosaminoglycans (GAGs) deposition. Current therapies (e.g., glucocorticoids) show limited efficacy with high relapse rates. Emerging evidence implicates JAK-STAT pathway activation via thyrotropin receptor antibodies (TRAb) in the pathogenesis of PTM, suggesting JAK inhibitors, such as Tofacitinib, as potential therapy.</p> Case Presentation <p>A 39-year-old man with GD and Graves’ orbitopathy (GO) presented with bilateral pretibial non-pitting edema and itchy erythematous nodules. Histopathology from skin biopsy confirmed GAGs deposition and elevated TRAb (&gt; 40 IU/L). After transient response to intralesional glucocorticoids, oral tofacitinib (5&#xa0;mg twice daily) was initiated. Significant resolution of edema (body surface area: 12%→3%) and GO occurred within 1 month, sustained over 6 months without adverse events.</p> Conclusion <p>Tofacitinib demonstrated rapid and durable efficacy in refractory PTM, likely by suppressing JAK-STAT-mediated fibroblast activation and pro-inflammatory cytokine release. This supports its role as a potential targeted oral therapy for PTM.</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

Effective treatment of pretibial myxoedema with tofacitinib: a case report and analysis of immunopathogenesis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月21日

查看全文
  • Chen-xi Zhao,
  • Ming-dan Zhao,
  • Xin Li

摘要

Background

Pretibial myxoedema (PTM), a rare extrathyroidal manifestation of Graves’ disease (GD), is characterized by dermal glycosaminoglycans (GAGs) deposition. Current therapies (e.g., glucocorticoids) show limited efficacy with high relapse rates. Emerging evidence implicates JAK-STAT pathway activation via thyrotropin receptor antibodies (TRAb) in the pathogenesis of PTM, suggesting JAK inhibitors, such as Tofacitinib, as potential therapy.

Case Presentation

A 39-year-old man with GD and Graves’ orbitopathy (GO) presented with bilateral pretibial non-pitting edema and itchy erythematous nodules. Histopathology from skin biopsy confirmed GAGs deposition and elevated TRAb (> 40 IU/L). After transient response to intralesional glucocorticoids, oral tofacitinib (5 mg twice daily) was initiated. Significant resolution of edema (body surface area: 12%→3%) and GO occurred within 1 month, sustained over 6 months without adverse events.

Conclusion

Tofacitinib demonstrated rapid and durable efficacy in refractory PTM, likely by suppressing JAK-STAT-mediated fibroblast activation and pro-inflammatory cytokine release. This supports its role as a potential targeted oral therapy for PTM.