@article{10.11648/j.ijcd.20250802.15,
  author = {Valentina Broshtilova and Nencho Smilov and Yoanna Velevska-Vatova and Irina Yungareva and Alexander Trenovski and Sonya Marina},
  title = {Wells Syndrome (Eosinophilic Cellulitis): Current Clinical, Histopathological, and Therapeutic Aspects},
  journal = {International Journal of Clinical Dermatology},
  volume = {8},
  number = {2},
  pages = {69-75},
  doi = {10.11648/j.ijcd.20250802.15},
  url = {https://doi.org/10.11648/j.ijcd.20250802.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcd.20250802.15},
  abstract = {Wells syndrome, also known as eosinophilic cellulitis, is a rare, relapsing inflammatory dermatosis characterized by erythematous and edematous plaques, accompanied by a distinctive histopathological feature known as flame figures. Since its initial description by G. Wells in 1971, fewer than one hundred well-documented cases have been reported in both children and adults. This review summarizes the clinical, histopathological, and therapeutic aspects of Wells syndrome, with particular emphasis on diagnostic challenges and emerging treatment options. A systematic analysis of classical and contemporary literature, including case series and clinical observations, was conducted. The discussion encompasses the clinical presentation, histological characteristics, presumed etiopathogenesis, and therapeutic outcomes. Clinically, the disease manifests as acute-onset erythematous, urticarial, or annular plaques that often resemble infectious cellulitis but fail to respond to antibiotic therapy. Histopathological examination typically reveals a dense eosinophilic infiltrate with flame figures and granulomatous elements. Although the disease course is generally benign, it is prone to recurrence. Systemic corticosteroids remain the mainstay of treatment; however, recurrent or refractory cases may require agents such as dapsone, cyclosporine, or methotrexate. Recent advances include the use of biologic therapies targeting the IL-5 and IL-4/IL-13 pathways—such as omalizumab, mepolizumab and dupilumab—as well as JAK inhibitors, which have shown promising results in improving disease control and reducing relapse frequency. Further research is needed to establish standardized treatment protocols and optimize long-term management strategies.},
 year = {2025}
}

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TY  - JOUR
T1  - Wells Syndrome (Eosinophilic Cellulitis): Current Clinical, Histopathological, and Therapeutic Aspects
AU  - Valentina Broshtilova
AU  - Nencho Smilov
AU  - Yoanna Velevska-Vatova
AU  - Irina Yungareva
AU  - Alexander Trenovski
AU  - Sonya Marina
Y1  - 2025/12/09
PY  - 2025
N1  - https://doi.org/10.11648/j.ijcd.20250802.15
DO  - 10.11648/j.ijcd.20250802.15
T2  - International Journal of Clinical Dermatology
JF  - International Journal of Clinical Dermatology
JO  - International Journal of Clinical Dermatology
SP  - 69
EP  - 75
PB  - Science Publishing Group
SN  - 2995-1305
UR  - https://doi.org/10.11648/j.ijcd.20250802.15
AB  - Wells syndrome, also known as eosinophilic cellulitis, is a rare, relapsing inflammatory dermatosis characterized by erythematous and edematous plaques, accompanied by a distinctive histopathological feature known as flame figures. Since its initial description by G. Wells in 1971, fewer than one hundred well-documented cases have been reported in both children and adults. This review summarizes the clinical, histopathological, and therapeutic aspects of Wells syndrome, with particular emphasis on diagnostic challenges and emerging treatment options. A systematic analysis of classical and contemporary literature, including case series and clinical observations, was conducted. The discussion encompasses the clinical presentation, histological characteristics, presumed etiopathogenesis, and therapeutic outcomes. Clinically, the disease manifests as acute-onset erythematous, urticarial, or annular plaques that often resemble infectious cellulitis but fail to respond to antibiotic therapy. Histopathological examination typically reveals a dense eosinophilic infiltrate with flame figures and granulomatous elements. Although the disease course is generally benign, it is prone to recurrence. Systemic corticosteroids remain the mainstay of treatment; however, recurrent or refractory cases may require agents such as dapsone, cyclosporine, or methotrexate. Recent advances include the use of biologic therapies targeting the IL-5 and IL-4/IL-13 pathways—such as omalizumab, mepolizumab and dupilumab—as well as JAK inhibitors, which have shown promising results in improving disease control and reducing relapse frequency. Further research is needed to establish standardized treatment protocols and optimize long-term management strategies.
VL  - 8
IS  - 2
ER  - 

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