To propose that hidradenitis suppurativa (HS) should be redefined as an autoinfectious disease rather than purely autoinflammatory, based on microbiological, immunological, metabolomic, therapeutic, and genetic evidence.
Approach:
Microbiological Evidence: The presence of viable bacteria in HS lesions was confirmed through prolonged cultures and metagenomic analyses, showing a correlation between bacterial load and disease severity.
Immunological Response: A robust immune response was observed in healthy keratinocytes exposed to anaerobic Gram-negative bacteria, suggesting a significant role of bacteria in HS pathology.
Comparative Analysis: Similar bacterial floras were identified in other inflammatory diseases, indicating a potential common mechanism involving dysbiosis and immune response.
Key Findings:
HS lesions contain live bacteria in the dermis, which is atypical for normal skin.
Bacterial flora in HS correlates with disease severity, showing increased diversity and antimicrobial resistance.
Hypergammaglobulinemia is common in HS patients and correlates with disease severity.
Interpretation:
The findings suggest that HS may involve an abnormal immune response to the patient's own skin flora, leading to autoinfection rather than solely autoinflammation.
Limitations:
Current studies have not fully characterized the bacterial flora or the immune response in HS.
Lack of investigation into antibodies against the bacterial flora in HS lesions.
Conclusion:
The evidence suggests a need for further investigation into the classification of HS, integrating microbiological and immunological perspectives.
Secukinumab becomes the only interleukin-17A inhibitor approved for pediatric patients aged 12 years and older with moderate to severe hidradenitis suppurativa.
