acne vulgaris

Introduction

acne is a chronic inflammatory skin disease of the sebaceous follicle.
the hormonal factor, innate immunity and the microbiome play a crucial role in the onset of acne lesions.
dysbiosis with an unbalanced presence of Cutibacterium acnes (C. acnes), characterized by a loss of C. acnes phylotype diversity and C. acnes biofilm production, is another proof for acne ¹⁾

drug-induced acneiform lesions
- Janus kinase inhibitors appear to have a 3.8x higher odds of causing acneiform lesions ²⁾
  - acneiform lesions appear quickly after initiating JAKi
  - no relationship with hyperseborrhoea or loss of diversity of Cutibacterium acnes or proliferation of phylotype 1AI, or proliferation or disappearance of S. epidermidis has been demonstrated in JAK-acne ³⁾
  - JAK1 and JAK3 proteins (but not JAK2) were reported to be overexpressed in acne lesions
- epidermal growth factor or methyl ethyl ketone inhibitors

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