Acne and hidradenitis suppurativa

Abstract

Acne and hidradenitis suppurativa (HS) both centre on hair follicles. They often occur together as part of the acne tetrad, but are found in distinct localizations. Acne is primarily defined by the presence of comedones and inflammatory lesions. However, in HS the intertriginous localization and chronicity play equally important roles for the diagnosis to the inflammatory lesions. Genetics, bacteria, environmental factors and innate inflammation have all been found to play a role in acne and/or HS. Surprisingly, there is little overlap between the findings so far. The genetics of acne and HS are distinct, bacteria have not been shown convincingly to play a role in HS, and the important risk factors obesity and smoking in HS cannot be easily translated to acne. The one driving factor central to both diseases is innate inflammation, most strikingly involving interleukin-1. Hence the interleukin-1 family, as already shown in autoinflammatory conditions associated with acne, could represent attractive treatment targets.

Risk of keratinocyte carcinoma among patients with hidradenitis suppurativa

“…DOI: 10.1111/bjd.19259 Dear Editor, Lichen planopilaris (LPP) is a difficult-to-treat condition leading to permanent hair loss and scarring. 1 Pathobiologically, LPP shows T-cell-mediated interferon-c-driven loss of keratin 15-positive hair follicle (HF) epithelial stem cells (eHFSCs) due to immune privilege (IP) collapse and pathological epithelial-to-mesenchymal transition (EMT). 1,2 This exhausts the eHFSC pool, impacting the HF's capacity to regenerate and cycle, ultimately resulting in HF destruction, fibrosis and scarring.…”

“…1 Pathobiologically, LPP shows T-cell-mediated interferon-c-driven loss of keratin 15-positive hair follicle (HF) epithelial stem cells (eHFSCs) due to immune privilege (IP) collapse and pathological epithelial-to-mesenchymal transition (EMT). 1,2 This exhausts the eHFSC pool, impacting the HF's capacity to regenerate and cycle, ultimately resulting in HF destruction, fibrosis and scarring. 1 Defective or insufficient peroxisome proliferator-activated receptor (PPAR)-c signalling in eHFSCs has been implicated in LPP pathogenesis, 3 which can be partly rescued by PPAR-c agonists.…”

“…We performed a case-control study comparing the incidence of BCC and SCC between patients with HS and people with acne vulgaris, which is also an inflammatory disorder of the pilosebaceous unit. 1 Using an age-, sex-, and race-matched 1 : 2 case-control study design, patients with at least one International Classification of Disease, 9th or 10th Revision (ICD-9/10) code for HS or acne vulgaris were identified in our institutional database of seven hospitals (Partners HealthCare, 2000-2019). HS and acne diagnosis codes were validated by reviewing electronic medical records of a random 10% sample of each group for descriptions of characteristic lesions arising within relevant anatomical sites, supplemented with pathology reports, when available.…”

Autoinflammation behind the curtain

“…However, medicine changes slowly and it can take many years for new findings to be integrated into clinical thinking. The four scholarly reviews in this issue of the BJD address this slow pivot that is currently taking place in dermatology …”

“…The four scholarly reviews in this issue of the BJD address this slow pivot that is currently taking place in dermatology. [1][2][3][4] Two decades ago, a whole new class of inflammatory diseases was identified 5 that had been previously classified incorrectly as autoimmune conditions. These diseases produce sterile inflammation without concomitant detectable autoimmune-primed B or T cells.…”