Incidence of hidradenitis suppurativa among tobacco smokers: a population-based retrospective analysis in the U.S.A.

Abstract

Incidence of HS appears to be doubled among tobacco smokers. These findings may support evidence-based counselling efforts for the cessation of smoking in populations at risk for HS.

North American clinical management guidelines for hidradenitis suppurativa: A publication from the United States and Canadian Hidradenitis Suppurativa Foundations

“…Approximately 70% to 75% of patients with HS smoke and 10% to 15% are past smokers. 153,158,184,185 Some data suggest an association between smoking status and HS severity, duration, and failure of treatment response 158,184,186 ; however, other studies have not found an association with HS activity 187 or quality of life. 184 In 2 cases, women with HS stopped smoking and had complete remission.…”

T helper 17 cell/regulatory T-cell imbalance in hidradenitis suppurativa/acne inversa: the link to hair follicle dissection, obesity, smoking and autoimmune comorbidities

“…83,84 The incidence of HS is doubled among tobacco smokers. 85 Recent evidence underlines that smoking adversely affects the Th17/Treg balance. Smoking has been associated with increased expression of Th17 cells, IL-17 expression and impaired numbers or function of Tregs.…”

A systematic review and critical evaluation of immunohistochemical associations in hidradenitis suppurativa

“…These results may be influenced by heterogeneous sampling methods, laboratory processing methods and data analysis 15 . An additional complicating factor is that clinical comorbidities which are strongly associated with disease activity in HS, such as obesity 16 , diabetes 17 , inflammatory bowel disease 18 , and smoking 19 also impact inflammatory cell activity in the skin 18,[20][21][22] . Hence it remains unclear whether the presence or absence of these conditions may confound the findings of immunohistochemical studies in HS 15,23 and whether clinical stratification of patients is required to identify distinct pathogenic pathways, which may be amenable to pharmacological intervention.…”