Smoking Cessation and Risk of Hidradenitis Suppurativa Development.

Abstract

Importance: Although tobacco smoking is established as a risk factor for hidradenitis suppurativa (HS), studies on the effects of smoking cessation on HS are limited, and evidence is lacking.

Objective: To examine the association between changes in smoking status and the development of HS.

Design, setting, and participants: This population-based cohort study enrolled participants from the Korean National Health Insurance Service database who had undergone 2 consecutive biennial health examinations (2004-2005 and 2006-2007) as the primary cohort. Within the primary cohort, the secondary cohort comprised individuals who underwent all biennial health examinations throughout the follow-up period and maintained the same smoking status from 2006 to 2007 to the end of the follow-up period. Data were analyzed from July to December 2023.

Exposures: Changes in smoking habit status.

Main outcomes and measures: Risk of HS development. The HS risk according to change in smoking status between the 2 consecutive health examinations was estimated using a Cox proportional hazards model.

Results: Of the 6 230 189 participants enrolled, the mean (SD) age was 47.2 (13.5) years, and 55.6% were male. During 84 457 025 person-years of follow-up, 3761 HS events occurred. In the primary cohort, compared to those who consistently reported active smoking at both checkups (ie, sustained smokers), lower HS risk was seen among those who were confirmed to smoke initially but quit by the second checkup (ie, smoking quitters) (adjusted hazard ratio [AHR], 0.68; 95% CI, 0.56-0.83), those who maintained cessation status throughout (AHR, 0.67; 95% CI, 0.57-0.77), and those who reported never smoking at either checkup (ie, never smokers) (AHR, 0.57; 95% CI, 0.52-0.63). Those who initially quit smoking but resumed by the second checkup and those who had no previous smoking history but started at the second checkup (ie, new smokers) exhibited similar HS risk as sustained smokers. The secondary cohort results aligned with those of the primary cohort, showing a more pronounced risk reduction with smoking cessation (AHR, 0.57; 95% CI, 0.39-0.83). Considering time-smoking interaction, the cumulative incidence and the risk of HS in smoking quitters were similar to those in sustained smokers in the early stages of observation. However, 3 to 4 years after smoking cessation, the rate decelerated, resembling that of never smokers, and there was a statistically significant decrease in the risk that persisted (between 3 and 6 years from the index date: AHR, 0.58; 95% CI, 0.36-0.92; and ≥12 years from the index date: AHR, 0.70; 95% CI, 0.50-0.97). New smokers initially paralleled never smokers but accelerated after 2 to 3 years, reaching sustained smokers' levels.

Conclusions and relevance: In this cohort study, quitting smoking and sustaining a smoke-free status were associated with a reduced risk of HS development compared to continuous smoking. In contrast, resuming or initiating smoking may have as detrimental an effect on HS development as continual smoking.