Smoking and Hidradenitis Suppurativa (Acne Inversa): What the Evidence Actually Shows – and Why It's Complicated

The relationship between smoking and hidradenitis suppurativa (HS) is one of the most consistently documented modifiable risk relationships in dermatologyDermatology: The medical specialty concerned with diagnosing and treating skin conditions. Acne Inversa is often managed by dermatologists, although surgery and other specialties may also be involved.DermatologyThe medical specialty concerned with diagnosing and treating skin conditions. Acne Inversa is often managed by dermatologists, although surgery and other specialties may also be involved.Read more in the glossary. Across multiple meta-analyses, current smokers have roughly a three- to four-fold higher risk of HS than non-smokers. Disease severity increases with duration of smoking. Response to first-line therapy is poorer in smokers. Recurrence after surgery is more likely in smokers. By any reasonable reading of the evidence, smoking is the best-documented modifiable patient-level factor influencing HS.

This article addresses the smoking question directly, without the two evasive manoeuvres that often surround it in patient education. The first evasion is minimising understatement – listing smoking among “lifestyle factors” without conveying the strength of the association. The second is moralising lecturing – treating cessation as a matter of willpower rather than a difficult behavioural change with its own evidence base. Neither is particularly helpful. The honest version: the evidence linking smoking and HS is strong, the mechanism is biologically plausible, the benefit of cessation is real though incomplete, and quitting is hard. All of this is true at the same time.

For educational purposes only. Smoking cessationSmoking Cessation: The single most evidence-supported lifestyle change in Acne Inversa. Benefit is real but often slow — many patients see improvement over months, not weeks.Smoking CessationThe single most evidence-supported lifestyle change in Acne Inversa. Benefit is real but often slow — many patients see improvement over months, not weeks.Read more in the glossary strategies should be developed together with your GP or a cessation specialist, who can provide appropriate medication, behavioural support, and follow-up.

Key Takeaways

• Current smoking is associated with a 3–4-fold increased HS risk in pooled meta-analyses; population-based incidence data show roughly double the HS incidence in smokers compared with non-smokers.
• Disease severity increases with pack-years smoked; response to both medical and surgical treatment is poorer in smokers.
• The mechanism likely involves both nicotine effects on follicular biology and immune function, as well as the broader inflammatory effects of combustion products.
• Cessation is associated with reduced HS development risk in newly developing disease and with improved postoperative outcomes; whether cessation produces marked improvement in established disease is supported by suggestive but limited evidence.
• Combined pharmacotherapy plus behavioural support is the most effective cessation approach. Nicotine replacement therapy, varenicline, and bupropion all have an evidence base and can be used in HS patients.
• E-cigarettes are not a clean substitute, and their long-term effects specifically on HS are unproven.

What the Evidence Actually Shows

The current data on smoking and HS, from multiple sources of varying study quality:

Meta-analyses of cross-sectional and case-control studies. Acharya and Mathur’s 2020 meta-analysis (published in the Journal of the American Academy of Dermatology) reports an odds ratio of 4.26 (95% CI 3.68–4.94) for current smoking and HS, based on a pooled analysis of multiple studies. A more recent 2024 meta-analysis (23 studies, approximately 29.5 million patients across healthcare system datasets) reports a pooled odds ratio of 3.10 (95% CI 2.60–3.69). Both findings are statistically robust and clinically meaningful.

Population-based incidence data. Garg et al.’s population-based retrospective analysis from the US identified approximately 3.9 million tobacco smokers and 8.0 million non-smokers in health records. HS incidence was 0.20% among smokers versus 0.11% among non-smokers (adjusted odds ratio 1.90, 95% CI 1.84–1.96). The lower odds ratio in this analysis compared with cross-sectional meta-analyses reflects the more conservative incidence framework, but the doubling of incidence remains clinically meaningful.

Severity correlations. Several studies have shown that pack-years smoked (a measure of cumulative smoking exposure) correlate with HS severity by Hurley stageHurley Stage: A clinical classification system for assessing the severity of Acne Inversa in three stages: Stage I (single abscesses without sinus tracts), Stage II (recurrent abscesses with isolated sinus tracts), Stage III (extensive sinus tracts and scarring across an entire region). Named after Dr. Helen Hurley.Hurley StageA clinical classification system for assessing the severity of Acne Inversa in three stages: Stage I (single abscesses without sinus tracts), Stage II (recurrent abscesses with isolated sinus tracts), Stage III (extensive sinus tracts and scarring across an entire region). Named after Dr. Helen Hurley.Read more in the glossary. The Dutch cohort analysis reported by Schrader et al. found pack-years to be an independent predictor of severity in multivariate analysis. The effect is dose-dependent: more smoking is associated with more severe disease.

Treatment response. A retrospective cohort study by Denny and Anadkat (2017) found that current smokers had a poorer response to first-line HS therapy than non-smokers. The mechanism is not fully characterised but is consistent with broader observations that smoking impairs response to immunomodulatory therapy across several inflammatory diseases.

Postoperative outcomes. Smoking is associated with poorer wound healing across surgical specialties generally, and specifically in HS surgery. Higher rates of wound dehiscence, infection, delayed healing, and recurrence have been documented. Smoking cessation in the perioperative period (typically at least 4 weeks before and 4 weeks after surgery) is associated with substantial reduction in surgical complications.

Effects of cessation. A Korean cohort study (Park et al., JAMA Dermatology, 2024) showed that participants who quit smoking and remained smoke-free had a reduced subsequent risk of developing HS compared with continuous smokers; participants who resumed or started smoking had an increased risk. This addresses the question of cessation in HS-naive populations rather than established disease, but is consistent with a causal contribution of smoking. For patients with established HS, smaller observational studies suggest that cessation may produce a moderate improvement in disease activity, but the evidence is less robust than for prevention.

The combined weight of the evidence is unusual for a dermatological condition – most lifestyle-disease associations are weaker and more contested. The smoking-HS association is one of the stronger ones in dermatology, comparable in its robustness to the association between smoking and psoriasis severity.

Why Smoking Worsens HS: Plausible Mechanisms

The mechanistic picture is not fully understood, but several pathways are well supported.

Nicotine effects on follicular biology. Nicotine affects the function of hair follicleHair Follicle: The tube-shaped pocket in the skin from which a hair grows. In Acne Inversa, the follicle becomes plugged and eventually ruptures, spilling its contents into surrounding tissue and triggering the inflammatory cascade that defines the disease.Hair FollicleThe tube-shaped pocket in the skin from which a hair grows. In Acne Inversa, the follicle becomes plugged and eventually ruptures, spilling its contents into surrounding tissue and triggering the inflammatory cascade that defines the disease.Read more in the glossary keratinocytes and may promote follicular occlusionFollicular Occlusion: The blockage of hair follicles is considered a key starting point in the development of Acne Inversa. When a follicle becomes obstructed, inflammation can spread deep into tissue, leading to nodules, abscesses, and sinus tracts.Follicular OcclusionThe blockage of hair follicles is considered a key starting point in the development of Acne Inversa. When a follicle becomes obstructed, inflammation can spread deep into tissue, leading to nodules, abscesses, and sinus tracts.Read more in the glossary – the early initiating step of HS lesion formation. Nicotine also alters the function of sebaceous and apocrine glandsApocrine Gland: A type of sweat gland concentrated in the armpits, groin, around the nipples, and the anus. Long considered the origin of Acne Inversa — hence the name 'hidradenitis' — apocrine glands sit near the follicles HS affects but are bystanders, not the trigger.Apocrine GlandA type of sweat gland concentrated in the armpits, groin, around the nipples, and the anus. Long considered the origin of Acne Inversa — hence the name 'hidradenitis' — apocrine glands sit near the follicles HS affects but are bystanders, not the trigger.Read more in the glossary. These effects are plausibly relevant to HS pathogenesis.

Effects on neutrophils and innate immunityInnate Immunity: The fast, broad, non-specific arm of the immune system: neutrophils, macrophages, complement, cytokines. The dominant problem in Acne Inversa.Innate ImmunityThe fast, broad, non-specific arm of the immune system: neutrophils, macrophages, complement, cytokines. The dominant problem in Acne Inversa.Read more in the glossary. Cigarette smoke alters neutrophil function in ways that may contribute to the abnormal inflammatory response characteristic of HS. Smoking increases neutrophil migration to sites of inflammation and alters their response to bacterial stimuli.

Effects on the IL-17 and Th17 axis. The IL-17/Th17 inflammatory pathway is central to HS pathogenesis (and is the basis for the IL-17 inhibitor biologicsBiologic: A class of medications derived from living cells that target specific components of the inflammatory process. For Acne Inversa, biologics such as adalimumab and secukinumab are used when other treatments are insufficient.BiologicA class of medications derived from living cells that target specific components of the inflammatory process. For Acne Inversa, biologics such as adalimumab and secukinumab are used when other treatments are insufficient.Read more in the glossary now approved for HS). Smoking has documented effects on Th17 cell differentiation and IL-17 production that are biologically consistent with worsening IL-17-driven diseases, including HS.

Tissue hypoxia. Smoking reduces tissue oxygenation both through carbon monoxide binding to haemoglobin and through vasoconstriction. Hypoxic skin is more susceptible to inflammation, impaired wound healing, and impaired immune defence – all relevant to HS.

Direct toxic effects of combustion products. Cigarette smoke contains thousands of compounds beyond nicotine, many of which are toxic to skin cells and promote oxidative stress. These effects may explain why smokeless tobacco use, which delivers nicotine without combustion, might be less strongly associated with HS than cigarette smoking – although data on smokeless tobacco specifically in HS are limited.

Microbiome effects. Smoking alters the cutaneous and oral microbiome in ways that may influence inflammatory skin diseases.

That several mechanisms act simultaneously is consistent with the magnitude of the observed clinical effect.

What Cessation Achieves and What It Doesn’t

An honest framing of what quitting smoking is likely to achieve.

For people who don’t yet have HS: Cessation reduces the risk of developing HS in the future, particularly compared with continued smoking. This is supported by the recent Korean cohort data. For young people with a family history of HS, smoking cessation (or never starting) is one of the more meaningful available modifiable interventions.

For people with established HS: Cessation likely produces some improvement in disease activity, but the magnitude is variable and not as dramatic as the inverse association in cross-sectional data might suggest. Some patients report substantial improvement after quitting; others see little change in established disease. The reasons for individual variation are not well characterised – possibly disease chronicity at the time of cessation, possibly genetic factors, possibly the contribution of other unaddressed risk factors.

For people with established HS preparing for surgery: Cessation in the perioperative period substantially reduces surgical complications and wound healing problems, and likely lowers recurrence rates. This effect is robust and is one of the more clearly justified arguments for cessation in HS patients with established disease.

For people on biologic therapy: Smoking is associated with poorer response to biologics across several inflammatory diseases, plausibly including HS. Cessation may improve treatment response, although specific HS data on this are limited.

The realistic framing for an HS patient considering cessation: it’s probably not a cure, but it will likely make every other intervention you try more effective and will reduce the long-term disease burden. That is a substantial benefit, even if smaller than the inverse epidemiological correlation might suggest.

Why Quitting Is Hard

The empirical reality of smoking cessation: it is one of the most difficult behavioural changes available. Average success rates for unaided cessation attempts range from 3% to 7% sustained at one year. Most people who successfully quit require multiple attempts before succeeding – six to thirty attempts are typical, not unusual.

This is not because smokers lack willpower. Nicotine is highly addictive – comparable to or more addictive than several controlled substances. The withdrawal syndrome includes irritability, anxiety, low mood, sleep disturbance, difficulty concentrating, and strong cravings, peaking in the first week and subsiding over weeks to months. The behavioural component of smoking – the rituals, the social associations, the contexts that trigger cravings – persists even after the physical withdrawal has resolved.

The conclusion: cessation is most likely to succeed when approached as a structured project with pharmacological and behavioural support, not as a test of willpower.

The strongest evidence-based cessation approaches:

Nicotine replacement therapy (NRT) – patches, gum, lozenges, inhalers, sprays. Delivers nicotine without combustion products and reduces withdrawal severity. Roughly doubles or triples success rates compared with unaided cessation. Combining a long-acting form (patch) with a short-acting form (gum or lozenge) for acute cravings is more effective than either alone. Available over the counter in most countries; in Germany, NRT products are widely available in pharmacies.

Varenicline (Champix in Europe, Chantix in the US). A partial nicotinic receptor agonist. Roughly doubles cessation success rates compared with placeboPlacebo: An inactive substance, usually identical in appearance to the real drug, used in clinical trials to control for the meaningful placebo response in Acne Inversa.PlaceboAn inactive substance, usually identical in appearance to the real drug, used in clinical trials to control for the meaningful placebo response in Acne Inversa.Read more in the glossary. Prescription-only. The side effect profile includes nausea, vivid dreams, and (rarely) mood changes that warrant clinical monitoring.

Bupropion (Zyban for the cessation indication). An atypical antidepressant with established cessation efficacy. Prescription-only. May be particularly useful in patients with comorbid depression. Contraindicated in patients with a history of seizures.

Combined pharmacotherapy and behavioural support. The Cochrane review and the broader evidence base consistently show that combining medication with structured behavioural support – counselling, group support, telephone quitlines, structured cessation programmes – achieves the highest success rates, substantially better than either component alone.

In Germany, support for smoking cessation is available through GPs, specialised cessation programmes, and (partially) through statutory health insurance. The German Cancer Research Center operates a nationwide smoking cessation telephone helpline. Pharmacies offer some cessation counselling.

E-Cigarettes and Vaping

The role of e-cigarettes in cessation and in ongoing HS management is, honestly, uncertain.

For cessation, there is some evidence supporting their use as a transitional tool away from combustible cigarettes. Several large randomised trials, including evidence supported by the UK’s NICE, suggest they may be more effective for cessation than NRT in some users. They deliver nicotine without combustion products, addressing the combustion-related harm pathway.

Specifically for HS, evidence on e-cigarettes is essentially non-existent. Several considerations apply:

• E-cigarettes still deliver nicotine, which has direct effects on follicular biology that may be relevant to HS independent of combustion.
• Some e-cigarette devices (particularly older or black-market products) produce substantial aerosol contaminants that may have their own toxicity.
• The 2019 EVALI outbreak (vaping-associated lung injury) was strongly linked to illicit cannabis vape cartridges containing vitamin E acetate; regulated nicotine vaping products from licensed manufacturers were not implicated, but the event underscores that not all vaping products are equivalent.
• Long-term safety data on chronic e-cigarette use are still accumulating.

A reasonable framing: if e-cigarettes help you successfully move away from combustible cigarettes, the net harm reduction is likely positive. Indefinite continued e-cigarette use without further reduction is less clearly beneficial for HS. Treating e-cigarettes as a temporary cessation tool rather than a permanent substitute is consistent with current public health recommendations in most European countries.

A Practical Approach to Cessation in HS

If you have HS and are considering cessation, the practical structure that tends to work:

1. Discuss it with your GP or a cessation specialist. A structured approach with appropriate medication and follow-up is substantially more effective than unsupported attempts.
2. Choose a quit date in advance. Not so soon that you can’t prepare; not so far off that you postpone it indefinitely. Two to four weeks in advance is typical.
3. Plan for the difficult phase. Identify situations and triggers that will be difficult, plan substitute actions, organise social support. The first two weeks are usually the hardest.
4. Use pharmacological support. NRT, varenicline, or bupropion, depending on your situation. Combination NRT (patch plus gum or lozenge) for those using NRT.
5. Access behavioural support. Cessation counselling, group programmes, telephone quitlines, or smartphone apps. Multiple sources of support correlate with better outcomes.
6. Expect setbacks and plan for them. Most successful quitters had multiple attempts before succeeding. A relapse is not a failure; it’s information about what to do differently next time.
7. Address other modifiable factors. Weight management, moderate alcohol consumption, stress management, and other lifestyle factors interact with cessation success. Addressing them together is often more sustainable than addressing them sequentially.
8. Consider timing relative to other treatments. If surgery is planned, cessation in the perioperative window has particularly strong evidence. When starting biologic therapy, cessation may improve response.
9. Use HS-related motivation, but don’t rely on it alone. Specific motivation regarding HS can help start a cessation attempt; sustained motivation usually comes from broader sources (family, finances, general health) over the months to years required for lasting cessation.

A Note on Moral Framing

Conversations about smoking cessation in medical settings can drift toward moralising – explicit or implicit messages that the patient is harming themselves through personal failure. This framing is unhelpful and counterproductive.

Smoking is a behaviour shaped by addiction, social context, life history, mental health, and structural factors. Patients who smoke have usually heard repeatedly that they should quit and are aware that smoking is bad for their health. What is generally missing is not awareness or motivation, but access to effective cessation support delivered in a non-judgemental framework.

If you are an HS patient who smokes, and your dermatologist’s primary engagement is to lecture you about it, that is not maximally helpful clinical practice. A more useful conversation focuses on whether you’re interested in a cessation attempt, what would help, what previous attempts looked like, and what specific support could be organised.

If you are an HS patient who has tried to quit and was not successful, that is the typical pattern rather than a personal failure. The next attempt has a reasonable chance of success with better support and an adjusted strategy.