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Hidradenitis suppurativa (HS) Learning Zone
Declaration of sponsorship Novartis Pharma AG

HS Overview

Declaration of sponsorship Novartis Pharma AG
Read time: 100 mins
Last updated:16th Sep 2021
Published:16th Sep 2021

Hidradenitis suppurativa (HS) is a physically painful and psychologically distressing systemic disease. Explore:

  • The symptoms and immense burden in our interview with Dr Joslyn Kirby
  • Pathophysiological mechanisms in our infographics of early and advanced disease
  • Diagnostic techniques and the need for earlier diagnosis

HS epidemiology

Estimates of the prevalence of hidradenitis suppurativa (HS) vary widely and are determined by the method of data collection1. Currently, assessments of three main types of studies are used to produce estimates of prevalence and give important insights into the populations impacted by this disease; self-reporting, registry-based, and group examination studies1.

What is the global prevalence of hidradenitis suppurativa?

In recent years a range of studies have estimated the global prevalence of hidradenitis suppurativa as being between 0.00033–4.1% and more recent studies in the United States and Europe have potentially narrowed this range to 0.7–1.2%2–15.

However, in a systematic review and meta-analysis (N = 118,760,093) of hidradenitis suppurativa cases, differences in prevalence were found when stratifying by geographic region (Figure 1)16. The highest prevalence was seen in Europe 0.8% (0.5–1.3%), followed by the USA 0.2% (0.1–0.4%), Asia-Pacific 0.2% (0.01–2.2%), and South America 0.2% (0.01–0.9%)16.

T1 HS_Fig1.png

Figure 1. Forest plot of pooled hidradenitis suppurativa prevalence, stratified by geographic region (Adapted16).

One of the studies included in the systematic review and meta-analysis was a population-based observational and case–control study of hospital episode statistics from the UK Clinical Practice Research Datalink (CPRD)9.

In this study, it was also found that around 30% of hidradenitis suppurativa patients were previously unrecognised and 18,417 cases had a history of 1–4 flexural skin boils, potentially giving rise to a higher prevalence of 1.19%9.

Hidradenitis suppurativa is often underdiagnosed and has a worldwide mean diagnostic delay of approximately seven years17

The results from these studies broadly align with data collected across various western European countries that have utilised self-reporting through validated questionnaires15. However, selection and classification bias may impact the reliability of prevalence estimates as they are dependent on data from secondary and tertiary-level health care institutions18.

Does hidradenitis suppurativa prevalence differ by demographic?

In paediatric patients and adults, hidradenitis suppurativa appears to exhibit similar clinical features and endocrine comorbidities19,20. However, hidradenitis suppurativa is most highly prevalent between the third and fourth decades of life2,3,8,21–23. Moreover, hidradenitis suppurativa appears to be very rare in women before menarche, although paediatric cases have been described24.

In the study by Ingram et al., it was also noted that the peak hidradenitis suppurativa prevalence of 15.1 per 1,000 occurred in the fifth decade of life (Figure 2). It was also shown that the mean female to male ratio was 2.9 to 1 across the age groups9.

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HS symptoms


Explore how HS develops from early to late stages as well as the importance of engaging patients and finding the right treatment for every patient.

Hidradenitis suppurativa (HS), also known as acne inversa, is a chronic, inflammatory disorder of the skin that is defined by the nature and localisation of the skin alterations18. An understanding of the symptoms can both aid diagnosis and promote recognition of the immense burden of this disease.

What are the symptoms of hidradenitis suppurativa?

Patients with hidradenitis suppurativa develop painful and inflamed nodules, abscesses and pus-discharging tunnels (known as sinus tracts and fistulas) between skin folds of the armpits, groin, gluteal, and perianal areas of the body34.

The most impactful symptom reported by almost all hidradenitis suppurativa patients is chronic pain, which ranges from mild to moderate intensity35. Usually resulting from the inflammatory nodules or abscesses associated with the disease, pain is reported by 97% of patients during their disease course35.

Studies have shown that compared to other dermatological conditions, the pain associated with hidradenitis suppurativa may be of a higher intensity36–38

This pain has been described by patients as hot, burning, pressing, stretching, cutting, sharp, taut, splitting, gnawing, sore, throbbing or aching35,36.

Due to the severe pain and purulent secretions that restrict movement and produce an unpleasant smell, the physical manifestation of hidradenitis suppurativa profoundly impacts the lives of patients39.

T1 HS_Fig3.png

Figure 3. Common skin on skin locations in which hidradenitis suppurativa can develop (Adapted40).

Pruritus is also a frequently mentioned symptom39, which has been shown in two previous studies to have a prevalence of 41.2–67.6%35,41. Although no specific correlation was found between pruritus intensity and disease severity, the intensity of the pruritus was associated with a negative impact on quality of life35,41.

How do the symptoms of hidradenitis suppurativa progress?

When hidradenitis suppurativa begins to develop, it usually progresses through the following stages:

  • Area of skin feels uncomfortable
  • Tender, deep nodule(s) appear
  • Nodule(s) grow and start to join together
  • Large, painful, abscesses break open
  • Blackhead-like spots
  • Abscesses heal slowly (if at all) and return; scars form

Comparatively little is known about the long-term evolution of hidradenitis suppurativa. Some studies using self-reported real-world data have shown that approximately one third of patients achieve remission, while one third remain unchanged or worsen. One third also achieve amelioration, possibly due to improved coping over time42.

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HS burden of disease


Join Dr Joslyn Kirby to find out about the impact of hidradenitis suppurativa on patients and the large psychological burden they face.

Hidradenitis suppurativa has a substantially negative impact on quality of life that can persist for years due to an immense physical and psychological burden, including painful lesions, stigmatisation, and an increased risk of suicide39,46,47.

How does hidradenitis suppurativa impact quality of life?

According to studies of quality of life impairment, patients with hidradenitis suppurativa have greatly reduced physical and mental health (Figure 4)37,48.

T1 HS_Fig4.png

Figure 4. Impact of hidradenitis suppurativa on patient quality of life as measured by the Short Form 36 items survey, with scores representing the percentage of the total possible score achieved (Adapted39).

Using Short Form 36 items survey (SF-36) general health questionnaire scores, these studies have found that the domains with notably lower scores were role physical, bodily pain, general health, perception, social functioning, and role emotional compared to the general population37,48.

Patients have reported negative impacts on their sex life49 as well as their professional lives, which can negatively affect their economic situation50,51

In more severe disease (Hurley stage III), physical functioning, vitality, and mental health were also found to be significantly deteriorated48.

Collectively, these burdens can have an immense negative impact on the quality of life of the patient. Notably, a psychological burden is especially prevalent in hidradenitis suppurativa patients due to this impact on quality of life52.

What is the psychological burden of hidradenitis suppurativa?

Patients with dermatoses are generally considered to be at a higher risk of psychiatric disorders compared to the overall population52,53. However, patients with hidradenitis suppurativa are thought to be particularly at risk, due to the impact on quality of life caused by their symptoms and associated comorbidities52.

A Finnish nationwide registry study (N = 4,381) aimed to clarify the association between hidradenitis suppurativa and its psychiatric comorbidities. In the study, hidradenitis suppurativa patients were compared to patients with psoriasis, due to their elevated risk of psychological comorbidities, and melanocytic nevi52.

It was found that the total prevalence of psychotic disorders was 4.7% in the hidradenitis suppurativa group compared with 3.3% in the psoriasis group (OR 1.46, 95% CI 1.24–1.72) and 1.7% in the melanocytic nevi group (OR 2.74, 95% CI 2.29–3.28)52.

Notably, gender differences were observed (Figure 5) with mental disorders being more frequently observed in female (OR 1.28; 95% CI 1.15–1.41) than male (OR 1.46, 95% CI 1.28–1.66) patients with hidradenitis suppurativa (25.5% and 22.0%, respectively).

T1 HS_Fig5.png

Figure 5. Gender differences in the odds ratios for psychiatric disorders in hidradenitis suppurativa patients (Adapted52). CI, confidence interval.

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HS pathophysiology


Gain an overview of these complex pathophysiological mechanisms in our expert interview with Dr Joslyn Kirby.

The current understanding of the pathophysiology of hidradenitis suppurativa is limited18. The underlying pathological mechanisms of hidradenitis suppurativa (HS) appear to be complex and multifaceted, simultaneously involving neutrophilic dermatosis, a strong anti-inflammatory component, and the potential involvement of B cells, TH1 cells, and TH17 cells18.

How does hidradenitis suppurativa develop?

Beginning at the hair follicle, the earliest histologically detectable events in hidradenitis suppurativa include18:

  • Perivascular and perifollicular immune cell infiltration
  • Hyperkeratosis
  • Hyperplasia of the infundibular epithelium (infundibular acanthosis)

These alterations of the infundibular epithelium induce follicular occlusion, or ‘plugging’, followed by a stasis of follicular content, anaerobic bacterial proliferation, and hair follicle dilatation (Figure 1)18.

Specific causes of the HS pathogenetic process have yet to be determined. However, various trigger factors have been implicated including lifestyle factors, genetic predisposition, intertriginous skin type, and specific microbiota18

As follicular cells become damaged, bacterial components and danger-associated molecular patterns (DAMPs) are released, which may further stimulate inflammatory responses. It has been suggested that local macrophages may become activated, leading to the secretion of pro-inflammatory cytokines, such as interleukin (IL)-1β and tumour necrosis factor (TNF)(Figure 6)18.

T1 HS_Fig6.png

Figure 6. Initial events involved in the pathogenesis of hidradenitis suppurativa (Adapted18). AP-1, activator protein 1; CCL, chemokine (C-C motif) ligand; CXCL, chemokine (C-X-C motif) ligand; IL, interleukin; NF-κB, nuclear factor-κB; NLRP3, NACHT, LRR and PYD domain-containing protein 3; TH, T helper; TLR, toll-like receptor; TNF, tumour necrosis factor.

Bacterial sensing may also be strengthened through the increased expression of Toll-like receptor 2 (TLR2) by local macrophages or dendritic cells18.

Once secreted, IL-1β and TNF act on various cell types with partially overlapping effects (Figure 6). IL-1β induces the production of chemokines, with the most prominent chemokines attracting neutrophilic granulocytes. TNF activates endothelial cells, causing a stronger expression of adhesion molecules, and also stimulates an assortment of chemokines that attract neutrophils, T cell subsets, and monocytes into the skin18.

The importance of TNF involvement in the initial pathogenic events of HS is highlighted by patient responses to anti-TNF therapy18

The induction of chemokines and endothelial cell activation leads to an intense infiltration of immune cells into the developing lesions followed by the development of monocytes into macrophages and dendritic cells18.

While their precise role in the pathogenesis of hidradenitis suppurativa has yet to be elucidated, various other cells are also seen to be prevalent in hidradenitis suppurativa lesions, including18:

  • Mast cells
  • Natural killer cells
  • B cells
  • Plasma cells

Notably, hidradenitis suppurativa differs from other immune-mediated skin disorders, such as psoriasis, due to the strong expression of the anti-inflammatory mediator IL-1018.

In patients with hidradenitis suppurativa who also smoke tobacco, nicotine can increase intracellular cAMP levels, possibly enhancing cutaneous IL-10 production18

Following induction by pro-inflammatory cytokines, such as TNF, IL-10 in macrophages can inhibit immune responses by suppressing monocyte and macrophage pro-inflammatory cytokine production. This leads, both directly and indirectly, to a reduced T cell activation18.

When does hidradenitis suppurativa progress?

The sequential progression of hidradenitis suppurativa is still poorly understood. However, the events seen in advanced disease can be distinguished from the initial pathogenic events (Figure 2)18.

As hidradenitis suppurativa progresses, a diverse range of immune cells permeate the skin and secrete specific cytokines18

In the skin of hidradenitis suppurativa patients, T cells produce high levels of interferon-γ (IFNγ) and IL-17, similar to the levels seen in psoriasis patients. In a previous study, CD4+ T cell enrichment was shown to secrete IFNγ and IL-17 in ex vivo experiments, implying that T helper (TH) cells can produce these mediators18.

IL-12 and IL-23 are also present within the skin of hidradenitis suppurativa patients. These cytokines support the function of TH1 and TH17 cells and can be produced by dendritic cells or macrophages18.

IFNγ activates macrophages and tissue cells, which may be essential for local T cell activation18

In the hidradenitis suppurativa lesions, the infiltration of immune cells from blood vessels is triggered by the activation of dermal endothelial cells by IFNγ. A positive feedback loop then forms, with IFNγ inducing the secretion chemokines, such as CXCL10, that attract TH1 cells (Figure 7)18.

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HS diagnosis


Join Dr Joslyn Kirby to discover the factors that can influence the risk of developing HS, including genetics and lifestyle.

Appropriate early dentification and treatment of hidradenitis suppurativa is essential for minimising the risk of disease progression and the development of associated comorbidities.

However, as emerging hidradenitis suppurativa lesions appear similar to other disorders, such as abscesses or boils, the disease is often underdiagnosed and has led to a worldwide mean diagnostic delay of approximately seven years17.

How do you diagnose hidradenitis suppurativa?

Hidradenitis suppurativa diagnosis is based on the nature and location of skin lesions as well as the disease course, which can be defined as persistent (lesions present for at least 6 months) or recurrent (>2 skin lesions occurring or recurring within 6 months)34,60.

Large international studies have shown that there is an average delay of 7–10 years between the onset of disease and the diagnosis17,43

Typical hidradenitis suppurativa skins lesions are characterised by purulence, malodorous discharge, pain, and discomfort during daily life activities34.

The location and type of these lesions are used to support the diagnosis of hidradenitis suppurativa. Patients may present with one or multiple types of lesions simultaneously, which typically include60:

  • Inflammatory nodules
  • Abscesses
  • Inflamed and draining sinus tracts or fistulas
  • Rope-like scarring
  • Open comedones
  • Bridged scars
  • Post-inflammatory double-ended pseudocomedones (resembling a ‘tombstone’)

Lesions generally appear in intertriginous areas or other areas such as the nape of the neck, the trunk, extremities, or the retroauricular area. However, the location of these lesions in specific areas of the body is influenced by biological sex (Table 1)7,61,62.

Table 1. Differences in hidradenitis suppurativa lesion prevalence between men and women (Adapted7,61,62).

Lesions with higher prevalence in men  Lesions with higher prevalence in women 
• Armpits 
• Perineal or perianal regions 
• Buttocks 
• Gluteal cleft
• Groin, specifically upper inner thigh 
• Submammary regions 
• Inframammary regions 

A family history can also be used to support the diagnosis of hidradenitis suppurativa accompanied by various additional clinical signs, including recurrent atypical lesions in intertriginous areas, such as folliculitis and open comedones; the presence or history of a pilonidal sinus; and typical lesions in atypical locations, such as the inner thigh or the waist61,63.

What diagnostics can be used for hidradenitis suppurativa?

In cases of hidradenitis suppurativa that are uncertain, biopsies can be used to reject other potential disorders, such as pyoderma gangrenosum, squamous cell carcinoma or lymphomas18. However, skin biopsies are not usually required for the diagnosis of hidradenitis suppurativa18.

The type of alteration determines the histopathological characteristics of hidradenitis suppurativa. These can range from early cysts, nodules or abscesses to inflamed sinus tracts or rope-like scars64. In ruptured cysts, pan-keratin immunostaining as well as haematoxylin and eosin staining can also be used to visualise the keratin fragments and debris that become dispersed in the dermis65.

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References

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