What is Hidradenitis Suppurativa?
Hidradenitis suppurativa (HS) is a chronic, inflammatory, recurrent, debilitating skin disease of the hair follicle that presents after puberty with painful, deep-seated nodules, abscesses, draining sinus tracts, and scarring, predominantly affecting intertriginous areas such as the axillae, inguinal regions, and anogenital areas. 1
Clinical Presentation
Diagnosis relies on three clinical findings:
- Typical HS lesions (painful inflammatory nodules, abscesses, comedones, sinus tracts, and scarring) 1
- Predilection for intertriginous body sites (most commonly axillae, inguinal, anogenital regions, but also mammary, submammary, buttocks, and pubic areas) 1, 2
- Recurrent disease pattern 1
Epidemiology and Risk Factors
- Prevalence ranges from 0.1% to 2% of the population, with European studies suggesting approximately 1% prevalence 1, 3
- Predominantly affects patients in their third and fourth decades of life, with female preponderance 1
- Higher prevalence in patients of African descent and lower socioeconomic status 1
- Strong association with smoking and obesity, which are critical modifiable risk factors 1, 4, 5
Disease Severity Classification
Hurley staging is the recommended clinical classification system:
- Hurley Stage I: Recurrent nodules and abscesses with minimal scarring 1
- Hurley Stage II: One or limited number of sinuses and/or scarring within a body region 1
- Hurley Stage III: Multiple or extensive sinuses and/or scarring 1
Additional assessment tools include inflammatory lesion counts (abscesses and inflammatory nodules), pain visual analog scale scores, and Dermatology Life Quality Index (DLQI) 1
Pathophysiology
HS pathogenesis involves:
- Follicular occlusion and rupture as the primary initiating event, triggered by infundibular hyperkeratosis 5
- Genetic susceptibility (γ-secretase/Notch pathway mutations in some familial cases) 1
- Dysregulation of innate and adaptive immune pathways, particularly type 1 and type 17 helper T cells, with elevated tumor necrosis factor-α, interleukin-1β, and interleukin-17 1, 5
- Microbiome alterations and biofilm formation, though HS is not primarily an infectious disease 1, 5
Systemic Nature and Comorbidities
HS should be viewed as a systemic inflammatory disease with significant comorbidities requiring routine screening:
- Metabolic syndrome and diabetes (check HbA1c and/or fasting glucose) 1, 6
- Depression and anxiety (significantly impairs quality of life beyond other skin diseases) 1, 6, 3
- Cardiovascular disease risk factors (increased cardiovascular mortality) 4, 7, 6
- Inflammatory bowel disease and spondyloarthritis 6, 3
- Squamous cell carcinoma in chronic HS-affected skin 1
- Smoking status (mandatory assessment as tobacco worsens outcomes) 1, 4
Impact on Quality of Life
HS significantly reduces quality of life due to:
- Severe, chronic pain from inflamed lesions 1, 3
- Purulent drainage requiring wound care 4, 3
- Restricted mobility from lesion location and scarring 3, 5
- Psychosocial consequences including social isolation and sexual dysfunction 1
- Long diagnostic delays (often years before correct diagnosis) 1, 3
Treatment Principles
Management requires combining medical and surgical approaches based on disease severity:
- Mild disease (Hurley I): Topical clindamycin 1% twice daily for 12 weeks, combined with antiseptic washes (chlorhexidine 4% or benzoyl peroxide) 4
- Moderate disease (Hurley II): Clindamycin 300 mg twice daily plus rifampicin 300-600 mg daily for 10-12 weeks (response rates 71-93%) 4, 7
- Severe disease (Hurley III): Adalimumab (160 mg at week 0,80 mg at week 2, then 40 mg weekly) with surgical consultation for definitive management 4
Adjunctive measures are essential: