Hidradenitis suppurativa types

One of the most established ways to describe hidradenitis suppurativa focuses on two broad phenotypes: follicular and inflammatory. These terms describe how the disease behaves rather than acting as strict diagnostic labels.

• Follicular subtype: This form often appears earlier in life and mainly involves nodules. People with this presentation may also have acne or other follicular disorders. Abscesses tend to occur less frequently, and the disease course may progress more slowly.
• Inflammatory subtype: This presentation usually follows a more aggressive course. Patients experience recurrent, painful abscesses that may join up and form sinus tracts. Ongoing inflammation often leads to scarring, persistent discharge, and a higher level of physical discomfort and psychological distress.

Clinicians use these phenotypes to better understand disease behaviour and to guide decisions around the monitoring and the treatment of hidradenitis suppurativa. 

Another approach classifies hidradenitis suppurativa according to where lesions develop and how they cluster across the body. A commonly cited framework describes four main clinical patterns:

• Axillary–mammary–inguinal subtype: Lesions mainly affect the armpits, under the breasts, and the groin. This pattern is more frequently seen in women, and hormonal factors may influence symptom severity and flare-ups.
• Follicular subtype: In this anatomical classification, HS appears alongside other follicular conditions and tends to involve widespread nodules.
• Gluteal subtype: This form primarily affects the buttocks and perianal region. The location can complicate management due to friction, moisture, and challenges with local care.
• Syndromic subtype: In a smaller group of patients, HS occurs as part of a broader autoinflammatory syndrome, such as PASH or PAPASH. These patients may also develop conditions like pyoderma gangrenosum or inflammatory arthritis, and often benefit from coordinated, multidisciplinary care.

These patterns help clinicians recognize less typical forms of HS and adapt treatment strategies to specific anatomical challenges. 

More recent studies have applied statistical and cluster analysis techniques to large patient groups to identify distinct HS subtypes. This research has described up to six clinical subgroups defined by shared comorbidities, inflammatory markers, and patient-reported outcomes. Examples include subtypes associated with diabetes, Crohn’s disease, asthma, psychiatric conditions, familial disease patterns, or a predominance in female patients.

Each subgroup shows differences in systemic inflammation, metabolic features, quality of life impact and response to treatment. These findings reinforce the idea that HS is not a single disease entity but a collection of related conditions with overlapping mechanisms. As research into genetic and molecular drivers continues, these classifications may support more personalized and targeted treatment approaches in the future.