Hidradenitis suppurativa: 7-year diagnostic gap, early treatment

By Olivia Hart

Patients with hidradenitis suppurativa (HS) wait an average of roughly 7 years for diagnosis, according to a 2015 global study by Saunte and colleagues in the British Journal of Dermatology. The delay has a clinical consequence: medical therapy rarely reverses tunnels and scars once they form, leaving surgery as the main option.

In a Derm On Air episode, host Cynthia Trickett, MPAS, PA-C, of North Dallas Dermatology Associates, spoke with Leigh Ann Pansch, MSN, FNP-BC, DCNP, a dermatology nurse practitioner in Cincinnati, Ohio, about HS immunology and the timing of systemic treatment.

Why does HS biology make timing matter?

Recognition of HS as a systemic inflammatory disease is reshaping treatment timing. The discussion supports intervention before tunnels and scarring become permanent, although researchers have not resolved whether follicular occlusion or systemic inflammation comes first.

Innate immune cells, including macrophages and keratinocytes, act alongside adaptive B and T cells. Memory T cells persist within established tunnels, while no single inflammatory pathway dominates every stage of disease.

Because no single pathway dominates at every stage, Pansch summarized the therapeutic goal as “broad control of inflammation rather than precise targeting of one cell type.” The strategy therefore seeks control across inflammatory layers instead of treatment aimed at one cell population.

What do the phase 3 trials show?

Adalimumab (Humira) inhibits tumor necrosis factor-α. In the phase 3, placebo-controlled PIONEER I and II trials, Kimball and colleagues reported these week 12 clinical response rates:

• PIONEER I: 41.8% with adalimumab versus 26.0% with placebo at week 12.
• PIONEER II: 58.9% with adalimumab versus 27.6% with placebo at week 12.

The PIONEER trials found serious adverse event rates with adalimumab similar to placebo. Kimball and colleagues published the results in the New England Journal of Medicine in 2016.

Secukinumab (Cosentyx), an IL-17A inhibitor, met primary endpoints in SUNSHINE and SUNRISE, two phase 3 trials in moderate-to-severe HS. The identical, multicenter, randomized, placebo-controlled, double-blind studies produced week 16 and week 52 results, which Kimball and colleagues reported in The Lancet in 2023.

Bimekizumab (Bimzelx), an inhibitor of IL-17A and IL-17F, also met phase 3 primary endpoints. BE HEARD I and II were two 48-week, randomized, double-blind, placebo-controlled, multicenter trials; Kimball and colleagues reported their results in The Lancet in 2024.

Oral candidiasis ranked among bimekizumab’s more frequent adverse events. For secukinumab and bimekizumab, the discussion cited primary-endpoint success without numerical effect estimates; the quantified comparison came from adalimumab.

Where does JAK inhibition fit?

Topical ruxolitinib (Opzelura) and oral upadacitinib (Rinvoq) remain under investigation for HS. Pansch described their immune effect: “Rather than suppressing immunity, these agents downshift an overactive immune response toward normal function.”

The discussion placed JAK inhibition on the next frontier. That mechanism supports the episode’s timing message: downshift inflammation before permanent structural changes develop.

What does earlier treatment change for patients?

For a patient newly diagnosed with HS, the practical change is that systemic therapy becomes a tissue-preserving intervention rather than a fallback after tunnels and scars appear. The window resembles psoriatic arthritis, where joint damage accrues irreversibly once inflammation goes unchecked.

Counseling also shapes uptake. The discussion said to frame HS as immune mediated rather than as a consequence of weight, smoking, diet, or hygiene; this framing may reduce stigma and support earlier acceptance of systemic therapy.

Closer follow-up gives hesitant patients time to decide. It also creates more opportunities to initiate systemic therapy before established tunnels and scars make reversal unlikely. Earlier diagnosis and treatment initiation therefore form the core of a tissue-preserving strategy.

As investigators continue studying topical ruxolitinib and oral upadacitinib, earlier diagnosis and systemic treatment offer the clearest route to preserving tissue before permanent tunnels and scars develop.