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  • Presentation

Pearls and Updates in the Medical Management of Hidradenitis Suppurativa

Description

The talk reviewed hidradenitis suppurativa (HS) as a common, underdiagnosed inflammatory skin disease with major quality-of-life impact, significant racial disparities in diagnosis and care, and a complex pathogenesis involving follicular plugging, microbiome changes, immune activation, and genetic factors. The speaker emphasized that HS ranges from mild follicular/nodular disease to severe inflammatory disease with tunnels, scarring, and irreversible tissue damage, so early recognition and treatment are important. Traditional severity measures like Hurley stage can miss meaningful improvement, while trial endpoints such as HiSCR better capture response. For mild HS, useful options include spironolactone, selected oral contraceptives, oral antibiotics, and topical ruxolitinib, which is promising and may help patients avoid systemic therapy. Acute flares can be managed with intralesional steroids and antibiotics, with frequent flares prompting escalation of overall therapy. For moderate-to-severe disease, the talk reviewed biologics and other advanced therapies: adalimumab remains a standard anti-TNF option, infliximab is highly effective though off-label, and therapeutic drug monitoring plus methotrexate may help when response wanes. Newer FDA-approved IL-17 inhibitors, secukinumab and bimekizumab, offer strong efficacy with relatively favorable safety, though candidiasis and possible IBD concerns require attention. JAK inhibitors such as upadacitinib and povorcitinib are promising but need careful safety monitoring because of infection, lab abnormalities, and thrombosis risks. IL-23 inhibitors have been disappointing in HS trials, while ertapenem may serve as a rescue or bridge therapy. GLP-1 agonists may benefit patients with obesity or metabolic comorbidities, though evidence is still limited. Overall, the message was to treat HS early, set expectations that improvement is gradual and flares may still occur, and use biologics and other advanced therapies before irreversible progression occurs.

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Conclusions

  • Hidradenitis suppurativa is more common than once thought, frequently underdiagnosed, and still affected by major disparities in access to timely care.
  • HS arises from interacting follicular, microbial, immune, and genetic factors, but its exact biological drivers and progression remain incompletely understood.
  • Because HS can progress from mild follicular disease to irreversible scarring and tunnel formation, early recognition and treatment escalation are important.
  • Clinical phenotype and disease activity are more informative than Hurley stage alone for tracking treatment response and guiding management.
  • Mild HS can often be managed with topical, hormonal, and antibiotic approaches, while advanced disease usually requires systemic therapy.
  • Topical ruxolitinib appears promising for early or mild HS and may offer a useful low-risk option before systemic treatment is needed.
  • For acute flares, intralesional steroids and antibiotics can reduce symptoms and may prevent emergency department visits when used promptly.
  • Biologics should be considered early in patients with worsening, frequent flares, significant inflammatory burden, or rapid progression to avoid missing a therapeutic window.
  • Anti-TNF therapy remains effective, with adalimumab as the established first approved biologic and infliximab often highly effective in severe disease despite being off-label.
  • Dose optimization and therapeutic drug monitoring, including consideration of methotrexate to limit anti-drug antibodies, can improve durability of anti-TNF response.
  • IL-17 inhibitors, especially secukinumab and bimekizumab, are effective approved options for moderate to severe HS and may rival or exceed anti-TNF efficacy in some patients.
  • JAK inhibitors are a promising emerging class for HS, but their use requires caution because of risks such as infection, cytopenias, and thrombosis.
  • IL-23 inhibitors have not yet shown convincing benefit in HS, suggesting that IL-23-independent inflammatory pathways may be more relevant in the disease.
  • Ertapenem can be a useful short-term rescue or bridge-to-surgery therapy, but relapse after discontinuation is common.
  • GLP-1 agonists may help some HS patients, likely through weight loss and metabolic or anti-inflammatory effects, but stronger evidence is still needed.
  • The overall HS treatment landscape is expanding rapidly, with multiple novel mechanisms offering hope for better disease control in the future.
  • Management of HS should be individualized and shared with patients, balancing disease severity, phenotype, comorbidities, and patient preferences while aiming to prevent irreversible damage.
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