Inspiration Point

From Presentation to Clinic: Managing HS and IBD

Written by Admin | June 12, 2026

Managing chronic inflammatory diseases requires a keen diagnostic eye and a dynamic approach to treatment. At the RAPIDS 2026 conference in Fort Lauderdale, Eileen Cheever, PA-C, sat down with Dr. Jennifer Hsiao to discuss key clinical pearls, practice-changing updates, and concrete strategies for handling complex cases of Hidradenitis Suppurativa (HS) and Inflammatory Bowel Disease (IBD).

Here are the critical takeaways, diagnostic clues, and treatment toolkits from their conversation to help elevate your dermatology practice.

1. Unmasking Extraintestinal IBD: HS vs. Cutaneous Crohn’s

Perianal tunnels and drainage present a classic diagnostic crossroads: Is it HS, Cutaneous Crohn's disease, or are both coexisting?

The Diagnostic Clues

  • The "Knife-Cut" Fissure: When evaluating groin folds, examine the morphology closely. While HS often presents with superficial dermal tunnels, cutaneous Crohn’s typically reveals deep, straight-lined, "knife-cut" fissures or ulcers.
  • Anatomical Depth: A true perianal fistula that connects directly to the rectum or pierces through the anal sphincter is not HS. This indicates deep pathology that requires investigation.
  • The Quick IBD Screening Test: Ask patients two highly specific questions:
    1. Does abdominal pain wake you up at night?
    2. Do you experience constant or bloody diarrhea?

Next Steps for the Clinician

If a patient triggers these red flags, order a pelvic MRI (with and without contrast) to accurately map the tunnels' depth. Additionally, send a fecal calprotectin test—an elevated level indicates neutrophil excretion in the stool and strongly suggests active intestinal inflammation.

Don't hesitate to cross the aisle and build strong, collaborative relationships with local gastroenterologists to co-manage these patients.

2. Don’t Miss the Signs: Nutritional Deficiencies in IBD

Skin manifestations can often be the first clue to underlying systemic malabsorption or highly restrictive diets in IBD patients. Keep an eye out for these distinct cutaneous patterns:

Nutrient Deficiency Cutaneous Presentation
Zinc Psoriasiform plaques distributed around the mouth (perioral) and extremities (acral).
Vitamin C Perifollicular petechial hemorrhages and characteristic "corkscrew" hairs.
Vitamins B & D Angular cheilitis, glossitis, and photo-distributed rashes.

Mindset Shift for Providers: Anyone with a known history of IBD should be actively screened for HS, and vice versa. Always ask IBD patients if they experience painful nodules in the axillae or groin—dermatologists are uniquely positioned to catch HS early and dramatically improve patient quality of life.

3. Redefining the HS Pathophysiology Paradigm

For years, HS was strictly taught as a disease of mechanical follicular occlusion—the follicle plugs, ruptures, and cause a cascade of dermal inflammation.

However, current research points to a shift in this timeline: Are these patients immunologically primed by smoldering perifollicular inflammation before the occlusion even occurs? Viewing inflammation as the primary inciting event reinforces why early, aggressive anti-inflammatory intervention is paramount to halting disease progression and preventing irreversible scarring.

The Diagnostic Triad

To confidently diagnose HS, ensure the patient meets these three criteria:

  1. Typical Lesions: Abscesses, nodules, tunnels, and scarring.
  2. Typical Locations: Intertriginous zones (axillae, groin, inframammary folds, buttocks)—though atypical presentations can occur.
  3. Chronicity and Recurrence: A single armpit abscess might look like an MRSA furuncle, but if the patient notes a similar lesion occurred a few months prior, it is HS until proven otherwise.

4. Lowering the Threshold for Biologics

A crucial takeaway from RAPIDS 2026 is that biologics are no longer a "last resort" reserved exclusively for end-stage cases. They are highly effective core therapies that perform best when introduced early.

According to internationally validated HS severity scores, a patient with just one abscess and two inflammatory nodules qualifies as having moderate HS. If a patient presents with limited lesions but reports severe pain, diminished quality of life, and a history of failing oral antibiotics, they are a prime candidate for biologic therapy.

5. The Evolving Pipeline: What’s New and Next?

The HS therapeutic landscape is expanding rapidly. Providers now have access to three FDA-approved targeted options, with oral options on the horizon:

  • Current Approved Biologics: Adalimumab (TNF inhibitor), Secukinumab (IL-17A inhibitor), and Bimekizumab (IL-17A and F inhibitor).
  • The Next Wave (JAK Inhibitors):
    • Povorcitinib: A selective JAK-1 inhibitor delivered orally that has met its Phase 3 endpoints.
    • Upadacitinib: Already widely utilized in dermatology, currently in active Phase 3 trials for HS.

6. Building Your Ultimate HS Flare Toolkit

An effective long-term management strategy must include an actionable, day-one "flare plan" so patients know exactly how to manage acute breakouts at home.

                                 

7. Advanced Strategies: Stacking Therapies for Refractory Disease

When patients hit an "efficacy ceiling" on biologic monotherapy, combining mechanisms of action (multimodal stacking) can be considered. Because safety data is still limited in dermatological literature, selection must be highly deliberate:

  • Preferred Combination (Injectable + Oral): An IL-17 inhibitor combined with a JAK inhibitor provides excellent synergy with a manageable safety profile.
  • Secondary Combination (Dual Injectable): A TNF inhibitor combined with an IL-17 inhibitor can be effective, though patients must be monitored closely for an increased risk of infection.
  • The "Never" Combination: Avoid combining a TNF inhibitor with an IL-1 inhibitor. Rheumatoid arthritis data demonstrate a significantly elevated risk of serious, systemic infections with this pairing.

Moving Forward

By shifting our mindset toward early biologic intervention, using specific diagnostic clues to differentiate HS from cutaneous Crohn's, and equipping patients with a robust flare toolkit, we can fundamentally alter the disease trajectory for those with these challenging inflammatory conditions.

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