When Perianal Disease Isn't Just HS
Recapping her RAPIDS lectures in Fort Lauderdale, Dr. Jennifer Hsiao walked the hosts through the overlap between hidradenitis suppurativa (HS) and cutaneous Crohn's disease. Her 'don't miss' point: when a patient presents with perianal tunnels and drainage, don't stop at HS — ask whether underlying Crohn's could be driving the picture. The two can coexist, so a good full skin exam still matters even when IBD is on the table.
Hsiao pointed to a practical screening approach: an IBD screening question focused on abdominal pain that wakes patients at night and constant or bloody diarrhea, paired with a fecal calprotectin (a neutrophil-derived protein whose presence in stool suggests intestinal inflammation). Together, the question and the test help clinicians decide whether to refer to GI or proceed as HS.
On the skin side, she flagged knife-cut fissures in the groin folds — deeper, very straight-lined fissures or ulcers rather than the superficial dermal tunnels of HS — as a clue to screen for IBD. A true fistula in the perianal area that connects to the rectum or pierces the anal sphincter is 'not HS,' she said, and warrants investigation; a pelvic MRI without contrast can characterize how deep the tunnel goes and help distinguish the two.
Nutritional Deficiencies That Show Up on the Skin
IBD patients — and anyone on a restrictive diet — can present with vitamin deficiencies that manifest cutaneously, Hsiao explained. Zinc deficiency, a real risk in IBD, can produce psoriasiform plaques around the mouth and in acral areas. Vitamin C deficiency can show up as corkscrew hairs and perifollicular hemorrhage, and she noted several others including B vitamins and vitamin D.
Her takeaway for the clinic: when a rash follows a telltale pattern — photodistributed, acral, or oral findings like angular cheilitis or glossitis — keep nutritional deficiency on the differential rather than defaulting to 'just psoriasis.'
One Mindset Shift for IBD Patients
Asked for a single change in approach, Hsiao was direct: anyone with IBD should be screened for HS. If an IBD patient comes in for a skin check, ask about lesions in the axillae and groin — or check those areas — because dermatology providers may be the first to detect HS and meaningfully improve quality of life with therapy.
She also encouraged building relationships with local GI colleagues who are open to collaborating. For patients who have both HS and IBD, a single biologic may be chosen to cover both conditions — for example infliximab infusions, which can be easier to obtain for IBD than for HS — making the interdisciplinary relationship genuinely synergistic.
Diagnosing HS and the Case for Treating Earlier
Hsiao level-set the three diagnostic criteria for HS: typical lesions (abscesses, nodules, tunnels, scarring), in typical intertriginous locations (axillae, inframammary, groin, buttock — while noting some patients present outside these areas), and chronicity/recurrence. That last piece is key: a single armpit abscess with a history of prior lesions is HS until proven otherwise, and reframing it as chronic inflammatory disease rather than a one-time MRSA furuncle changes the whole treatment plan.
On pathophysiology, she described a shift in thinking. HS has long been framed as a follicular occlusion disease — follicle occludes, ruptures, dermal inflammation ensues, and repeated cycles create tunnels. But newer thinking asks whether perifollicular inflammation comes first and is 'smoldering' until a trigger sets it off. If inflammation is the inciting event, targeting it earlier may mitigate disease progression.
That reasoning fed into her message on biologics: they are not medications to save for the worst cases. Biologics are approved for moderate-to-severe HS, and validated international severity scores classify a patient with one abscess and two inflammatory nodules as moderate. Providers don't need to wait for ten lesions and multiple draining tunnels. She added a nuance — context matters. Three lesions on a patient's 'worst day in two years' is different from three lesions on their best day in a while.
New Therapies and a Practical Flare Toolkit
HS now has three FDA-approved biologics: adalimumab (TNF inhibitor), secukinumab (IL-17A inhibitor), and bimekizumab (IL-17A and F inhibitor). Hsiao highlighted the buzz around JAK inhibition as the next mechanism of action — povorcitinib, a JAK1-selective inhibitor, met its phase 3 endpoints and could potentially be approved as early as next year, while upadacitinib is in active phase 3 trials. A new mechanism delivered orally makes this an exciting stretch for a disease where three therapies are 'not enough.'
For flares, Hsiao emphasized sending patients home from day one with a clear plan: what to do at home and when to call. Her toolkit includes a 'pill in pocket' antibiotic (doxycycline, augmentin, or clindamycin — something that worked before), topicals (topical clindamycin, resorcinol, with topical ruxolitinib in phase 3 trials), and in-office intralesional Kenalog. A tip: she'll go above 10 mg/cc — up to 40 mg/cc — for very inflamed lesions or tunnels, injecting to the base of the lesion. Some drainage from tunnel ends is unavoidable and shouldn't be discouraging. She also uses punch incision and drainage over an 11-blade, since the punch lets the lesion keep draining rather than closing and recurring. Prednisone isn't her preference, but a short 10–14 day course can bridge some patients until long-term therapy kicks in.
For refractory cases, Hsiao described stacking therapies while counseling carefully given limited derm data and infection risk. Her go-to combinations include a TNF inhibitor with an IL-17 inhibitor (the two FDA-approved classes) and an IL-17 inhibitor with a JAK inhibitor — the latter pairing an injectable with an oral and, in her view, carrying less infection concern than combining a JAK with a TNF. One combination she avoids: anti–IL-1 plus anti-TNF, citing rheumatoid arthritis data showing increased risk of serious infection.