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  • Presentation

Neutrophilic Dermatoses in IBD Patients: Diagnosis and Management

Description

The talk reviewed neutrophilic dermatoses seen in patients with inflammatory bowel disease, emphasizing that these are sterile, immune-driven skin inflammations that may track with intestinal disease activity or follow a separate course, requiring close dermatology-GI co-management. It focused on pyoderma gangrenosum and Sweet syndrome, the two most common entities in IBD. For pyoderma gangrenosum, the speaker highlighted risk factors such as Crohn’s disease, colonic disease, female sex, and prior IBD surgery, and described key diagnostic clues including painful ulcers with violaceous overhanging borders, peripheral pustules, bridging epithelium, and characteristic cribriform or wrinkled-paper scarring. Diagnosis relies on clinical features, exclusion of infection, biopsy showing neutrophilic inflammation, and tools such as the Delphi consensus criteria. Treatment was framed in three parts: rapidly stopping acute inflammation with systemic steroids, cyclosporine, or infliximab; maintaining control of the underlying IBD with therapies such as TNF-alpha inhibitors, IL-12/23 or IL-23 inhibitors, and sometimes JAK inhibitors; and allowing time for wound healing. Integrin inhibitors were noted as ineffective for PG, and IL-17 inhibitors should be used cautiously in IBD. Sweet syndrome was described as an abrupt, painful eruption of red edematous papules, plaques, or nodules, often on the head, neck, or upper extremities, with fever and systemic illness; it frequently correlates with active IBD and is diagnosed by major and minor criteria including neutrophilic dermal infiltrate without vasculitis, fever, lab abnormalities, and steroid response. Management again centers on systemic steroids for rapid control and TNF inhibitors or azathioprine in selected cases, while recognizing that azathioprine or anti-TNF drugs can paradoxically induce Sweet syndrome. The speaker briefly also mentioned amicrobial pustulosis of the folds and bowel-associated dermatosis-arthritis syndrome, both sterile inflammatory conditions in IBD that may require steroids, dapsone or colchicine, antibiotics when relevant, and optimization of IBD therapy.

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Conclusions

  • Neutrophilic dermatoses in IBD are best understood as sterile, dysregulated inflammatory skin diseases that may either parallel bowel activity or follow an independent course requiring separate dermatologic treatment.
  • Pyoderma gangrenosum is strongly associated with IBD, especially in women with Crohn’s disease, colonic or perianal involvement, and prior surgery, and it should prompt clinicians to consider occult IBD in younger patients.
  • PG is diagnosed mainly by clinical pattern recognition and exclusion of infection, with key clues including a violaceous overhanging border, pustules at the edge, epithelial stranding, cribriform scarring, wrinkled-paper scarring, and pathergy after biopsy or trauma.
  • Successful PG management requires three steps: rapidly suppress acute inflammation, optimize IBD-directed maintenance therapy, and then allow gradual wound healing with supportive care.
  • For acute PG, fast-acting immunosuppression such as systemic corticosteroids, cyclosporine, or infliximab is most effective, and early improvement in pain, drainage, redness, and edema is expected within about a week.
  • For longer-term PG control in IBD patients, TNF-alpha inhibitors are the preferred shared therapy, while IL-12/23, IL-23, and JAK inhibitors may also be useful in selected cases.
  • Integrin inhibitors are not effective for PG, and IL-17 inhibitors should be used cautiously in patients with IBD.
  • Sweet syndrome is less common than PG in IBD but often tracks with active intestinal disease, especially in women with colonic disease and other extraintestinal manifestations.
  • Sweet syndrome is suggested by abrupt onset of painful red plaques or nodules, often on the head, neck, or upper extremities, and by systemic illness such as fever and malaise.
  • Sweet syndrome diagnosis is supported by neutrophilic dermal infiltrate without vasculitis plus compatible minor criteria, including fever, lab abnormalities, a trigger, and rapid steroid response.
  • Sweet syndrome usually responds quickly to systemic corticosteroids, often within 24 to 72 hours, and failure to respond should prompt reconsideration of the diagnosis.
  • Maintenance treatment for Sweet syndrome should be aligned with IBD therapy, with TNF-alpha inhibitors again emerging as a key overlap option.
  • Clinicians should recognize paradoxical medication-induced Sweet syndrome, particularly with anti-TNF agents and azathioprine, because stopping the offending drug may be sufficient and rechallenge can cause recurrence.
  • Amicrobial pustulosis of the folds and bowel-associated dermatosis-arthritis syndrome are additional IBD-associated neutrophilic eruptions that are sterile, inflammatory, and managed with systemic anti-inflammatory therapy plus optimization of bowel disease control.
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