Ulcerative pyoderma gangrenosum in a 78-year-old woman treated with brodalumab: A case report

Abstract

Pyoderma gangrenosum is a rare neutrophilic dermatosis, that is, often recalcitrant to conventional therapies. Biologics targeting specific inflammatory pathways, including IL-17, are emerging as alternative treatment options in refractory cases. We report a case of severe, ulcerative pyoderma gangrenosum in a 78-year-old woman with complex comorbidities, including advanced sarcoma and prior venous thromboembolism, which precluded use of several immunosuppressive agents. The patient was refractory to corticosteroids, dapsone, and roflumilast, and developed recurrent Gram-negative infections. Initiation of brodalumab, an anti-IL-17RA monoclonal antibody, led to rapid ulcer improvement and sustained clinical response, with successful tapering of systemic steroids. Brodalumab may offer a safe and effective treatment option in refractory pyoderma gangrenosum, particularly in patients with contraindications to conventional therapies. This case supports further evaluation of IL-17 pathway inhibition in neutrophilic dermatoses.

Introduction

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis characterized by painful, rapidly progressive skin ulcers. ¹ Although its pathogenesis remains incompletely defined, dysregulated neutrophil function and upregulation of cytokines such as TNF-α, IL-1β, and IL-17 are implicated.^1–3 First-line therapies typically include corticosteroids or cyclosporine, with biologic agents considered in refractory cases. ⁴

We present a case of biopsy-confirmed ulcerative PG in an elderly patient with prior high-grade pleomorphic spindle cell sarcoma, significant surgical and thrombotic complications and failure of conventional treatments. She achieved clinical remission with brodalumab, an IL-17 receptor A inhibitor.

Case report

A 78-year-old woman was referred to dermatology in October 2024 for evaluation of a rapidly enlarging and exquisitely painful ulcer at the site of prior high-grade pleomorphic spindle cell sarcoma resection on the left thigh. Her postoperative recovery had been complicated by flap failure, bilateral deep vein thromboses, pulmonary embolism, and chronic anticoagulation with apixaban. Dermatologic examination revealed a 13 × 5 × 5 cm ulcer with violaceous undermined borders and ~20% necrotic tissue (Figure 1(a)). The ulcer had been worsening with serial surgical debridements, prompting concern for pathergy. A punch biopsy was obtained from the ulcer edge for histopathology and tissue cultures.

Figure 1.

Serial clinical photographs showing ulcer evolution in ulcerative pyoderma gangrenosum treated with brodalumab. (a) Initial presentation (October 2024): large necrotic ulcer measuring 13 × 5 × 5 cm with violaceous undermined borders and fibrinous base. (b) Pre-brodalumab worsening (November 2024): expansion to 15 × 9 × 4 cm with seropurulent exudate despite systemic corticosteroids and dapsone. (c) Early response (2 weeks post-brodalumab initiation, December 2024): decreased necrosis and early granulation tissue. Measured size: 13.0 × 7.0 × 4.5 cm. (d) Continued improvement (January 2025): improved granulation, shallower depth, and reduced pain; off prednisone. Size: 15.5 × 7.8 × 3.0 cm. (e) Ongoing healing (March 2025): 80% granulation, decreasing ulcer depth and no active inflammation. Size: 16.0 × 6.5 × 2.5 cm. (f) Later follow-up (June 2025): re-epithelialization, depth 0.5 cm, pain-free with no discharge. Size: 12.0 × 7.0 × 0.5 cm.

While awaiting results, a work-up to rule out underlying causes of PG was performed, including complete blood count, inflammatory markers, autoimmune serologies, serum protein electrophoresis, and imaging. Empiric therapy with oral doxycycline and nonadherent silver foam dressings was initiated to cover possible secondary infection while minimizing trauma and avoiding pathergy.

Five days later, biopsy and culture results returned, demonstrating a dense dermal neutrophilic infiltrate without evidence of vasculitis or infection, satisfying criteria for PG. The clinical diagnosis was further supported by a PARACELSUS score ⩾10 based on rapid progression, undermined borders, severe pain, and exclusion of infection or alternative etiologies. At that time, empiric antibiotics were discontinued, and treatment was escalated to systemic prednisone (50 mg daily with a taper) and dapsone (50 mg daily), with cessation of surgical debridement in favor of nontraumatic, moisture-preserving foam dressings.

Despite this regimen, the ulcer expanded to 15 × 9 × 4 cm over 4 weeks, with increased pain and a persistent fibrinous base (Figure 1(b)). Prednisone was re-escalated to 50 mg, dapsone was increased to 100 mg, and oral roflumilast (250 µg daily) was added for its anti-neutrophilic and steroid-sparing effects. Wound care was intensified with Silvercell packing and foam dressings. However, the patient experienced recurrent Gram-negative infections, complicating further immunosuppression.

Given ongoing ulcer progression and the patient’s comorbidities precluding additional systemic immunosuppressants, brodalumab (210 mg subcutaneously every 2 weeks) was initiated under compassionate access in November 2024. At the time, she remained on prednisone 30 mg and roflumilast. Dapsone was discontinued and trimethoprim-sulfamethoxazole prophylaxis was introduced. Prednisone was tapered weekly by 5–10 mg, then more slowly thereafter.

Pain management included topical lidocaine 3%, pregabalin, acetaminophen, and intermittent oxycodone, with a focus on preserving function while minimizing opioid use. Clinical improvement was evident within 2 weeks of brodalumab initiation (Figure 1(c)). By January 2025, the ulcer was granulating, pain-free, and prednisone had been discontinued (Figure 1(d)). Progressive healing continued, with reduced depth and no signs of active inflammation by March (Figure 1(e)). At follow-up in June 2025, the ulcer had decreased to 12.0 × 7.0 × 0.5 cm with visible re-epithelialization (Figure 1(f)). At last follow up in December 2025, the ulcer was completely healed and brodalumab taper to every 4 weeks.

Discussion

This case illustrates the utility of brodalumab in treating severe PG unresponsive to standard therapy. IL-17 signaling, particularly via IL-17RA, has been implicated in neutrophil recruitment and cytokine amplification in PG pathogenesis. ⁵ Brodalumab inhibits IL-17RA, thereby blocking multiple IL-17 isoforms including IL-17A, IL-17C, and IL-17F. ⁵

Over five cases of secukinumab-treated PG have demonstrated favorable outcomes, ⁶ alongside more than 20 cases treated with ustekinumab (anti-IL-12/23) and guselkumab (anti-IL-23p19), especially in patients with coexisting inflammatory bowel disease or arthritis.^7,8 A 2022 systematic review by Maronese et al. summarized these findings, noting growing support for IL-17 and IL-23 blockade in PG management. ² However, these therapies are not reimbursed by public insurance plans in many jurisdictions, limiting their accessibility.

To our knowledge, this is among the first published cases demonstrating sustained remission of PG with brodalumab, expanding on two prior reports of clinical response.^9,10 Brodalumab was selected in this case based on its broader cytokine blockade, lack of contraindications in cancer survivors, and availability through compassionate access. The patient tolerated treatment well, experienced rapid stabilization, and achieved complete corticosteroid tapering. Importantly, brodalumab offered a steroid-sparing, infection-avoiding alternative in a frail elderly patient with a complex vascular and oncologic history.

This case supports further evaluation of IL-17RA inhibition in PG, particularly in complex or immunosuppression-limited settings. Clinical trials are needed to define its role within therapeutic algorithms and to optimize dosing and monitoring strategies.

Conclusion

In this case of refractory ulcerative PG with contraindications to conventional immunosuppressants, brodalumab led to sustained clinical response and corticosteroid sparing. IL-17RA inhibition may be a promising therapeutic approach in selected PG patients.