A 43-year-old man with a history of ulcerative colitis (UC) treated with infliximab for 2 years presented with a 4 × 3 cm2 hemorrhagic bullous lesion with bluish serpiginous border, and surrounding erythema was noted on the left dorsal foot. The lesion later progressed to a large painful ulcer despite treatment with broad-spectrum antibiotics. Excisional biopsy and debridement were performed (Figure 1A,B). Bacterial, Mycobacterium tuberculosis, and fungal cultures were negative. Laboratory tests were negative for antinuclear antibody, extractable nuclear antigen antibody, rheumatoid factor IgM, human leukocyte antigen B27, anti-neutrophil cytoplasmic antibody, thyroid function tests, and screening for hematologic and solid malignancies. Skin biopsy revealed abundant neutrophil infiltration and microabscess formation in the dermis and epidermis. Based on the patient's history of UC, histopathological findings, and rapid progression to expanding ulcers with characteristic violaceous undermined edges and a necrotic base, pyoderma gangrenosum (PG) was diagnosed. The patient was started on systemic corticosteroid therapy with azathioprine and cyclosporine; however, the treatment response was poor. Treatment was switched to adalimumab every 2 weeks with prednisolone at a dose of 5 mg/day. Rapid ulcer healing and considerable improvement were observed at the 6-month follow-up appointment (Figure 2). PG is a rare inflammatory form of neutrophilic dermatosis that typically presents as painful necrotic skin ulcers with undermined violaceous borders.1, 2 PG is associated with systemic diseases, such as inflammatory bowel disease (IBD), inflammatory arthritis, and malignancies. Notably, IBD demonstrates the strongest association with PG, with approximately 30% of patients with PG having IBD. In IBD patients, a large cohort study found a cumulative prevalence of PG of 0.75% across 5 years. There is no significant difference in PG incidence between Crohn's disease (CD) and UC patients. Additionally, the mortality risk in patients with PG is significantly elevated, with a 72% higher risk of death compared to IBD patients without PG.3 The diagnosis of PG is a clinical diagnosis of exclusion. The differential diagnosis includes infectious conditions such as cellulitis, necrotizing fasciitis, vascular diseases, vasculitis, and malignancy.4 It can be challenging due to lack of specific clinical, histopathological, laboratory findings, and the absence of validated diagnostic criteria, often leading to misdiagnosis.5 Therefore, when PG is suspected, a comprehensive evaluation based on the patient's medical history is crucial. In conclusion, clinicians should consider PG in IBD patients, as early recognition and management are essential to prevent complications. The authors declare no conflicts of interest. Informed consent was obtained.
Pai et al. (2026) studied this question.