Pyoderma gangrenosum (PG) is classified as a neutrophilic dermatosis, often presenting as a rapidly enlarging ulcer and associated with inflammatory bowel disease, specifically ulcerative colitis and Crohn's disease. PG has been typically reported to occur after trauma and surgical procedures. We present a unique case of PG following multiple breast augmentation procedures and illustrate various therapeutic strategies to prevent recurrence during subsequent breast reconstruction. The combination of cyclosporine and prednisone was successfully used to prevent PG in this patient when given before and after her third breast surgery.   &nbsp.

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis that may cause rapid tissue destruction when it involves the periocular region. We report a 17-year-old patient with ulcerative colitis who developed progressive upper eyelid ulceration initially treated as preseptal cellulitis and later suspected necrotizing infection. Despite broad-spectrum antibiotics, the lesion worsened. Clinical findings, sterile cultures, associated cutaneous lesions, and a PARACELSUS score of 17 strongly supported the diagnosis of PG, prompting immediate systemic corticosteroid therapy before histopathologic confirmation. Adjunctive wound care included topical hypochlorous acid therapy and ophthalmic antibiotic ointment. Histopathology subsequently confirmed PG. Complete re-epithelialization was achieved within 3 weeks without eyelid malposition, functional sequelae, or recurrence during 8 months of follow-up. This case highlights the value of the PARACELSUS score in facilitating early diagnosis of periocular PG and supports prompt tissue-preserving management to prevent irreversible eyelid damage.

PAPA syndrome (pyogenic sterile arthritis, pyoderma gangrenosum, and acne) is a rare autosomal dominant autoinflammatory disorder caused by mutations in the PSTPIP1 gene. In pediatric patients, arthritis often precedes cutaneous manifestations by several years, leading to frequent misdiagnosis as septic arthritis. Treatment is challenging, with IL-1 inhibitors being the most pathophysiology-based first-line therapy, but their accessibility is limited by high costs. We reported an 11-year-old Chinese boy with a 7-year history of recurrent, migratory arthritis. Trio whole-exome sequencing identified a heterozygous PSTPIP1 c.770A>G (p.Glu257Gly) variant, classified as likely pathogenic. The father carried the same variant; he had experienced arthralgias in early childhood but became asymptomatic after age 10 without any treatment, demonstrating incomplete penetrance. This variant is extremely rare, reported in only one of 16 patients in the Eurofever registry, all of European descent, making this the first Asian case. Due to financial constraints, IL-1 inhibitors were inaccessible. Tofacitinib (3.5 mg twice daily, adjusted from adult dose based on body surface area) was initiated in February 2026. After 2 months, joint swelling and pain decreased significantly. As of July 10, 2026, no recurrence of joint swelling and pain had been observed during follow-up. However, radiography revealed irreversible structural damage (bone demineralization, joint space narrowing, osteophyte formation), and the patient still had limited mobility. Rehabilitation specialists advised against aggressive range-of-motion exercises and recommended home-based ultrasound and electrical stimulation to prevent muscle atrophy. Long-term follow-up is ongoing. PAPA syndrome should be considered in children with culture-negative, antibiotic-unresponsive recurrent arthritis, even without skin findings. Early genetic diagnosis can prevent unnecessary procedures. For patients who cannot access IL-1 inhibitors, tofacitinib may reduce inflammation, but it cannot reverse established joint damage. Given the relatively short follow-up duration, the long-term durability of response, safety, and impact of tofacitinib on disease progression remain to be determined. This report provides early, preliminary evidence of JAK inhibitor use in this population, contributing initial data to the limited Asian literature.

The treatment of inflammatory skin diseases has moved from broad immunosuppression toward mechanism-based therapy with targeted biologics and small molecules. Psoriasis exemplifies this shift: interleukin-23 (IL-23)/T helper 17 (Th17) blockade can achieve near-complete clearance, yet persistent tissue-resident memory T cells may sustain disease memory and drive relapse after treatment withdrawal. The papers highlighted in this issue link tissue memory, genotype, treatment durability, and pathway-directed therapy across different skin diseases. Together, they emphasize that precision dermatology must look beyond visible clearance toward biological remission and durable disease control.