Pyoderma gangrenosum caused by secukinumab successfully treated with risankizumab: a case report and literature review

Dear Editor, Pyoderma gangrenosum (PG) is an uncommon ulcerative inflammatory skin disease characterized by a pathological abundance of neutrophils in the absence of infection.1 It is known that drugs can be a triggering factor for PG, and several recent articles have reported PG induced by biologics.1 However, biologics can also be used to treat recalcitrant PG.2 We report a case of PG occurring under treatment with secukinumab against psoriasis. Switching to risankizumab effectively controlled both the PG and psoriasis. A 68‐year‐old man presented to our department with a painful, reddish, tumorous lesion on his right shoulder (Fig. 1a), which had expanded to 80 mm in diameter. The patient had a 10‐year history of psoriasis vulgaris, and had previously presented with disseminated scaly erythema on his face, trunk and limbs, along with joint pain. At that time, he had a negative rheumatoid factor test and was diagnosed with psoriatic arthritis. He had been started on adalimumab, which had to be stopped 1 month later due to a drug eruption. He had then been switched to secukinumab, and the rashes and joint pain had gradually alleviated. The shoulder lesion appeared after 3 years of secukinumab treatment. The patient had no history of inflammatory bowel disease or haematological disorders. (a–c) Clinical images and course: (a) before the switch to risankizumab, there was an erythematous tumour, 80 mm in diameter, on the right shoulder, for which culture tests were negative; (b) 1 week later, the tumour had collapsed and discharged pus, leaving ulceration; (c) 3 months after the switch to risankizumab, the tumour and ulcer had largely resolved, leaving postinflammatory pigmentation (no recurrence was observed 1 year after the switch to risankizumab). Bacterial cultures from the shoulder lesion were taken three times and were all negative. Histopathology revealed dense inflammatory neutrophilic infiltrates (Fig. 2), but no fungi were detected by Grocott staining. (a,b) Histopathological findings from a biopsy of the skin tumour showed various inflammatory cell infiltrates. Most of the infiltrating cells were neutrophils, and prominent dermal oedema and epidermal spongiosis were noted. Haematoxylin and eosin, original magnification (a) × 40; (b) × 200. Based on these clinical, laboratory and histopathological findings, PG, probably associated with secukinumab, was suspected. Secukinumab was stopped. The tumorous lesion regressed gradually and became ulcerative (Fig. 1b). To control the psoriasis and PG, we started risankizumab 2 months after secukinumab cessation. Following 3 months of risankizumab treatment, the lesion had largely resolved, leaving postinflammatory pigmentation (Fig. 1c). It did not recur during a follow‐up of 1 year, and both the psoriasis and the psoriatic arthritis were well controlled (Table 1). Reported cases of pyoderma gangrenosum occurring while under treatment with secukinumab. PG, pyoderma gangrenosum. a Time between starting secukinumab treatment and developing PG. Reported cases of pyoderma gangrenosum occurring while under treatment with secukinumab. PG, pyoderma gangrenosum. a Time between starting secukinumab treatment and developing PG. The literature includes reports of secukinumab triggering PG as well as reports of secukinumab improving PG. In hidradenitis suppurativa, secukinumab was reported to show a ‘potential double pathogenetic face’, i.e. both an ameliorating effect and an exacerbating effect.2 Our case of PG might have manifested this paradoxical exacerbating effect. The interleukin (IL)‐23/IL‐17 pathway is considered to be related to the pathogenesis not only of psoriasis but also of PG. There are three reports of PG occurring under secukinumab for psoriasis (Table 1).1, 3, 4 All of these cases were ulcerative and were treated with corticosteroids, ciclosporin or ustekinumab. A compensatory increase in IL‐23 induced by IL‐17 inhibition might be associated with the pathogenesis of PG.3 Guenova et al. reported that IL‐23 is abundantly elevated and IL‐12 is not elevated in PG lesions.5 Furthermore, Petty et al. reported a case of PG induced by secukinumab successfully treated by a switch to ustekinumab.3 In our case, both the PG and psoriasis were successfully controlled by risankizumab. These data indicate that IL‐23, rather than IL‐12, plays an important role in the pathogenesis of PG, and that IL‐23‐targeting therapies can be a treatment option for PG.