Bullous pemphigoid emerged after secukinumab controlled psoriasis but not the underlying immune shift
A 68-year-old man with long-standing severe plaque psoriasis developed bullous pemphigoid after 10 injections of secukinumab, despite a clear early response of his psoriatic plaques. The sequence is clinically important because the eruption did not appear at the height of uncontrolled psoriasis; it appeared after visible improvement, when a new blistering phenotype interrupted a biologic course that had been helping the original disease.
The case follows the patient for more than two years after the first blistering episode and shows how difficult it can be to steer treatment when psoriasis and bullous pemphigoid coexist. The skin disease was not the only problem. Serology, direct immunofluorescence, and later follow-up all pointed to a deeper immunologic discordance: the blisters settled, yet the BP-associated antibody and complement signals remained active in the background.
Ten secukinumab injections were enough to change the phenotype
At presentation in March 2023, the patient had more than 20 years of plaque psoriasis and extensive skin involvement, with approximately 95% body surface area affected and a psoriasis area and severity index of at least 10. Prior therapies had been limited to topical corticosteroids, oral acitretin, and UVB phototherapy, each producing only partial or temporary benefit. Secukinumab 300 mg subcutaneously was started on the standard schedule, and the response was brisk: the psoriatic lesions improved after the first two injections.
The clinical turn came in October 2023 after a total of 10 injections. Severe pruritus developed, followed by numerous tense bullae, vesicles, erosions, and crusts across the head and neck, trunk, and extremities. Nikolsky’s sign was negative, and the oral and genital mucosae were spared. In a blistering disorder, the morphology matters. Tense bullae on erythematous skin, together with a negative Nikolsky sign, immediately pushes the differential toward a subepidermal autoimmune process rather than a simple drug rash or epidermal necrolysis.
Eosinophils, IgE, BP180, and complement painted a classic BP pattern
Laboratory testing was not subtle. Leukocytosis was present, with a white blood cell count of 13.80 × 10^9/L and an absolute neutrophil count of 8.50 × 10^9/L. Peripheral eosinophilia was striking, with eosinophils accounting for 16.4% of leukocytes and an absolute eosinophil count of 2.30 × 10^9/L. Total immunoglobulin E reached 693 kU/L. Anti-BP180 antibody exceeded 400 RU/mL, and anti-BP230 antibody measured 344.06 RU/mL.
Skin biopsy added the tissue-level evidence. Histopathology showed a subepidermal cleft with eosinophils, neutrophils, and lymphocytes in the superficial dermis, while direct immunofluorescence demonstrated linear IgG and C3 along the basement membrane zone. Those findings fit bullous pemphigoid tightly and explain the blistering biology: autoantibodies against hemidesmosomal antigens trigger complement activation, recruit eosinophils, and weaken epidermal adhesion at the dermal-epidermal junction.
Secukinumab was stopped, and the patient received prednisone 30 mg/day, cyclosporine 175 mg/day, minocycline 200 mg/day, nicotinamide 400 mg/day, topical corticosteroids, and symptomatic antipruritic treatment. No new blisters appeared after three days. The existing bullae dried, crusted, and healed, and eosinophil counts normalized before discharge.
Clinical remission did not erase the BP signal
After control was achieved, prednisone was tapered by 5 mg every 4 weeks and discontinued in April 2024 without new bullae. Cyclosporine continued until the same month. BP remained clinically quiet, but psoriasis became increasingly difficult to control, which forced a series of sequential therapeutic decisions that were not uncomplicated.
Tildrakizumab was started in May 2024 because of persistent psoriasis activity. A second injection was given one month later, and transient improvement followed, but eczematous lesions later appeared and the drug was stopped in September 2024. Ustekinumab began in January 2025 and continued for about five months, yet psoriasis still did not come under adequate control. When the patient returned in June 2025, the skin showed moderate plaque psoriasis, with dark-red scaly plaques on the trunk and extremities, coalescing plaques on the lower limbs, and erosions on both lower legs. Typical tense bullae were absent.
The paradox was clear on follow-up testing. Eosinophils had fallen to 5.9%, with an absolute count of 0.40 × 10^9/L, but total IgE had climbed to greater than 1,100 kU/L. Anti-BP180 remained above 400 RU/mL, anti-BP230 had dropped to 10.22 RU/mL, and direct immunofluorescence still showed C3 along the basement membrane zone. Clinically, BP was quiet. Immunologically, the disease footprint remained visible.
Deucravacitinib controlled psoriasis without BP relapse
Because psoriasis remained inadequately controlled and the patient declined further biologic therapy, oral deucravacitinib 6 mg once daily was started after contraindications were excluded and risks were discussed. Topical calcipotriol, fluticasone propionate, and tapinarof, plus oral rupatadine, were added. Psoriasis improved from moderate to mild severity before discharge, and no vesicles or bullae developed.
He continued deucravacitinib until December 2025, then stopped it on his own. During treatment, psoriasis stayed mild and no blistering recurred. At the latest structured telephone follow-up, roughly 6 months after discontinuation, the patient reported stable mild psoriasis and no return of bullae, marked pruritus, erosions, or mucosal involvement.
The case has a narrow but important clinical message. Pathway-specific therapy can suppress one immune-dominant dermatosis while leaving another to surface, and clinical quiescence can coexist with persistent BP180 positivity and residual complement deposition. In patients who develop blistering during secukinumab exposure, follow-up should extend beyond rash clearance, because the skin may look quiet even when the autoimmune signal has not fully disappeared.
Why this long follow-up matters in a single patient
Most published reports on BP during IL-17A inhibitor therapy stop at onset or short-term resolution. This case extends the timeline across more than two years and shows how the treatment sequence itself became part of the disease story. Secukinumab controlled psoriasis first, then coincided with BP emergence. Later, sequential biologic choices did not provoke BP relapse clinically, yet the antibody and immunopathologic profile stayed abnormal for a prolonged period.
The bedside consequence is straightforward: patients with psoriasis who develop tense bullae during IL-17A inhibition need biopsy confirmation, immunologic testing, and longer observation than a short rash follow-up would provide. Persistent BP180 elevation and C3 deposition may not equal active blistering on a given day, but they do argue for continued surveillance when the therapeutic target shifts again.