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Management with secukinumab of tumour necrosis factor inhibitor‐induced pulmonary sarcoidosis‐like reaction in a patient with psoriasis

With about 90 reported cases, drug-induced sarcoidosislike reactions (DISRs), which typically manifest in the lungs, are a rare adverse effect of tumour necrosis factor (TNF) inhibitor treatment. Among the TNF inhibitors used for psoriasis, etanercept seems to pose the highest risk of inducing DISR. While discontinuation of the TNF inhibitor is recommended when DISR occurs, knowledge about the role of more modern biologics in the management of DISR is inadequate. A 27-year-old man with long-standing severe chronic plaque psoriasis was started on etanercept 50 mg/week. Previous treatments with acitretin, methotrexate (MTX), phototherapy and a 3-month course of adalimumab had failed. MTX 15 mg/week was reinitiated 6 months after the commencement of etanercept because etanercept alone failed to control the psoriasis sufficiently. Three years after initiation of etanercept, at the age of 30 years, the patient was diagnosed with DISR. His symptoms were mild coughing and exertional dyspnoea. The diagnosis of DISR was made upon radiological examination including a pulmonary computed tomography scan and chest radiography, which showed stage 3 sarcoidosis with early fibrosis and coarse reticulonodular changes (Fig. 1) and the histological findings of a bronchial biopsy showing the presence of noncaseating granulomas formed by epithelioid histiocytes and multinucleated giant cells (Fig. 2). The results of the patient’s pulmonary function tests (PFT) deteriorated over 3 consecutive years, with mild restrictive changes manifesting as a drop in forced expiratory vital capacity (FVC) from 108 to 81% of predicted value, and the diffusing capacity of the lungs for carbon monoxide (DLCO) from 94 to 87% of predicted value. Therefore, treatment with etanercept and MTX was stopped and replaced by ciclosporin (3 mg/kg). Owing to insufficient action and ciclosporin-induced hypertension, secukinumab (300 mg/month after the loading dose) was subsequently introduced and ciclosporin discontinued. Eight months after commencement of secukinumab, the patient’s psoriasis was well controlled, with radiographic and PFT improvement (FVC 97% of predicted value; DLCO 94% of predicted value; Fig. 1). It is estimated that 1 in 2800 patients treated with a TNF inhibitor develops DISR. TNF inhibitor-induced sarcoidosis-like reactions are considered a paradoxical reaction with unknown underlying pathophysiology. It is hypothesized that the cause of DISR may either be the cytokine imbalance due to TNF suppression or an infection unmasked by TNF inhibitor treatment. More recently, other biologics including ustekinumab have been associated with DISR. Although TNF inhibitor-induced, sarcoidosis-like reaction is considered a class effect, there have been reports of successful management after switching to another TNF inhibitor. Toussirot et al. reported a case on the successful use of secukinumab in a patient with certolizumab-induced, renal sarcoidosis-like reaction and underlying axial spondylarthritis without further recurrence over a 6-month period. The benefits of the interleukin-17A inhibitor secukinumab over TNF inhibitors in patients with DISR could be explained by the findings that secukinumab does not increase the risk of tuberculosis infection and by the underlying clinical and immunological similarities between both conditions. The presented case suggests that secukinumab is a promising treatment option in the management of