Abstract
A 60-year-old man with severe chronic plaque psoriasis and psoriatic arthritis (PsA) was started on infliximab (5 mg kgMINUS SIGN 1) having developed secondary failure to adalimumab and etanercept. His baseline antinuclear antibody (ANA) and double-stranded DNA (dsDNA) antibody were both negative.
Nine months later, he developed severe, pleuritic left-sided chest pain, dyspnoea, weight loss, new arthralgia and fevers. His autoantibodies were repeated with the onset of his symptoms and showed a weakly positive ANA 1 : 140 (human epithelial type-2 speckled nuclear pattern) and dsDNA (weak immunofluorescence for Crithidia DNA).
Computed tomography of the chest revealed bilateral small pleural effusions, an elevated right hemi-diaphragm and atelectasis of the left lung base. Lung function tests showed reduced forced expiratory volume in 1 s (FEV1) 2.01% (predicted 2.94%), FEV1/forced vital capacity 74% (predicted 86%) and transfer factor for carbon monoxide 4.82 (predicted 8.48).
Infective aetiologies were excluded. The diagnosis of 'infliximab-induced lupus with pleuropulmonary involvement and shrinking lung syndrome' was made, and met the American College of Rheumatology (ACR) criteria for tumour necrosis factor (TNF)-induced lupus: serositis (pleuritis), new nonerosive arthritis, ANA and dsDNA positivity, and a temporal relationship of resolution of symptoms after TNF cessation.
One year after infliximab cessation and prednisolone (20 mg reducing course over 15 months) his ANA and dsDNA antibodies were negative and his lupus-related symptoms had resolved. Five years later he is now managed on ustekinumab [anti-interleukin (IL)-12/23] every 3 months with no recurrence of symptoms or residual fibrosis.
Lung function tests are now normal.