Hypertriglyceridaemia during treatment with adalimumab in psoriatic arthritis

Conflicts of interest: none declared. Sir, Adalimumab, the first fully human antitumour necrosis factor (TNF)‐α antibody developed to date, has been shown to be useful in the treatment of inflammatory diseases such as rheumatoid arthritis, Crohn disease and psoriatic arthritis, and it has also demonstrated a safety profile similar to other anti‐TNF‐α agents. There are currently no available data about triglyceride (TG) alterations in patients during treatment with adalimumab. We report a 39‐year‐old man with a 1‐year history of oligoarticular asymmetrical type psoriatic arthritis. Minimal plaque psoriasis developed 2 months before the articular involvement; the patient had no comorbidities, in particular, no features of metabolic syndrome. There was no family history of hypertriglyceridaemia or hypercholesterolaemia. Given the lack of efficacy of previous therapies with disease‐modifying antirheumatic drugs, the patient was considered as ‘high need’ for biologic therapy. Baseline Psoriasis Area and Severity Index (PASI) was 8 and Ritchie index1 was 6. Before starting treatment, complete laboratory tests were performed, including chest X‐ray, full blood count, urea, creatinine, transaminases, cholesterol, TGs, antinuclear antibodies, antidouble‐stranded DNA antibodies, antiextractable nuclear antigens, antiphospholipid antibodies (lupus anticoagulant and anticardiolipin), tumour markers, blood culture and urine culture; no significant alterations were found. A Mantoux test was negative. Anticitrullin antibody and rheumatoid factor were normal while C‐reactive protein was 13 mg L−1. Hence we started systemic therapy with adalimumab 40 mg every 2 weeks administered subcutaneously as monotherapy. Blood tests were repeated every 4 weeks. After the first 4 weeks of treatment an improvement of skin condition and articular performance (PASI 4 and Ritchie index 2) was observed, without any side‐effects. After 8 weeks of treatment (PASI 3.2 and Ritchie index 2) the patient developed hypercholesterolaemia (267 mg dL−1; normal 100–200), hypertriglyceridaemia (449 mg dL−1; normal 100–180) and weakness; we decided to continue treatment and after 3 months of therapy the patient developed a severe weakness and a remarkable hypertriglyceridaemia (689 mg dL−1) while total serum cholesterol levels remained unchanged (264 mg dL−1). Because of these important alterations we decided to discontinue therapy with the biological drug and after 4 weeks the TG level was 220 mg dL−1, cholesterol level was 224 mg dL−1 and weakness was notably improved.