LAUSR

A 26-year-old Filipino man presented to his rheumatologist with symptoms of weakness in his lower limbs after noticing that activities such as running and walking up stairs had become quite difficult. He had not performed any excessive physical activity in the preceding days nor used any illicit substances or over the counter medications. On examination, he had reduced 4/5 power in the proximal muscles of his lower limbs with preserved distal power. His lower limb tone, reflexes, sensation and coordination were normal as was the rest of the neurological examination. He had no muscle tenderness, rash or synovitis of any joints and in particular no discomfort on internally rotating the hips in flexion. Initial blood tests revealed a C-reactive protein (CRP) of 9.3 mg/L and an elevated creatinine kinase of 5564U/L. Twomonths prior he had presentedwith 1week of pain and swelling in both knees and ankles. A synovial fluid aspirate of the knee was inflammatory with a white cell count of 36 000 10/L and his CRP was 82.5 mg/L. The HLAB27 gene test was positive and he had negative rheumatoid factor and cyclic citrullinated peptide antibodies. A pelvic X-ray showed bilateral sacroiliitis. He was diagnosed with an acute spondyloarthritis and commenced on meloxicam 15 mg daily and sulfasalazine with the dose up-titrated to 2 g per day. This achieved resolution of his joint symptoms and the meloxicam was ceased. He was not taking any othermedications including over the counter preparations. He had been otherwise healthy with no history of psoriasis, inflammatory bowel or eye disease. Spondyloarthritides are not clinically associated with myositis and therefore tests were performed to investigate for any other possible cause of myopathy or inflammatory myositis. No other condition related to myopathy was found. The patient had normal thyroid function and negative results for HIV and hepatitis B and C. Antinuclear, myositis specific and anti-neutrophil cytoplasmic antibodies were negative, as were antibodies to extractable nuclear antigens and double-stranded DNA. The sulfasalazine was immediately ceased after his presentation with weakness due to concerns of drug-induced myopathy. He was observed closely and 2 weeks after ceasing sulfasalazine he had normal lower limb power, no synovitis and his creatinine kinase level had returned to within the normal range. This supported the clinical suspicion that the patient’s myopathy was drug-induced secondary to sulfasalazine with the adverse reaction rated as ‘probable’ with a score of 7 on the Naranjo scale. Sulfasalazine is a conventional disease modifying antirheumatic drug used in inflammatory arthritis and inflammatory bowel disease. It has recognised side-effects of gastrointestinal upset, skin reactions, hepatotoxicity and rare cases of severe leukopenia or agranulocytosis. Druginduced myopathy is one of the most common causes of muscle disease. Many medications have been implicated as causative of myopathy either via direct toxicity or immunemediated mechanisms, in particular, statins, glucocorticoids, hydroxychloroquine and colchicine. It is more likely that this was a direct muscle toxicity because of the rapid resolution on ceasing the sulfasalazine. This is only the second ever published report of sulfasalazine-induced myopathy and highlights the importance of clinicians being mindful of unexpected medication side-effects and always considering the possibility of drugs as a cause of myopathy.