LAUSR

Dear Editor, Statin is commonly prescribed for treatment of dyslipidemia and prevention of cardiovascular disease. Musculoskeletal manifestations ranging from asymptomatic elevation of creatine kinase (CK), myalgia and muscle weakness, to life-threatening rhabdomyolysis, are welldescribed complications of statin use. More recently, statin has been recognized to be associated with immune-mediated necrotizing myopathy (IMNM). We report here a patient with statin-associated IMNM who presented with atypical manifestations which included subcutaneous edema of the limbs and persistent bulbar weakness, despite spontaneous resolution of limb weakness and normalization of CK after cessation of statin, in addition to the absence of autoantibody against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR). To the best of our knowledge, these features have not been previously described. A 68-year-old man who had attended the dermatology out-patient clinic for pemphigus foliaceus complained of a 1-month history of muscle weakness associated with fatigue. Treatment of pemphigus in the past with high-dose prednisolone had shown good response and he was on prednisolone 5 mg daily as maintenance therapy. There was proximal muscle weakness and elevated CK of 10 215 U/L (normal range: < 170 U/L). Rhabdomyolysis was ruled out. He had dyslipidemia and had been on treatment with simvastatin for the past 7 years. Statin was promptly discontinued given the possibility of statin-induced myopathy. The patient refused further investigations. He presented 2 months later with increasing lethargy, progressive muscle weakness, dysphagia and swelling of both upper and lower limbs. Rheumatology consultation was sought. He admitted to choking on solid food; however, there was no slurred speech, diplopia, ptosis or breathlessness. There was no family history of muscle disease. He denied consumption of supplements or herbal remedies. Physical examination revealed brawny non-pitting edema over all extremities, which was more pronounced in the upper arms. Cutaneous signs of dermatomyositis were absent. Muscle power was assessed using the Medical Research Council (MRC) score: neck flexion was 5, shoulder abduction and adduction was 4 bilaterally, hip flexion and extension was 4 bilaterally, other muscle groups were 5. Examination of the other systems was essentially unremarkable. Investigation revealed CK of 9065 U/L. There was hypoalbuminemia at 26 g/L (normal: > 35 g/L) but no proteinuria. Erythrocyte sedimentation rate was 20 mm/h, C-reactive protein (CRP) was 131.5 mg/L (normal: < 5 mg/L) and hemoglobin was 10.1 g/dL. Renal function and thyroid function tests were normal. Hepatitis B, hepatitis C and human immunodeficiency virus serology were negative. Immunology was negative for antinuclear antibody, rheumatoid factor, anti-Jo-1 antibody and anti-signal recognition particle (anti-SRP) antibody. Tumor markers including prostate specific antigen, carcinoembryonic antigen, CA 19-9 and alphafetoprotein were within normal limits. Chest radiography and electrocardiography were unremarkable. Screening for internal malignancy, which comprised upper endoscopy, ENT (ear, nose and throat) examination and computed tomography (CT) of thorax, abdomen and pelvis did not reveal any evidence of malignancy. Biopsy of the left deltoid muscle was undertaken in order to arrive at a definitive diagnosis. In the interim period while waiting for the muscle biopsy report, muscle strength over his shoulder and pelvic girdles improved spontaneously to an MRC score of 5. This was accompanied by normalization of CK. Of note, his prednisolone dose had remained at 5 mg daily. Nonetheless, his dysphagia persisted. Endoscopic evaluation of swallowing revealed severe oropharyngeal dysphagia characterized by poor epiglottic deflection