Characteristic features on histology are myocyte necrosis and regeneration without significant inflammation.1 5 9 10 While histology is required to confirm diagnosis in the autoantibody unfavorable NAM, specific histological features are not required to classify patients with autoantibody positive NAM.4 Best treatment options and long-term prognosis for NAM are incompletely defined. Statin-associated NAM, a subtype has only been described in the literature in about 550 cases with an estimated incidence of two to three cases in 1?000?000 patients exposed to statins per year.3 We describe Sesamolin a case of statin-associated NAM presenting as severe oropharyngeal dysphagia and acutely progressing to severe symmetrical muscle weakness while receiving treatment with high-dose corticosteroids. This case aims to increase awareness of an atypical presentation pattern of this rare disease, highlights the need for a high index of suspicion in patients with a remote history of statin use and the importance of early recognition and having a low threshold to start aggressive immunosuppressive therapy. Case presentation A 71-year-old African-American man with a medical history of hypertension, peripheral artery disease and a remote history of simvastatin use, which was changed to high-dose atorvastatin and later discontinued due to abnormal liver function assessments, presented with 2?weeks of dysphagia, dysphonia, hoarseness, excess salivation and a 2.7?kg weight loss. He described dysphagia to both solids and liquids with a feeling of food getting stuck in his throat. No myalgia was reported, but he pointed out he had moderate fatigue and weakness which he attributed to his inability to eat. On examination, the patient was normotensive with blood pressure of 126/70?mm?Hg, heart rate of 60 bpm and a respiratory rate of 18/min. He had severe oropharyngeal dysphagia with pooled secretions in his oropharynx on swallow evaluation. Muscle strength was 5/5 in bilateral upper and lower extremities with normal gait. Investigations Given the nature of his symptoms, a mechanical obstruction due to a neoplasm was suspected. CT scan of his head, neck, chest, stomach and pelvis were essentially unfavorable except for peri-carinal lymph nodes, which were less than 1?cm. Upper gastrointestinal endoscopy revealed normal oesophagus and oesophagram could not be performed due to severe risk of aspiration. Flexible laryngoscopy showed normal vocal cords with no laryngeal masses or lesions. Non-contrast brain MRI performed to evaluate brainstem stroke was unremarkable, and there was also no evidence of a demyelinating disorder around the MRI although suspicion for this aetiology was low based on the patients presentation and isolated symptoms. Due to absence of mechanical causes of oropharygeal dysphagia and the patients atypical presentation, electromyography?(EMG)/nerve conduction Sesamolin study was done. This test revealed evidence of myopathy with features of muscle membrane irritability suggestive of necrotising or inflammatory myopathy. With this new obtaining, myositis workup was initiated. Pertinent positives were creatine kinase (CK) of 15?595?u/L (normal, 25?to?90), C-reactive protein of 9.76?mg/dL?(normal, 0?to?0.5), urine myoglobin? 12?700?mcg/L (normal,? 28) and aldolase of 131.5?u/L (normal, 1?to?8?u/L). Of note, alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase were persistently elevated throughout his admission ranging from 266 to 581?u/L (normal, 5 to 35), 169 to 370?u/L (normal, 0?to?40) and 589?to?894?u/L (normal, 85?to?210), respectively. Enzyme-linked immunosorbent assay revealed anti- 3-hydroxy-3-methylglutaryl-coenzyme receptor (HMGCR) antibodies? 200 models. Biopsy of the left quadriceps muscle showed active PPP1R53 myopathic changes including fibre size variation, individual fibre necrosis and regenerating fibres without significant inflammatory nodule or rimmed vacuoles (physique 1). Immunohistochemical staining for the major histocompatibility complex class 1 showed membranous and cytoplasmic staining of the necrotising myopathic fibres with no significant background inflammation. Similar features were seen on with complement C5-9 staining. The left quadriceps muscle was chosen for muscle biopsy to Sesamolin avoid misinterpretation as the EMG was done on right side of the body. Open in a separate window Physique 1 Quadriceps muscle biopsy (haematoxylin and eosin stain). (A) Transverse section showing fibre size variation with randomly admixed atrophic fibres and scattered necrotic fibres. (B) Longitudinal section showing a necrotic fibre with numerous intra-fibre macrophages.?Scale bars: 100 micrometres..