Bergner et al. Journal of Medical Case Reports 2011, 5:409 http://www.jmedicalcasereports.com/content/5/1/409 progressive proximal muscle weakness of six weeks’ duration; slight, intermittent proximal muscle pain; dys- pnea; and oliguria. He was treated with irbesartan and hydrochlorothiazide (CoAprovel® 150/12.5 mg Sanofi Pharma Bristol - Myers Squibb SNC, 174 Avenue de France F - 75013 Paris, France) because of arterial hypertension and tamsulosin (Pradif T® Boehringer Ingelheim GmbH, Dufourstrasse 54 CH 4002 Basel, Switzerland) because of weak urinary flow. He did not drink alcohol but smoked one pack of cigarettes per day. At the time of admission, the patient was alert, his body temperature was 38.6°C, his blood pressure was 140/80 mmHg, his heart rate was 80 beats/minute, his breathing rate was 20 breaths/minute, and his oxygen saturation level was 85% while breathing ambient air. He had edema in his lower legs. Painless muscle weak- ness prevented him from standing or sitting. He had normal strength in both his hands and his feet, but active lifting of his head, legs, and arms was barely pos- sible while he was supine, and his speech was slurred. His reflexes, eye movements, and cranial nerve function were normal. He had no skin lesions. A chest X-ray showed right lung infiltration consistent with aspiration pneumonia. No signs of lung fibrosis were observed. His electrocardiogram was normal. His laboratory values were as follows: hemoglobin 148 g/L, leukocyte count 14.7 × 109/L, erythrocyte sedimentation rate 14 mm/ hour, creatine kinase 121,530 U/L, C-reactive protein 39 mg/L, creatinine 51 μmol/L, BUN 6.4 mmol/L, sodium 122 mmol/L, and potassium 4.3 mmol/L. His serum 25- OH vitamin D level and thyroid gland function were normal, and his human immunodeficiency virus test was negative. MRI of his legs showed edema of the proximal muscles, particularly of both adductors. A biopsy of adductor muscle tissue was performed. Histological and immunohistochemical tests (inflammation marker, membrane attack complex, and major histocompatibility complex class I) showed signs of muscle necrosis (Figure 1, Figure 2) and diffuse muscle infiltration of T lympho- cytes (Figure 3), but no signs of an autoimmune process. Additional serological tests for hepatitis B, hepatitis C, anti-nuclear antibodies, anti-neutrophil cytoplasmic anti- bodies, anti-double-stranded DNA antibodies, anti-mito- chondrial M2 antibodies (anti-Mi2), anti-signal recognition particle (anti-SRP) antibodies, anti-Jo-1 anti- bodies and anti-polymyositis/scleroderma antibodies (anti-PM-Scl) all yielded negative results. The patient was rehydrated with bicarbonate solution until his jugular veins were distended, and therapy with intravenous furosemide, ceftriaxone, methylprednisolone (500 mg/day), calcium, vitamin D, and alendronate was initiated. The patient’s proximal muscle weakness declined within three days. Within four days, his serum creatinine level rose to 190 μmol/L, which was Page 2 of 4 Figure 1 Cross-sectional slice of human skeletal muscle showing acute muscle fiber necrosis (hematoxylin and eosin stain; × 400 original magnification). accompanied by oliguria, and his serum creatine kinase level dropped from a maximum of 169,910 U/L to 34,897 U/L. His steroid therapy was modified to oral prednisone 80 mg/day. Seven days later he could walk again with support, and his urine output and serum creatinine level had normalized. After 28 days, his pre- dnisone treatment was tapered back to 35 mg/day, but within four days his serum creatine kinase rose again from 547 U/L to 1548 U/L without clinical Figure 2 Cross-sectional slice of human skeletal muscle (hematoxylin and eosin stain; × 400 original magnification). Regenerating muscle fibers can be seen as basophilic fibers with enlarged nuclei in the center of the image.