Bergner et al. Journal of Medical Case Reports 2011, 5:409 http://www.jmedicalcasereports.com/content/5/1/409 Page 3 of 4 Figure 3 Immunohistochemical staining for CD3 to display T lymphocytes. deterioration. His prednisone dosage was increased to 70 mg/day, and his serum creatine kinase declined to normal (246 U/L) within six weeks. The patient was dis- charged from the hospital free of symptoms after under- going orchiectomy on the 45th day following his initial admission. His serum creatine kinase and serum creati- nine were normal, and he was prescribed prednisone 50 mg/day. After his discharge from the hospital, predni- sone was tapered to 20 mg/day and his serum creatine kinase level rose slightly without clinical relapse. Nine months after discharge his prednisone therapy was stopped without a subsequent increase in his creatine kinase level. At his 12-month follow-up examination, the patient was in good clinical condition and had nor- mal laboratory values, including PSA. Discussion Myopathy with rhabdomyolysis and renal failure can have several causes. In the course of searching for a possible inflammatory myopathy, we found no clinical or serologi- cal signs of endocrinopathies, viral infections, or connec- tive tissue diseases and no immunohistochemical signs of autoimmune polymyositis or dermatomyositis. The nega- tive results of screening of our patient for these antibodies represent an additional argument against a diagnosis of autoimmune polymyositis, although anti-Jo-1 antibodies are found in 18% to 55% of these patients, anti-Mi-2 anti- bodies are found in 4% to 9%, anti-SRP antibodies are found in 4.8% to 11% of patients with autoimmune poly- myositis, and anti-PM-Scl antibodies are found in 25% of patients with concomitant polymyositis and scleroderma [8-10]. Although cancer-associated myopathy can be of inflammatory origin [11], we assume that a paraneoplastic etiology of the myositis in our patient is not probable. While cancer-associated myositis can ameliorate during cancer treatment [7], the treatment of cancer in our patient resulted in the development of clinical signs of myopathy. On the basis of his serum PSA and the fact that the size of the solitary node in his lung decreased during leuprolide acetate therapy, we assume that prostate cancer therapy was successful in our patient. We consider leuprolide acetate to be the cause of myopathy in our patient. We did not find an infectious cause of his myopathy. However, T lymphocytes were found. Thus, it is likely that a drug-induced T-lympho- cyte-mediated mechanism, not a direct toxic effect of leuprolide acetate, caused his muscle necrosis. We can- not explain the exact mechanism. Further studies are required to answer this question. To the best of our knowledge, this is the fourth such case reported in the literature. The three previously published cases manifested with proximal myopathy. While the muscle biopsy in the first case showed diffuse T-lymphocyte infiltration of the muscle and was treated with steroids [12], the biopsy in the second case revealed only mild, non-specific changes [13]. In the third case, no biopsy was performed [14]. In these three studies, the reported serum creatine kinase values were 2728 U/L, normal, and 1290 U/L, respectively, and within one to six months after leuprolide acetate therapy was discontinued, the patients’ symptoms of myopathy vanished. Renal failure did not occur. Conclusion In this case report, we highlight rare but severe side effects of leuprolide acetate therapy: inflammatory myo- pathy, severe rhabdomyolysis, and renal failure. To the best of our knowledge, this report describes the second case of leuprolide acetate-induced inflammatory myopa- thy and the first case of severe leuprolide acetate- induced rhabdomyolysis with renal failure. Consent Written informed consent was obtained from the patient for publication of this case report and any accompany- ing images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Acknowledgements We thank Professor Dr M Tolnay and Dr D Pfeiffer for providing us the histological images. Author details 1Department of Cardiology, Luzerner Kantonsspital, 6000 Luzern 16, Switzerland. 2Emergency Department, University Hospital Bern, 3010 Bern, Switzerland. Authors’ contributions MB and MR contributed equally to the case report. Both of them wrote the report and conducted the literature search. PE contributed to the discussion