The patient is a 44y old male of mixed black African and white ethnicity with Type 2 diabetes diagnosed in late 2006.
His GP checked his CK prior to starting simvastatin last year and found an activity of 1289 iu/L (Siemens Advia RR 30-210 iu/L). Allowing for sex and ethnicity I would not expect an activity greater than about 380 (unless you can advise differently). Further investigations at the time showed him to be euthyroid; Anti-Nuclear Antibodies were negative, and both C-reactive protein and cardiac troponin I were undetectable.
He appears to have been put on simvastatin anyway and the CK rose to 2153iu/L but his ALT remained unchanged. Serum biochemical indicators of liver and renal function have remained unremarkable.
After the statin was stopped the CK fell to 559iu/L ('half life' 105 days) in April. With this result the AST was 24 (<40)iu/L; the LDH 294 (<430)iu/L and the CK isoenzymes were predominantly CK-MM with a trace of CK-MB and no macro-CK. In May his HbA1c was 9.7 (<6.5)% and urine albumin/creatinine 33.4 (<2.5)mg/mmol. His most adverse total:HDL cholesterol ratio has been 6.6.
The patient has remained clinically well throughout with neither signs nor symptoms of myopathy. He does not exercise excessively and denies recreational drug use. The only patient with muscle glycogenosis and diabetes I have seen previously experienced pain and muscle swelling on exertion.
The reason for the elevated CK remains unexplained. Whilst this must presumably be due to muscle damage, I was surprised that other muscle enzymes were not raised. Unfortunately these were not measured whilst the CK peaked.
What else might be the cause of the raised CK?
Should he recommence statin therapy?
Would further investigations be helpful?
All views, comments and suggestions will be gratefully received and collated anonymously if offered privately.
Consultant Chemical Pathologist
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