Chronic Creatine Kinase Elevation Not Associated with HMG-CoA Reductase Inhibitor Treatment

Lin, Jennifer; Ito, Matthew K.

doi:10.1345/aph.18120

Ann Pharmacother

1999

DOI: 10.1345/aph.18120

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Chronic Creatine Kinase Elevation Not Associated with HMG-CoA Reductase Inhibitor Treatment

Jennifer Lin

Matthew K. Ito²

Abstract: It is important to be aware of different causes for CK enzyme concentration elevation, especially when it is used as a monitoring parameter during HMG-CoA reductase inhibitor treatment. In a case of persistent elevated CK enzyme concentration without evidence of myositis, renal insufficiency may be a contributing factor and malignancy must be ruled out.

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Cited by 3 publications

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Serum Creatine Kinase Elevation in a Medical Department

Kodatsch¹,

Finsterer²,

Stöllberger³

2001

Acta Med Austriaca

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Serum creatine kinase (CK) levels are diagnostic markers for acute myocardial infarction. Many other causes however, including neuromuscular disorders, may induce serum CK elevation as well. Aim of the study was to investigate the prevalence of potential causes for serum CK elevation in a medical department. In particular we were interested in the recognition of patients in whom serum CK elevation was due to a neuromuscular disorder. Included in this prospective study were 100 consecutive patients in whom the CK level, determined at admission, was increased (> 70 IU/l in female, > 80 IU/l in male patients). After admission we looked for the presence of causes known to induce CK elevation. Patients with no potential cause for CK elevation were invited for follow-up investigations three months later. If no potential cause could be found and if CK was elevated again on this occasion, the patient was referred for a comprehensive neurological investigation. The prevalence of patients with CK elevation was 11.2%. The 100 patients (44 female, 56 male) were aged from 23 to 94 (mean 67) years. In 95% CK elevation was only up to 500 IU/l. The most frequent cause for serum CK elevation was acute myocardial infarction in 32%. Further frequent causes were drug intake (32%), fall (24%), haematoma (17%), intramuscular injection (16%) and malignancy (11%). In 61% of the cases at least two potential causes for serum CK elevation could be detected. Neuromuscular disorders were found in only 2%. This study shows that serum CK elevation occurs in 11% of patients admitted to a medical department and can be explained by acute myocardial infarction in only 32%. In almost two thirds of the patients, more than one potential cause for serum CK elevation can be found thus making CK elevation a rather unspecific finding. Neuromuscular disorders are rarely found as a cause of serum CK elevation in a medical department.

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Serum Creatine Kinase Elevation in a Medical Department

Kodatsch¹,

Finsterer²,

Stöllberger³

2001

Acta Med Austriaca

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Risk-benefit of HMG-CoA reductase inhibitors in the treatment of HIV protease inhibitor-related hyperlipidaemia

Penzak

Chuck²

2002

Expert Opinion on Drug Safety

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HIV protease inhibitors decrease mortality and improve quality of life in patients with HIV infection. However, these drugs have been associated with serum lipid elevations, which may pose an increased risk of cardiovascular disease and pancreatitis. Treatment of protease inhibitor-related hyperlipidaemia (PIH) is complicated by drug interactions, which significantly increase concentrations of most 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins). Although pravastatin and atorvastatin effectively lower cholesterol and triglyceride concentrations in HIV-infected patients, a significant number of patients did not achieve their National Cholesterol Education Program low density lipoprotein concentration goals. Nonetheless, due to the increased risk of rhabdomyolysis with elevated statin concentrations, atorvastatin should be considered a second-line agent. The limited available PIH data supports the fact that pravastatin and atorvastatin are well-tolerated in HIV-infected individuals. More data are needed on the appropriate starting doses, maximum safe doses, role of combination statin-fibrate therapy, documentation of coronary heart disease benefit and incidence of myotoxicity and hepatotoxicity. Pravastatin has an acceptable risk-benefit ratio in PIH, while theoretical toxicity concerns exist with atorvastatin.

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COX-2 selective inhibitors: analysis of the renal effects

Perazella¹

2002

Expert Opinion on Drug Safety

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COX-2 selective inhibitors provide analgesia and blunt inflammation while also sparing the gastrointestinal tract from classic NSAID toxicity. Therapeutic effects are thought to result from inhibition of the inflammatory COX-2 isoform. Organ sparing is considered the result of preservation of homeostatic COX-1 enzyme function. Similar roles of the COX isoforms in the kidney would reduce NSAID-associated nephrotoxicity. However, human kidney tissue expresses COX-2 enzyme, suggesting a role for this isoform in maintenance of physiological renal processes. Available clinical data on the renal effects of COX-2 selective inhibitors in humans also demonstrate nephrotoxic potential.

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Chronic Creatine Kinase Elevation Not Associated with HMG-CoA Reductase Inhibitor Treatment

Cited by 3 publications

References 17 publications

Serum Creatine Kinase Elevation in a Medical Department

Serum Creatine Kinase Elevation in a Medical Department

Risk-benefit of HMG-CoA reductase inhibitors in the treatment of HIV protease inhibitor-related hyperlipidaemia

COX-2 selective inhibitors: analysis of the renal effects

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