HMG-CoA Reductase Inhibitors / Statins

How to Subscribe
MLS & MLT Comprehensive CE Package
Includes 146 CE courses, most popular
$95Add to cart
Pick Your Courses
Up to 8 CE hours
$50Add to cart
Individual course$20Add to cart
Need multiple seats for your university or lab? Get a quote
The page below is a sample from the LabCE course Pharmacology of Antihyperlipidemic Medications for Laboratory Professionals. Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

Learn more about Pharmacology of Antihyperlipidemic Medications for Laboratory Professionals (online CE course)
HMG-CoA Reductase Inhibitors / Statins

Drug examples: Atorvastatin, Simvastatin, Pravastatin. Drugs in this class share the suffix "statin."

Mechanism of action: Drugs in this class are HMG-CoA reductase inhibitors. Recall from a previous discussion that the enzyme HMG-CoA reductase is an essential enzyme in the cholesterol synthesis pathway. By inhibiting this enzyme, HMG-CoA reductase inhibitors decrease cholesterol levels. Clinical and scientific studies have demonstrated that statins also have an anti-inflammatory effect on the blood vessel wall, resulting in less atherosclerosis.

Use: Statins reduce LDL levels dramatically. High intensity statin therapy can reduce LDL cholesterol by as much as 50%. Reduction in the risk of coronary events, such as myocardial infarctions (MIs), have been demonstrated in patients who take statins. Furthermore, they have been shown to reduce the risk of ischemic stroke. The benefits from this drug are believed to be from both the anti-inflammatory and lipid lowering properties. Statins can also cause mild increases in HDL cholesterol and decrease triglyceride levels.

Drug toxicity: Muscle pain (myalgia) is the most common patient complaint with statins. An important laboratory application of statin therapy is the elevation of serum liver enzymes (AST and ALT). Clinicians will periodically order liver enzyme testing on patients taking statins to assess for this common side effect. It is important to realize that not all patients on statin therapy with elevated liver enzymes have hepatic damage. Having preexisting liver disease can lead to more dramatic changes in liver enzymes. A less common side effect is non-life-threatening muscle damage that leads to an increase in serum creatine kinase (CK) levels. An even less common side effect is rhabdomyolysis. In rhabdomyolysis, skeletal muscle breaks down rapidly and kidney damage occurs due to released myoglobin. In patients with rhabdomyolysis, a urine dip stick will be positive for blood (due to the similarities of myoglobin and hemoglobin) but no red blood cells (RBCs) are observed on microscopic analysis of the urine. CK levels will be in excess of 1,000 U/L due to extensive muscle breakdown.