Creatine kinase (CK) should not be measured following strenuous exercise or in the presence of any plausible alternative cause of CK increase as this makes value interpretation difficult. If concomitant administration cannot be avoided, the lowest dose of atorvastatin to achieve the therapeutic objective should be used and the patients should be appropriately monitored (see section 4.4).The use of ezetimibe alone is associated with muscle related events, including rhabdomyolysis.

The risk of myopathy may also be increased with the concomitant use of gemfibrozil and other fibric acid derivates, antivirals for the treatment of hepatitis C (HCV) (boceprevir, telaprevir, elbasvir/grazoprevir), erythromycin, niacin, or ezetimibe.

Patients should be started with Atorvastatin 10 mg daily. When compared to pravastatin the effects of atorvastatin were statistically significant (p=0.02). Atorvastatin is effective in reducing LDL-C in patients with homozygous familial hypercholesterolaemia, a population that has not usually responded to lipid-lowering medicinal products.

Atorvastatin should be prescribed with caution in patients with pre-disposing factors for rhabdomyolysis. should be avoided if possible.

Patients who develop any signs or symptoms suggestive of liver injury should have liver function tests performed. The median percent change, from baseline, in total atheroma volume (the primary study criteria) was -0.4% (p=0.98) in the atorvastatin group and +2.7% (p=0.001) in the pravastatin group (n=249).

It's used to lower cholesterol if you've been diagnosed with high blood cholesterol.It's also taken to prevent heart disease, including heart attacks and strokes.Your doctor may prescribe atorvastatin if you have a family history of heart disease, or a long-term health condition such as type 1 or type 2 diabetes or rheumatoid arthritis. The atorvastatin dose was permitted to be doubled if a subject had not attained target LDL-C of < 3.35 mmol/L at Week 4 and if atorvastatin was well tolerated.Mean values for LDL-C, TC, VLDL-C, and Apo B decreased by Week 2 among all subjects. Cohort B included 24 children, 10 to 17 years of age and at Tanner Stage ≥ 2.The initial dose of atorvastatin was 5 mg daily of a chewable tablet in Cohort A and 10 mg daily of a tablet formulation in Cohort B. Metabolites of atorvastatin are substrates of OATP1B1. Atorvastatin was not found to be carcinogenic in rats, but high doses in mice (resulting in 6–11 fold the AUC 0–24h reached in humans at the highest recommended dose) showed hepatocellular adenomas in males and hepatocellular carcinomas in females. This site uses cookies. - If symptoms resolve and CK levels return to normal, then re-introduction of atorvastatin or introduction of an alternative statin may be considered at the lowest dose and with close monitoring. Atorvastatin is also used to help reduce the risk of having a heart attack or stroke in people who have high blood pressure and coronary heart disease (CHD) or who are at risk of CHD. Triglycerides and cholesterol in the liver are incorporated into very low-density lipoproteins (VLDL) and released into the plasma for delivery to peripheral tissues. Due to the dual interaction mechanism of rifampin, (cytochrome P450 3A induction and inhibition of hepatocyte uptake transporter OATP1B1), simultaneous co-administration of atorvastatin with rifampin is recommended, as delayed administration of atorvastatin after administration of rifampin has been associated with a significant reduction in atorvastatin plasma concentrations. Pharmacotherapeutic group: Lipid modifying agents, HMG-CoA-reductase inhibitors, ATC code: C10AA05 Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme responsible for the conversion of 3-hydroxy-3-methyl-glutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Should an overdose occur, the patient should be treated symptomatically and supportive measures instituted, as required. The effect of intensive lipid lowering on major cardiovascular endpoints was not investigated in this study. If CK levels are significantly elevated (> 5 times ULN) at baseline, treatment should not be started. Atorvastatin should be used with caution in patients with hepatic impairment (see sections 4.4 and 5.2). Atorvastatin was negative for mutagenic and clastogenic potential in a battery of 4 in vitro tests and 1 in vivo assay.