Pitavastatin

Indications

Pitavastatin is used for: Hypercholesterolaemia, Hyperlipidaemias, Mixed dyslipidaemia, Cardiovascular disease,

Adult Dose

Oral Hypercholesterolemia Adult: 2 mg once daily. May increase to 4 mg qDay if necessary. Hepatic Impairment Contraindicated in active liver disease or unexplained transaminase elevations

Child Dose

Safety and efficacy not established

Renal Dose

Renal impairment: Moderate to severe (CrCl 15-60 mL/min, not on haemodialysis) and ESRD (on haemodialysis): Initial: 1 mg once daily. Max: 2 mg once daily.

Administration

May be taken with or without food.

Contra Indications

Patients with a known hypersensitivity to any component of this products. Pitavastatin is contraindicated in patients with active liver disease , which may include unexplained persistent elevations of hepatic transaminase levels.

Precautions

Patient w/ predisposing factors for myopathy; alcoholism. Renal impairment. Monitoring Parameters Monitor lipid panel (total cholesterol, HDL, LDL, triglycerides), hepatic transaminase levels; creatine phosphokinase (CPK). Lactation: Contraindicated

Pregnancy-Lactation

Interactions

Increased bioavailability w/ erythromycin and rifampicin. Increased risk of myopathy/rhabdomyolysis w/ gemfibrozil, colchicine, niacin and other fibrates. Potentially Fatal: Ciclosporin significantly increases pitavastatin exposure.

Adverse Effects

Side effects of Pitavastatin : Liver enzyme abnormalities, myalgia, muscle spasm, back pain, diarrhoea, constipation, pain in extremities, arthralgia, headache, dizziness, influenza, nasopharyngitis, abdominal discomfort, abdominal pain, dyspepsia, nausea, asthenia, malaise, fatigue, hepatitis, jaundice, hypoaesthesia, insomnia, depression, interstitial lung disease, erectile dysfunction, cognitive impairment (e.g. memory loss and impairment, confusion, forgetfulness, amnesia). Potentially Fatal: Myopathy and rhabdomyolysis w/ acute renal failure secondary to myoglobinuria; hepatic failure.

Mechanism of Action

HMG-CoA reductase inhibitor, inhibits rate-limiting step in cholesterol biosynthesis by competitively inhibiting HMG-CoA reductase