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Rosuvastatin
Allopathy
Prescription Required
DCGI (Drugs Controller General of India)
Schedule H
Rosuvastatin is an HMG-CoA Reductase Inhibitor belonging to Antilipemic Agent.
Rosuvastatin is an HMG-CoA reductase inhibitor used to lower lipid levels and reduce the risk of cardiovascular disease including myocardial infarction and stroke.
The peak plasma concentrations of Rosuvastatin were reached 3 to 5 hours following oral dosing. Both Cmax and AUC increased in approximate proportion to the Rosuvastatin dose. The absolute bioavailability of rosuvastatin is approximately 20%. The mean volume of distribution at the steady state of rosuvastatin is approximately 134 liters. Rosuvastatin is 88% bound to plasma proteins, mostly albumin. Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as a metabolite. Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces (90%). The elimination half-life (t1/2) of rosuvastatin is approximately 19 hours. After an intravenous dose, approximately 28% of total body clearance was via the renal route, and 72% by the hepatic route.
Rosuvastatin shows common side effects like Constipation, stomach pain, Dizziness, difficulty falling asleep or staying asleep, Depression, joint pain, Headache, memory loss or forgetfulness, and confusion.
Rosuvastatin is available in the form of an Oral Tablet and Oral Capsule.
Rosuvastatin is available in India, the US, Singapore, the UK, Malaysia, Spain, Canada, Russia, Japan, China, and Australia.
Rosuvastatin belongs to the Antilipemic Agent and acts as an HMG-CoA Reductase Inhibitor.
Rosuvastatin inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis (reduces the production of mevalonic acid from HMG-CoA); this then results in a compensatory increase in the expression of LDL receptors on hepatocyte membranes and stimulation of LDL catabolism. In addition to the ability of HMG-CoA reductase inhibitors to decrease levels of high-sensitivity C-reactive protein (hsCRP), they also possess pleiotropic properties including improved endothelial function, reduced inflammation at the site of the coronary plaque, inhibition of platelet aggregation, and anticoagulant effects.
The Data on the onset and duration of action of Rosuvastatin is not clinically established.
The Tmax of Rosuvastatin is approximately 3-5 hours.
Rosuvastatin is available in the form of Oral tablets and Oral Capsules.
Rosuvastatin Tablet and Capsule are taken orally usually once daily.
Rosuvastatin is used in the treatment of high blood cholesterol and triglycerides (fats) levels. This medicine works by blocking the production of unhealthy fats in your body and prevents the risk of heart problems and stroke (a condition that causes reduced oxygen supply to the brain).
Rosuvastatin is an HMG-CoA Reductase Inhibitor belonging to Antilipemic Agent.
Rosuvastatin selectively and competitively inhibits 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis. It increases the number of hepatic LDL receptors on the cell surface, thereby enhancing the uptake and catabolism of LDL. It also decreases apolipoprotein B, and triglyceride and increases HDL concentrations.
Rosuvastatin is approved for use in the following clinical indications
Adult indication
- Heterozygous familial hypercholesterolemia
- Homozygous familial hypercholesterolemia
- Prevention of atherosclerotic cardiovascular disease
- Transplantation
Pediatric indication
- Heterozygous familial hypercholesterolemia
- Homozygous familial hypercholesterolemia
Adult Dose
- Heterozygous familial hypercholesterolemia
High-intensity therapy: Oral: Initial: 20 or 40 mg once daily; if 20 mg once daily is initiated and tolerated, increase to 40 mg once daily.
- Homozygous familial hypercholesterolemia
High-intensity therapy: Oral: 40 mg once daily.
- Prevention of atherosclerotic cardiovascular disease
- Primary prevention:
Patients without diabetes, 40 to 75 years of age, and with LDL-C 70 to 189 mg/dL:
ASCVD 10-year risk 5% to <7.5%:
Moderate-intensity therapy: Oral: 5 to 10 mg once daily to reduce LDL-C by 30% to 49%.
ASCVD 10-year risk ≥7.5% to <20%:
Moderate-intensity therapy: Oral: 5 to 10 mg once daily to reduce LDL-C by 30% to 49%; higher risk patients with multiple risk-enhancing factors may benefit from higher doses to reduce LDL-C by ≥50%.
ASCVD 10-year risk ≥20%:
High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated.
- Patients with diabetes:
40-75 years of age without additional ASCVD risk factors:
Moderate-intensity therapy: Oral: 5 to 10 mg once daily to reduce LDL-C by 30% to 49%.
ASCVD risk ≥20% or multiple ASCVD risk factors:
High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated.
Patients with LDL-C ≥190 mg/dL and 20 to 75 years of age:
High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated.
Secondary prevention in patients with established ASCVD (eg, coronary heart disease, cerebrovascular disease [ischemic stroke or transient ischemic attack], peripheral arterial disease)
High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated
- Transplantation
Transplantation, post heart (off-label use)
Oral: Initial: 5 mg once daily starting 1 to 2 weeks after transplant, regardless of baseline cholesterol levels; increase dose based on response, tolerability, and use of concomitant medications up to 20 to 40 mg once daily.
Transplantation, post kidney (off-label use)
Oral: Initial: 5 mg once daily; increase dose based on response, tolerability, and use of concomitant medications up to 10 mg once daily.
Pediatric Dose
- Heterozygous familial hypercholesterolemia
Children 8 to <10 years (females >1year postmenarche):
Oral: 5 to 10 mg once daily; maximum daily dose: 10 mg/day.
Children ≥10 years and Adolescents (females >1year postmenarche):
Oral: 5 to 20 mg once daily; maximum daily dose: 20 mg/day.
- Homozygous familial hypercholesterolemia
Children ≥7 years and Adolescents: Oral:
Initial dose: 20 mg once daily. Maximum daily dose in adults is 40 mg/day. Although higher doses have been used (ie, 80 mg/day), additional benefit has not been reported.
Rosuvastatin is available in various strengths as 5mg, 10mg, 20mg and 40mg.
Rosuvastatin is available in the form of Oral Tablet and Oral Capsule.
- Dosage Adjustment in Kidney Patient
CrCl ≥30 mL/minute/1.73 m2: No dosage adjustment necessary.
CrCl <30 mL/minute/1.73 m2: 5 to 10 mg once daily.
- Dosage Adjustment in Hepatic impairment Patient
There are no specific dosage adjustments provided.
Rosuvastatin is contraindicated in patients with
- Patients with a known hypersensitivity to any component of this product. Hypersensitivity reactions including rash, pruritus, urticaria, and angioedema have been reported with Rosuvastatin.
- Patients with active liver disease may include unexplained persistent elevations of hepatic transaminase levels.
- Pregnancy.
- Lactation. Limited data indicate that Rosuvastatin is present in human milk. Because statins have the potential for serious adverse reactions in nursing infants, women who require Rosuvastatin treatment should not breastfeed their infants.
- Diabetes mellitus
Small increases in HbA1c (mean: ~0.1%) and fasting blood glucose have been reported with rosuvastatin; however, the benefits of statin therapy far outweigh the risk of dysglycemia.
- Skeletal Muscle Effects
Cases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with HMG-CoA reductase inhibitors, including Rosuvastatin. These risks can occur at any dose level but are increased at the highest dose (40 mg). Rosuvastatin should be prescribed with caution in patients with predisposing factors for myopathy (e.g., age ≥65 years, inadequately treated hypothyroidism, renal impairment). The risk of myopathy during treatment with Rosuvastatin may be increased with concurrent administration of some other lipid-lowering therapies (fibrates or niacin), gemfibrozil, cyclosporine, atazanavir/ritonavir, lopinavir/ritonavir, or simeprevir. Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors, including rosuvastatin, coadministered with colchicine, and caution should be exercised when prescribing Rosuvastatin with colchicines. Rosuvastatin therapy should be discontinued if markedly elevated creatine kinase (CK-enzyme) levels occur, or myopathy is diagnosed or suspected.
- Hematuria/proteinuria
Hematuria (microscopic) and proteinuria have been observed; more commonly reported in adults receiving rosuvastatin 40 mg daily. Typically, transient and not associated with a decrease in renal function. Consider dosage reduction if unexplained hematuria and proteinuria persist.
- Myasthenia gravis
May rarely worsen or precipitate myasthenia gravis (MG); monitor for worsening MG if treatment is initiated.
- Proteinuria And Hematuria
In the Rosuvastatin clinical trial program, dipstick-positive proteinuria and microscopic hematuria were observed among Rosuvastatin-treated patients. These findings were more frequent in patients taking Rosuvastatin 40 mg when compared to lower doses of Rosuvastatin or comparator HMG-CoA reductase inhibitors, though it was generally transient and was not associated with worsening renal function. Although the clinical significance of this finding is unknown, a dose reduction should be considered for patients on Rosuvastatin therapy with unexplained persistent proteinuria and/or hematuria during routine urinalysis testing.
- Concomitant Coumarin Anticoagulants
Caution should be exercised when anticoagulants are given in conjunction with Rosuvastatin because of its potentiation of the effect of coumarin-type anticoagulants in prolonging the prothrombin time/INR. In patients taking coumarin anticoagulants and Rosuvastatin concomitantly, INR should be determined before starting Rosuvastatin and frequently enough during early therapy to ensure that no significant alteration of INR occurs.
Alcohol Warning
Consumption of alcohol is not recommended during treatment with Rosuvastatin as it may lead to liver damage and other undesired effects.
Breast Feeding Warning
It is not known whether rosuvastatin is excreted in human milk, but a small amount of another drug in this class does pass into breast milk. In rats, breast milk concentrations of rosuvastatin are three times higher than plasma levels; however, animal breast milk drug levels may not accurately reflect human breast milk levels. Because another drug in this class passes into human milk and because HMG-CoA reductase inhibitors have the potential to cause serious adverse reactions in nursing infants, women who require Rosuvastatin treatment should be advised not to nurse their infants.
Pregnancy Warning
Adverse events have been observed in some animal reproduction studies. There are reports of congenital anomalies following maternal use of HMG-CoA reductase inhibitors in pregnancy; however, maternal disease, differences in specific agents used, and the low rates of exposure limit the interpretation of the available data. Cholesterol biosynthesis may be important in fetal development; serum cholesterol and triglycerides increase normally during pregnancy. The discontinuation of lipid-lowering medications temporarily during pregnancy is not expected to have a significant impact on the long-term outcomes of primary hypercholesterolemia treatment. Rosuvastatin should be discontinued immediately if an unplanned pregnancy occurs during treatment.
Common Adverse effects
- Myalgia, diabetes mellitus, constipation, nausea, cystitis, increased serum alanine aminotransferase, increased serum transaminases (including increased serum alkaline phosphatase, increased serum bilirubin), dizziness, headache, arthralgia, asthenia, increased creatine phosphokinase in blood specimen, Abnormal thyroid function test, increased gamma-glutamyl transferase, increased serum glucose, Abdominal pain, Hematuria, proteinuria, Elevated glycosylated hemoglobin (HbA1c), Hypersensitivity reaction.
Rare Adverse effects
- Gynecomastia, Pancreatitis, Thrombocytopenia, Autoimmune hepatitis, hepatic failure, hepatitis, jaundice, Angioedema, Drug reaction with eosinophilia and systemic symptoms, immune-mediated necrotizing myopathy, Cognitive dysfunction (reversible; includes amnesia, confusion, memory impairment), depression, peripheral neuropathy, sleep disorder (including insomnia, nightmares), Myoglobinuria, myopathy, myositis, rhabdomyolysis, Renal failure syndrome, Interstitial pulmonary disease.
- Cyclosporine
Cyclosporine increased rosuvastatin exposure and may result in an increased risk of myopathy. Therefore, in patients taking cyclosporine, the dose of Rosuvastatin should not exceed 5 mg once daily.
- Gemfibrozil
Gemfibrozil significantly increased rosuvastatin exposure. Due to an observed increased risk of myopathy/rhabdomyolysis, combination therapy with Rosuvastatin and gemfibrozil should be avoided. If used together, the dose of Rosuvastatin should not exceed 10 mg once daily.
- Protease Inhibitors
Coadministration of rosuvastatin with certain protease inhibitors has differing effects on rosuvastatin exposure and may increase the risk of myopathy. Simeprevir, which is a hepatitis C virus (HCV) protease inhibitor, or combinations of atazanavir/ritonavir or lopinavir/ritonavir, which are HIV-1 protease inhibitors, increase rosuvastatin exposure. For these protease inhibitors, the dose of Rosuvastatin should not exceed 10 mg once daily. The combinations of fosamprenavir/ritonavir or tipranavir/ritonavir, which are HIV-1 protease inhibitors, produce little or no change in rosuvastatin exposure. Caution should be exercised when rosuvastatin is coadministered with protease inhibitors.
- Coumarin Anticoagulants
Rosuvastatin significantly increased INR in patients receiving coumarin anticoagulants. Therefore, caution should be exercised when coumarin anticoagulants are given in conjunction with Rosuvastatin. In patients taking coumarin anticoagulants and Rosuvastatin concomitantly, INR should be determined before starting Rosuvastatin and frequently enough during early therapy to ensure that no significant alteration of INR occurs.
- Niacin
The risk of skeletal muscle effects may be enhanced when Rosuvastatin is used in combination with lipid-modifying doses (≥1 g/day) of niacin; caution should be used when prescribing with Rosuvastatin.
- Fenofibrate
When Rosuvastatin was coadministered with fenofibrate, no clinically significant increase in the AUC of rosuvastatin or fenofibrate was observed. Because it is known that the risk of myopathy during treatment with HMG-CoA reductase inhibitors is increased with concomitant use of fenofibrates, caution should be used when prescribing fenofibrates with Rosuvastatin.
- Colchicine
Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors, including rosuvastatin, coadministered with colchicine, and caution should be exercised when prescribing Rosuvastatin with colchicine.
The common side effects of Rosuvastatin include the following
Common
● Constipation, stomach pain, Dizziness, difficulty falling asleep or staying asleep, Depression, joint pain, Headache, memory loss or forgetfulness, confusion.
Rare
● Muscle pain, tenderness, or weakness (or if these symptoms continue after stopping rosuvastatin), lack of energy, fever, chest pain, dark, reddish urine; decreased amount of urine; weakness; and muscle aches, yellowing of the skin or eyes, dark colored urine, pain in the upper right part of the abdomen, nausea, extreme tiredness, weakness, unusual bleeding or bruising, loss of appetite, flu-like symptoms, rash, hives, itching, difficulty breathing or swallowing, swelling of the face, throat, tongue, lips, eyes, hands, feet, ankles, or lower legs, hoarseness.
- Pregnancy
Pregnancy Category X
Teratogenic effects: Rosuvastatin is contraindicated in women who are or may become pregnant. Serum cholesterol and triglycerides increase during normal pregnancy, and cholesterol products are essential for fetal development. Atherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the long-term outcomes of primary hyperlipidemia therapy. There are no adequate and well-controlled studies of Rosuvastatin in pregnant women. There have been rare reports of congenital anomalies following intrauterine exposure to HMG-CoA reductase inhibitors. In a review of about 100 prospectively followed pregnancies in women exposed to other HMG-CoA reductase inhibitors, the incidences of congenital anomalies, spontaneous abortions, and fetal deaths/stillbirths did not exceed the rate expected in the general population. However, this study was only able to exclude a three-to-fourfold increased risk of congenital anomalies over background incidence. In 89% of these cases, drug treatment started before pregnancy and stopped during the first trimester when pregnancy was identified. Rosuvastatin crosses the placenta in rats and rabbits. In rats, Rosuvastatin was not teratogenic at systemic exposures equivalent to a human therapeutic dose of 40 mg/day. At 10-12 times the human dose of 40 mg/day, there was decreased pup survival, decreased fetal body weight among female pups, and delayed ossification. In rabbits, pup viability decreased, and maternal mortality increased at doses equivalent to the human dose of 40 mg/day. Rosuvastatin may cause fetal harm when administered to a pregnant woman. If the patient becomes pregnant while taking Rosuvastatin, the patient should be apprised of the potential risks to the fetus and the lack of known clinical benefits with continued use during pregnancy.
- Nursing Mothers
It is not known whether rosuvastatin is excreted in human milk, but a small amount of another drug in this class does pass into breast milk. In rats, breast milk concentrations of rosuvastatin are three times higher than plasma levels; however, animal breast milk drug levels may not accurately reflect human breast milk levels. Because another drug in this class passes into human milk and because HMG-CoA reductase inhibitors have the potential to cause serious adverse reactions in nursing infants, women who require Rosuvastatin treatment should be advised not to nurse their infants.
- Pediatric Use
The safety and effectiveness of Rosuvastatin in patients 10 to 17 years of age with heterozygous familial hypercholesterolemia were evaluated in a controlled clinical trial of 12 weeks duration followed by 40 weeks of open-label exposure. Patients treated with 5 mg, 10 mg, and 20 mg daily Rosuvastatin had an adverse experience profile generally similar to that of patients treated with a placebo. Although not all adverse reactions identified in the adult population have been observed in clinical trials of children and adolescent patients, the same warnings and precautions for adults should be considered for children and adolescents. There was no detectable effect of Rosuvastatin on growth, weight, BMI (body mass index), or sexual maturation in pediatric patients (10 to 17 years of age). Adolescent females should be counseled on appropriate contraceptive methods while on Rosuvastatin therapy. Rosuvastatin has not been studied in controlled clinical trials involving prepubertal patients or patients younger than 10 years of age. Doses of Rosuvastatin greater than 20 mg have not been studied in the pediatric population. In children and adolescents with homozygous familial hypercholesterolemia, experience is limited to eight patients (aged 8 years and above). In a pharmacokinetic study, 18 patients (9 boys and 9 girls) 10 to 17 years of age with heterozygous FH received single and multiple oral doses of Rosuvastatin. Both Cmax and AUC of rosuvastatin were like values observed in adult subjects administered the same doses.
- Geriatric Use
Of the 10,275 patients in clinical studies with Rosuvastatin, 3159 (31%) were 65 years and older, and 698 (6.8%) were 75 years and older. No overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. Elderly patients are at higher risk of myopathy and Rosuvastatin should be prescribed with caution in the elderly.
There is no specific treatment in the event of an overdose. In the event of an overdose, the patient should be treated symptomatically, and supportive measures instituted as required. Hemodialysis does not significantly enhance the clearance of rosuvastatin.
Pharmacodynamic
Rosuvastatin dose-dependently reduces elevated LDL cholesterol and reduces total cholesterol and triglycerides and increases HDL cholesterol. A therapeutic response to Rosuvastatin is evident within 1 week of commencing therapy and 90% of the maximum response is usually achieved in 2 weeks. The maximum response is usually achieved within 4 weeks and is maintained after that. Individualization of drug dosage should be based on the therapeutic response.
Pharmacokinetics
- Absorption
In clinical pharmacology studies in men, peak plasma concentrations of rosuvastatin were reached 3 to 5 hours following oral dosing. Both Cmax and AUC increased in approximate proportion to the Rosuvastatin dose. The absolute bioavailability of rosuvastatin is approximately 20%. Administration of Rosuvastatin with food did not affect the AUC of rosuvastatin. The AUC of rosuvastatin does not differ following evening or morning drug administration.
- Distribution
The mean volume of distribution at the steady state of rosuvastatin is approximately 134 liters. Rosuvastatin is 88% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations.
- Metabolism
Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as a metabolite. The major metabolite is N-desmethyl rosuvastatin, which is formed principally by cytochrome P450 2C9, and in vitro studies have demonstrated that N-desmethyl rosuvastatin has approximately one-sixth to one-half the HMG-CoA reductase inhibitory activity of the parent compound. Overall, greater than 90% of active plasma HMG-CoA reductase inhibitory activity is accounted for by the parent compound.
- Excretion
Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces (90%). The elimination half-life (t1/2) of rosuvastatin is approximately 19 hours. After an intravenous dose, approximately 28% of total body clearance was via the renal route, and 72% by the hepatic route.
- Kostapanos MS, Milionis HJ, Elisaf MS. An overview of the extra-lipid effects of rosuvastatin. Journal of cardiovascular pharmacology and therapeutics. 2008 Sep;13(3):157-74.
- Sexton TR, Wallace EL, Macaulay TE, Charnigo RJ, Evangelista V, Campbell CL, Bailey AL, Smyth SS. The effect of rosuvastatin on thromboinflammation in the setting of the acute coronary syndrome. Journal of thrombosis and thrombolysis. 2015 Feb;39(2):186-95.
- Luvai A, Mbagaya W, Hall AS, Barth JH. Rosuvastatin: a review of the pharmacology and clinical effectiveness in cardiovascular disease. Clinical Medicine Insights: Cardiology. 2012 Jan;6:CMC-S4324.
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