Product Overview
[Drug Name]
Generic Name: Rosuvastatin Calcium Tablets
Trade Name: Erunda Rosuvastatin Calcium Tablets 10mg x 14 Tablets
[Main Ingredients]
The active ingredient of this product is rosuvastatin calcium. Chemical Name: Bis-[{E)-7-[4-(4-fluorophenyl)-6-isopropyl-2-{methyl(methylsulfonyl)amino]-pyrimidin-5-yl]|(3R,5)-3,5-dihydroxyhept-6-enoic acid] calcium salt (2:1) Molecular Formula: (C22H27FN3O6S)2Ca Molecular Weight: 1001.13
[Properties]
This product is a film-coated tablet that appears white or off-white after removal of the coating.
[Indications/Main Functions]
This product is indicated for patients with primary hypercholesterolemia (type Ia, including heterozygous familial hypercholesterolemia) or mixed dyslipidemia (type Ib), whose dyslipidemia is inadequately controlled with diet and other non-drug therapies (e.g., exercise therapy, weight loss). This product is also indicated for patients with homozygous familial hypercholesterolemia as an adjunct to diet and other lipid-lowering measures (e.g., LDL-C depletion therapy), or when these measures are inadequate.
[Specifications]
10mg x 14 tablets
[Dosage and Administration]
Before treatment begins, patients should follow a standard cholesterol-lowering diet and maintain this diet during treatment. The use of this product should be individualized, taking into account the patient's individual cholesterol level, expected cardiovascular risk, and potential risk of adverse reactions. For oral administration, the usual starting dose is 5 mg once daily. The selection of the starting dose should be based on the patient's individual cholesterol level, expected cardiovascular risk, and potential risk of adverse reactions. For patients requiring more robust low-density lipoprotein cholesterol (LDL-C) lowering, a starting dose of 10 mg once daily can be considered. This dose controls lipid levels in most patients. If necessary, the dose can be adjusted to the next higher dose level after 4 weeks of treatment. The maximum daily dose of this product is 20 mg. This product can be taken at any time of day, with or without food. Patients with Renal Impairment: No dose adjustment is required for patients with mild and moderate renal impairment. All doses of this product are contraindicated in patients with severe renal impairment. Patients with Hepatic Impairment: Systemic exposure to rosuvastatin was not increased in subjects with a Child-Pugh score of 7 or less. Increased systemic exposure was observed in subjects with Child-Pugh scores of 8 and 9. In these patients, renal function should be evaluated. There is no experience with the use of this product in patients with a Child-Pugh score of 9 or higher. This product is contraindicated in patients with active liver disease. Ethnicity: Increased systemic exposure has been observed in subjects of Asian descent. This factor should be considered when determining the dosage for patients of Asian descent. Dosage recommendations for patients with predisposing factors for myopathy: The recommended starting dose for patients with predisposing factors for myopathy (see [Precautions]) is 5 mg.
[Adverse Reactions]
See the package insert for details.
[Contraindications]
This product is contraindicated in patients with: Hypersensitivity to rosuvastatin or any of its ingredients; Active liver disease, including unexplained persistent elevations in serum transaminases and any elevation in serum transaminases exceeding three times the upper limit of normal (ULN); Severe renal impairment (creatinine clearance <30 ml/min); Myopathy; Concomitant use of cyclosporine; Pregnancy, lactation, and women of childbearing potential who are not using adequate contraception.
[Precautions]
Renal Effects:Proteinuria (as measured by dipstick) has been observed in patients treated with high doses, particularly 40 mg. The protein is primarily derived from the renal tubules and, in most cases, is transient or intermittent. Proteinuria is not considered a precursor to acute or progressive renal disease (see Adverse Reactions). Skeletal Muscle Effects: Skeletal muscle effects, such as myalgia, myopathy, and, rarely, rhabdomyolysis, have been reported in patients treated with all doses of ezetimibe, particularly in doses greater than 20 mg. Extremely rare cases of rhabdomyolysis have been reported with the concomitant use of ezetimibe and HMG-CoA reductase inhibitors. Drug interactions cannot be ruled out; caution should be exercised when these drugs are used together. Creatine kinase (CK) testing should not be performed after strenuous exercise or in the presence of plausible causes of elevated CK, as this can confound interpretation of the results. If baseline CK values are significantly elevated (>5×ULN), retesting should be performed within 5 to 7 days. If repeat testing confirms a baseline creatine kinase value >5×ULN, treatment should not be initiated. As with other HMG-CoA reductase inhibitors, caution should be exercised in patients with predisposing factors for myopathy/rhabdomyolysis. These factors include: renal impairment, hypothyroidism, personal or family history of hereditary muscle disorders, a history of muscle toxicity with other HMG-CoA reductase inhibitors or fibrates, alcohol abuse, and age >70 years. For patients who are taking fibrates concurrently, the potential benefits of treatment should be balanced against the potential risks, and clinical monitoring is recommended. Treatment should not be initiated if the baseline creatine kinase value is significantly elevated (>5×ULN). During treatment, patients should be instructed to immediately report unexplained muscle pain, weakness, or cramping, especially if accompanied by malaise and fever. Creatine kinase levels should be measured in these patients, and treatment should be discontinued if the creatine kinase value is significantly elevated (>5×ULN) or if muscle symptoms are severe and cause daylong malaise (even if the creatine kinase value is ≤5×ULN). If symptoms resolve and creatine kinase levels return to normal, consider restarting levofloxacin or switching to the lowest dose of another HMG-CoA reductase inhibitor with close observation. Regular monitoring of creatine kinase levels is not necessary for asymptomatic patients. Rare reports of immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, have been associated with statin use. IMNM is characterized by proximal muscle weakness and elevated serum creatine kinase, which persists despite discontinuation of statin therapy. Muscle biopsy reveals a necrotizing myopathy without significant inflammation; the condition improves with immunosuppressive therapy. In clinical studies, there was no evidence of increased effects on skeletal muscle in the small number of patients receiving levofloxacin concurrently with other therapies. However, an increased incidence of myositis and myopathy has been observed in patients receiving other HMG-CoA reductase inhibitors concomitantly with fibric acid derivatives (including gemfibrozil), cyclosporine, niacin, azole antifungals, protease inhibitors, or macrolide antibiotics. Concomitant use of gemfibrozil with some HMG-CoA reductase inhibitors can increase the risk of myopathy. Therefore, coadministration of this drug with gemfibrozil is not recommended. The benefits of combining this drug with fibrates or niacin to further improve lipid levels should be carefully weighed against the potential risks of this combination. Coadministration of rosuvastatin with fusidic acid is not recommended. Rhabdomyolysis (including fatalities) has been reported in patients receiving this combination. (See Drug Interactions.) This drug should not be used in any patient with an acute, severe illness suggestive of myopathy or with renal failure that predisposes to rhabdomyolysis (e.g., sepsis, hypotension, major surgery, trauma, severe metabolic, endocrine, or electrolyte abnormalities, or uncontrolled epilepsy). Similar to other HMG-CoA reductase inhibitors, this drug should be used with caution in patients who consume excessive alcohol and/or have a history of liver disease. Liver function tests are recommended before and three months after initiation of treatment. If serum transaminases increase more than three times the upper limit of normal, this drug should be discontinued or the dose reduced. For hypercholesterolemia secondary to hypothyroidism or nephrotic syndrome, the underlying condition should be treated before initiating this drug. Ethnic pharmacokinetic studies have shown that Asian subjects have higher drug exposure than Caucasians. Protease inhibitors: Increased systemic exposure of rosuvastatin has been observed in subjects receiving rosuvastatin concomitantly with various protease inhibitors (combined with ritonavir). The lipid-lowering benefits of this drug in HIV patients receiving protease inhibitors should be carefully considered, as should the potential for increased rosuvastatin plasma concentrations with concomitant protease inhibitor therapy. Coadministration of this drug with protease inhibitors is not recommended unless the dose of this drug is adjusted. Lactose intolerance: Patients with rare hereditary conditions such as galactose intolerance, lactase deficiency, or glucose-galactose malabsorption should not take this drug. Interstitial lung disease: Rare cases of interstitial lung disease have been reported with some statin therapy, particularly long-term. Symptoms include dyspnea, a dry, nonproductive cough, and a decline in overall health status (fatigue, weight loss, and fever). Statin therapy should be discontinued in patients suspected of developing interstitial lung disease. In patients with diabetes, use of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (including this product) has been reported to be associated with elevated glycated hemoglobin A1C (HbA1C) and fasting serum glucose levels. Clinical and biochemical monitoring should be performed in accordance with relevant guidelines for at-risk patients (fasting plasma glucose: 5.6-6.9 mmol/L, BMI >30 kg/m2, elevated triglycerides, and hypertension). Pediatric Patients: Rosuvastatin is limited to one year for pediatric patients aged 10-17 years who are at the stage of secondary sexual maturity according to Tenner staging, as assessed by linear growth (height), weight, and BMI (body mass index). After 52 weeks of study treatment, there were no effects on growth, weight, BM, or sexual maturation. Clinical trial experience in children and pediatric patients is limited, and the long-term (greater than one year) efficacy of rosuvastatin in adolescent patients is unknown. In 52-week clinical trials, pediatric and adolescent patients treated with rosuvastatin experienced elevations of creatine kinase greater than 10×ULN and muscle symptoms following exercise or increased physical activity more frequently than in adult clinical trials (see Adverse Reactions). Effects on Driving and Operating Machinery: Studies to determine the effects of this product on driving and operating machinery have not been conducted. However, based on its pharmacodynamic properties, this product is unlikely to affect these abilities. The potential for dizziness during treatment should be considered when driving and operating machinery.
