Product Overview
[Drug Name]
Trade Name: Simvastatin Tablets
Generic Name: Simvastatin Tablets
English Name: Simvastatin Tablets
[Indications]
1. Hyperlipidemia (1) For patients with primary hypercholesterolemia, heterozygous familial hypercholesterolemia, or mixed hypercholesterolemia, when dietary control and other non-drug treatments are not ideal, simvastatin can be used to reduce elevated total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, and triglycerides. Simvastatin also increases high-density lipoprotein cholesterol, thereby reducing the ratio of low-density lipoprotein/high-density lipoprotein and total cholesterol/high-density lipoprotein. (2) For patients with homozygous familial hypercholesterolemia, when dietary control and non-dietary treatments are not ideal, simvastatin can be used to reduce elevated total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B. 2. Coronary heart disease. (1) Reduce the risk of death. (2) Reduce the risk of death from coronary heart disease and non-fatal myocardial infarction. (3) Reduce the risk of stroke and transient ischemic attack. (4) Reduce the risk of myocardial revascularization surgery (coronary artery bypass grafting and percutaneous coronary angioplasty). (5) Delay the progression of atherosclerosis, including the occurrence of new lesions and total blockage.
[Main ingredient]
The main ingredient of this product and its chemical name is: simvastatin.
[Specification]
10mg*10 tablets
[Interaction]
1. When simvastatin is used in combination with other drugs that have a significant inhibitory effect on cytochrome P450 A4 at therapeutic doses (such as cyclosporine, mibefradil, itraconazole, ketoconazole, erythromycin, clarithromycin and nefazodone) or fibric acid derivatives or niacin, the risk of rhabdomyolysis is increased. 2. Concomitant use of this product with methylhydroxyglutaryl-Coenzyme A (HMG-CoA) reductase inhibitors may increase the incidence and severity of myopathy. These drugs include gemfibrozil and other fibrates, as well as lipid-lowering doses of niacin (≥1 g/day). Furthermore, elevated plasma levels of methylhydroxyglutaryl-Coenzyme A (HMG-CoA) reductase inhibitor activity may increase the risk of myopathy. Simvastatin and other methylhydroxyglutaryl-Coenzyme A (HMG-CoA) reductase inhibitors are metabolized by the cytochrome P450 isoenzyme 3A4. Several drugs that significantly inhibit this metabolic pathway at therapeutic doses can increase plasma levels of methylhydroxyglutaryl-Coenzyme A (HMG-CoA) reductase inhibitors and, therefore, increase the risk of myopathy. These drugs include cyclosporine, tetralins, the calcium channel blocker mibefradil, itraconazole, ketoconazole, and other antifungal azoles, the macrolide antibiotics erythromycin and clarithromycin, and the antidepressant nefazodone. 3. Coumarin derivatives: Clinical studies have shown that simvastatin can moderately enhance the anticoagulant effect of coumarin anticoagulants. Therefore, when adults begin early anticoagulant therapy and concurrently use simvastatin, the prothrombin time should be monitored frequently to ensure that the prothrombin time does not change significantly. Even after a stable prothrombin time has been achieved in patients taking coumarin derivatives, continued prothrombin time monitoring is recommended for a fixed period. The same procedure should be followed if the simvastatin dose is changed. Simvastatin therapy has not been reported to affect bleeding or prothrombin time in patients not taking anticoagulants.
[Precautions]
1. Patients should follow a standard cholesterol-lowering diet before and during simvastatin treatment. 2. Hepatic reactions. This drug should be used with caution in patients who consume significant amounts of alcohol and/or have a history of liver disease. Simvastatin should be contraindicated in patients with active liver disease or unexplained elevations in aminotransferases. In clinical trials, a small number of patients taking simvastatin experienced significant, persistent elevations in serum aminotransferases (over 3 times the normal value). However, after discontinuation of the drug, aminotransferase levels returned to pre-treatment levels, without jaundice, other concerning clinical signs or symptoms, or allergic reactions. Patients with elevated aminotransferases should be monitored closely before treatment. If the patient's aminotransferase levels continue to rise, particularly if the elevation exceeds 3 times the normal value and persists, the drug should be discontinued. As with other lipid-lowering drugs, moderate elevations in aminotransferases (less than 3 times the normal value) have also been reported in patients treated with simvastatin. These changes typically occur shortly after treatment with simvastatin, are generally transient, and are not associated with any symptoms, so discontinuation of the drug is not necessary. 3. Muscle Reactions: Mild, transient elevations in creatine kinase (CK, derived from skeletal muscle) are common in patients treated with simvastatin, but these elevations are not clinically significant. Myopathy should be considered in patients with diffuse myalgia, muscle weakness, and/or significant elevations in creatine kinase (CK) (greater than ten times the normal value). Patients should be instructed to report any unexplained signs of myopathy to their doctor immediately. Simvastatin treatment should be discontinued immediately if CK is significantly elevated or myalgia is diagnosed or suspected. Methylhydroxyglutaryl coenzyme A (HMG-CoA) reductase inhibitors should be discontinued in patients with acute or severe conditions suggestive of myopathy or those at risk for secondary acute renal failure due to rhabdomyolysis. 4. Ophthalmological examination. The incidence of lens opacities increases with age, even in the absence of any medication. Long-term clinical studies have shown that simvastatin has no adverse effects on the human lens. 5. Homozygous familial hypercholesterolemia. Because patients with homozygous familial hypercholesterolemia completely lack low-density lipoprotein (LDL) receptors, simvastatin is less effective in this patient population. 6. Hypertriglyceridemia. Simvastatin has only a moderate triglyceride-lowering effect and is not suitable for treating conditions characterized by elevated triglycerides (such as types I, IV, and V hyperlipidemia). 7. This drug should be used with caution in patients with excessive alcohol consumption and/or a history of liver disease.
[Dosage and Administration]
Patients should follow a standard cholesterol diet before starting simvastatin treatment and continue this diet during treatment. Hypercholesterolemia: The general initial dose is 10 mg daily, taken in the evening. For patients with mild to moderately elevated cholesterol levels, the initial dose is 5 mg daily. Dose adjustments should be made at least four weeks apart, with a maximum dose of 40 mg daily, taken in the evening. The simvastatin dose should be reduced when the LDL cholesterol level drops to 75 mg/dL (1.94 mmol/L) or the total cholesterol level drops below 140 mg/dL (3.6 mmol/L). Coronary Artery Disease: Patients with coronary artery disease can take 20 mg daily in the evening as a starting dose. If dose adjustment is necessary, refer to the instructions above (Usage and Dosage for Hypercholesterolemia). Concomitant Therapy: Simvastatin is effective when used alone or in combination with a bile acid sequestrant. For patients taking concomitant immunosuppressants, the recommended dose of simvastatin is 10 mg daily. Patients with Renal Impairment: Because simvastatin is not significantly excreted by the kidneys, no dosage adjustment is required for patients with moderate renal impairment. For patients with severe renal impairment (creatinine clearance [CQ] < 0.05), the dosage should be adjusted.
[Storage]
Store in a cool, dark, airtight container.
[Adverse Reactions]
Simvastatin is generally well tolerated, with most adverse reactions being mild and transient. In controlled clinical trials, fewer than 2% of patients discontinued simvastatin due to adverse reactions. In controlled clinical trials, adverse reactions (classified as possibly, suspected, or definitely) attributed to the drug with an incidence greater than or equal to 1% included abdominal pain, constipation, and flatulence. Adverse reactions with an incidence of 0.5% to 0.9% included fatigue, asthenia, and headache. Reports of myopathy are rare. The following adverse reactions have been reported in uncontrolled clinical trials or post-marketing use: nausea, diarrhea, rash, dyspepsia, pruritus, alopecia, dizziness, muscle cramps, myalgia, pancreatitis, paresthesia, and peripheral neuropathy. Symptoms of rhabdomyolysis, vomiting, and anemia, as well as rhabdomyolysis and hepatitis/jaundice, have rarely occurred. A significant hypersensitivity reaction syndrome, including one or more of the following features, has been reported rarely, including angioedema, lupus-like syndrome, polymyalgia rheumatica, vasculitis, thrombocytopenia, eosinophilia, elevated erythrocyte sedimentation rate (ESR), arthritis, arthralgia, urticaria, photosensitivity, fever, flushing, dyspnea, and malaise. Laboratory findings: Significant and persistent elevations of serum aminotransferases have been reported rarely. Liver function test abnormalities have been mild or transient. Elevations in serum creatine phosphokinase (CK), derived from skeletal muscle, have also been reported.
[Interactions]
1. The risk of rhabdomyolysis may increase when simvastatin is coadministered with other drugs that significantly inhibit cytochrome P450 A4 at therapeutic doses (e.g., cyclosporine, mibefradil, itraconazole, ketoconazole, erythromycin, clarithromycin, and nefazodone), or with fibric acid derivatives or niacin. Increased risk.
2. The incidence and severity of myopathy may be increased when this product is used in combination with methylhydroxyglutaryl-coenzyme A (HMG-COA) reductase inhibitors. These drugs include gemfibrozil and other fibrates, as well as lipid-lowering doses of niacin (greater than or equal to 1g/d). In addition, high plasma levels of methylhydroxyglutaryl-coenzyme A (HMG-COA) reductase inhibitor activity may also increase the risk of myopathy. Simvastatin and other methylhydroxyglutaryl-coenzyme A (HMG-COA) reductase inhibitors are metabolized by the cytochrome P450 isoenzyme 3A4. Several drugs that significantly inhibit this metabolic pathway at therapeutic doses can increase the blood levels of methylhydroxyglutaryl-coenzyme A (HMG-COA) reductase inhibitors and thereby increase the risk of myopathy. These drugs include cyclosporine, tetralins, the calcium channel blocker mibefradil, itraconazole, ketoconazole and other antifungal azoles, the macrolide antibiotics erythromycin and clarithromycin, and Nefazodone is an antidepressant.
3. Coumarin derivatives: Clinical studies have shown that simvastatin can moderately enhance the anticoagulant effect of coumarin anticoagulants. Therefore, when adults begin early anticoagulant therapy and concurrently use simvastatin, the prothrombin time should be checked frequently to ensure that the prothrombin time has not significantly changed. Even after a patient taking coumarin derivatives has achieved a stable prothrombin time, continued prothrombin time monitoring is recommended for a fixed period. If the simvastatin dose is changed, Follow the same procedure as above. Simvastatin therapy has not been reported to affect bleeding or prothrombin time in patients not taking anticoagulants.
[Contraindications]
1. Allergy to any ingredient.
2. Active hepatitis or unexplained persistent elevation of serum aminotransferases.
3. Concomitant use with the tetralin calcium channel blocker mibefradil.
[Manufacturer]
Shandong Lukang Pharmaceutical Group Saite Co., Ltd.
