primobolan

It is a decrease in plasma concentrations of triglycerides , low density lipoproteins , very low density lipoproteins  and total cholesterol . (with heterozygous familial and non-familial hypercholesterolemia, in mixed hyperlipidemia where the increased concentration of cholesterol in blood plasma is a risk factor)
Increasing the concentration of high density lipoprotein and reduces the ratio  cholesterol and total primobolan ratio in the blood plasma.
Starting manifestations effect – 2 weeks from the start of application, the maximum therapeutic effect is achieved after 4 – 6 weeks of therapy. Action is maintained with continued treatment, at the termination of treatment cholesterol concentration in blood plasma is gradually returning to its original value.  Simvastatin is well absorbed from the gastrointestinal tract. Food does not affect the absorption of simvastatin. After oral administration the maximum concentration is reached about 1-2 hours in the blood plasma and reduced by 90% after 12 h. Binding to plasma proteins is greater than 95%.Not accumulates. Extensively metabolized in the liver (hydrolyzed to form primary active derivative – beta-hydroxyacids and four other active metabolites). Excreted mainly as metabolites intestine (60%) for 4 days, 13% of kidney in an inactive form.

Patients with renal impairment Because primobolan simvastatin is excreted by kidneys in small numbers, there is no need for dose adjustment in patients with impaired renal and mild to moderate severity function. However, in patients with severe renal impairment (creatinine clearance of less than 30 ml / min), simvastatin should be used with caution. The initial dose of the drug in such cases should be 5 mg per day. It should be used with caution in doses above 10 mg / day, and if any doses deemed necessary, patients should be under close medical supervision. Patients of advanced age (over 65) The need for dose adjustment is not available.

 

Indications

Hypercholesterolemia (for patients older than 18 years):
• as an adjunct to diet when diet alone, and other non-pharmacological treatments is not enough to:
– reduce elevated concentrations of total cholesterol,  cholesterol, triglycerides, apolipoprotein B (apo B);
– increasing  cholesterol in patients with primary hypercholesterolaemia, including heterozygous familial hypercholesterolaemia (hyperlipidemia IIa type classification Fredrickson) or mixed hypercholesterolaemia (hyperlipidemia, type IIb Fredrickson classification);
• hypertriglyceridemia (hyperlipidemia type IV classification Frederickson);
• an adjunct to diet and other methods of treating patients with homozygous familial hypercholesterolemia to reduce elevated concentrations of total cholesterol;
• the primary disbetalipoproteinemiya (hyperlipidemia type III classification Fredrickson). patients with coronary heart disease  or high risk of cardiovascular complications (for patients older than 18 years) patients with a high risk of cardiovascular complications (if hyperlipidemia and without it), for example, patients with ischemic heart disease or predisposition to coronary artery disease, diabetes, stroke or other cerebrovascular disease history, patients with peripheral vascular disease is shown for the purpose of: • reducing the risk of total mortality by reducing as a result of coronary heart disease mortality; • reduce the risk of serious cardiovascular and coronary events:    – non-fatal myocardial infarction    – coronary death;    – stroke ;    – revascularization procedures. • reducing the risk of the need for operations to restore coronary blood flow; • reducing the risk of the need for recovery operations in peripheral blood flow and other non-coronary revascularization; • reduction in the risk of hospitalization due to primobolan angina. Use in children and adolescents 10 – 17 age with heterozygous familial hypercholesterolemia: t simultaneously with diet shown to reduce elevated concentrations of total cholesterol,  cholesterol, triglycerides, apo B in boys 10 – 17 years and girls 10 – 17 years at least 1 year after menarche, with heterozygous familial hypercholesterolemia.

 

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