primobolan acetate

Primobolan acetate agent derived synthetically from a fermentation product of Aspergillus terreus, is an inactive lactone, is hydrolyzed in the body to form a hydroxy-acid derivative. Active metabolite inhibits 3-hydroxy-Z-methyl-glutaryl-CoA reductase (HMG-CoA reductase), an enzyme that catalyzes the initial reaction of mevalonate HMG-CoA. Since the conversion of HMG-CoA to mevalonate is an early step in cholesterol synthesis, the use of primobolan acetate does not cause accumulation in the body is potentially toxic sterols. HMG-CoA is easily metabolized to acetyl-CoA, which is involved in many processes of primobolan acetate synthesis in the body. Reduces triglycerides (TG), low density lipoprotein (LDL), very low density lipoprotein (VLDL) cholesterol and total cholesterol in the blood plasma (in the case of heterozygous familial and non-familial forms of hypercholesterolemia, in mixed hyperlipidemia where cholesterol increased content of a risk factor). Reduces the ratio of LDL / HDL cholesterol (HDL-C) and total cholesterol / HDL ratio. The onset of action – within 2 weeks from the start of the reception, the maximum therapeutic effect is reached after 4-6 weeks. Action is maintained primobolan half life with continued treatment; upon termination of therapy, cholesterol returned to baseline (pre-treatment).


Absorption of primobolan acetate high. After oral administration the maximum plasma concentration is reached after 1,3-2,4 hours and reduced by 90% after 12 hours.Communication with plasma proteins is 95%. primobolan acetate is metabolized in the liver, it has the effect of “first pass” through the liver (mainly hydrolysed to its active form beta-hydroxy acid, and discovered other active and inactive metabolites). The half-life of the active metabolite is 1.9 h. Write mainly with faeces (60%) in the form of metabolites. Approximately 10-15% is excreted by the kidneys in an inactive form.

Indications Primary Hypercholesterolemia IIa and Type IIb (with the ineffectiveness of diet therapy in patients at increased risk of coronary atherosclerosis), combined hypercholesterolemia and hypertriglyceridemia, hyperlipoproteinemia, not amenable to correction special diet and exercise. Myocardial Infarction Prevention (to slow the progression of coronary atherosclerosis) stroke and transient ischemic attacks.

Contraindications : Hypersensitivity to the drug, increased sensitivity to other drugs statin series (HMG-CoA reductase), a history of liver failure, acute liver disease, increased activity of “liver” transaminases of unknown origin; pregnancy; lactation, age 18 years (safety and efficacy not established). Be wary appoint patients who abuse alcohol and / or have a history of liver disease; transplant patients undergoing immunosuppressive therapy (due to an increased risk of rhabdomyolysis and renal failure); in conditions that can lead to severe renal insufficiency primobolan cycle results, such as hypotension, acute infectious diseases heavy currents expressed metabolic and endocrine disorders, disorders of water and electrolyte balance, surgery (including dental), or injury; patients with low or high tone of the skeletal muscles of unknown etiology; epilepsy.

Dosage and administration The tablets are taken orally, once in the evening. In mild to moderate hypercholesterolemia starting dose is 5 mg; in severe hypercholesterolemia initial dose – 10 mg / day; if necessary, the dose can be increased not earlier than 4 weeks, the maximum daily dose – 80 mg. In ischemic heart disease starting dose is 20 mg (once in the evening); if necessary, gradually increased every 4 weeks to 40 mg. If the LDL content of less than 75 mg / dl (1.94 mmol / L), and -less total cholesterol 140 mg / dl (3.6 mmol / L), the dose should be reduced. In patients with chronic renal failure (creatinine clearance less than 30 ml / min) or receiving cyclosporine, fibrates, nicotinamide, the initial dose is 5 mg, the maximum daily dose -. 10 mg against immunosuppressive therapy recommended starting dose of 5 mg per day, the maximum daily dose is 5 mg per day. in the case of skip the current drug dose must be taken as soon as possible. If you come during the next dose, do not double the dose.

Side effect From the digestive system : dyspepsia (nausea, vomiting, gastralgia, abdominal pain, constipation or diarrhea, flatulence), hepatitis, jaundice, increased activity of “liver” transaminases, alkaline phosphatase, and creatinine phosphokinase (CPK); -ostry rarely pancreatitis. From the nervous system and sensory organs : asthenic syndrome, dizziness, headache, insomnia, convulsions, paresthesia, peripheral neuropathy, blurred vision, taste disturbance. On the part of the musculoskeletal system : myopathy, myalgia, muscle weakness ; rarely – rhabdomyolysis. Allergic and immunopathological reactions : angioedema, lupus-like syndrome, polymyalgia rheumatica, vasculitis, thrombocytopenia, eosinophilia, increased ESR, arthritis, arthralgia, urticaria, photosensitivity, fever, flushing of the skin, “tides” of blood to the skin of the face, shortness of breath. Dermatological reactions : skin rash, pruritus, alopecia. Other : anemia, palpitation, acute renal failure (due to rhabdomyolysis), reduced potency.


Treatment: If overdose is necessary to induce vomiting, take activated charcoal, symptomatic therapy. It is necessary to monitor liver and kidney function, the concentration of CK in the blood serum.

Interaction with other drugs increases the effects of anticoagulants and increases the risk of bleeding. Cytotoxic agents, antifungals (ketoconazole, itraconazole), fibrates, high doses of nicotinic acid, immunosuppressants, erythromycin, clarithromycin, protease inhibitors increase the risk of rhabdomyolysis. primobolan acetate improves the concentration of digoxin in the blood plasma. Cholestyramine and colestipol reduce bioavailability (perhaps through the use Aterostata 4 hours after the administration of these drugs, while noting additive effect).

Specific guidance Before treatment is necessary to carry out a study of liver function (to control the activity of “liver” transaminases every 6 weeks during the first 3 months, then every 8 weeks for the remainder of the first year, and then one every six months). Patients receiving Aterostat a daily 80 mg, 1 liver function monitored every 3 months. In cases when the activity of “liver” transaminase increases (exceeding 3 times the upper limit of normal), treatment is canceled. In patients with myalgia, myasthenia and / or marked increase in CPK drug treatment is stopped. Aterostat (as well as others. GMG inhibitors CoA reductase inhibitors) should not be applied at increased risk of rhabdomyolysis and renal failure (due to severe acute infection, hypotension, major surgery, trauma, severe metabolic disorders). Cancel lipid-lowering drugs during pregnancy has no significant effect on long-term treatment of primary hypercholesterolemia. Due to the fact that inhibitors of HMG-CoA reductase inhibitors inhibit the synthesis of cholesterol and cholesterol and other products of its synthesis play an essential role in the development of the fetus primobolan dosage, including the synthesis of steroids and cell membranes, primobolan acetate may have adverse effects on the fetus when assigning it to pregnant women (women of childbearing age should avoid conception). If in the course of treatment there is a pregnancy, the drug should be discontinued, and the woman warned of the possible danger to the fetus. Aterostat not shown in those cases where there is hypertriglyceridemia I, IV and V types. The drug is effective as a monotherapy and in combination with bile acid sequestrants. Before and during the course of treatment the patient should be on hypolipidemic diet. Patients with severe renal insufficiency treatment is carried out under the control of renal function. Patients are advised to promptly report unexplained muscle pain, weakness or weakness, particularly if accompanied by malaise or fever. steroiden kaufen

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