testosterone enanthate cycle

After repeated daily administration testosterone enanthate cycle of the drug pharmacokinetic parameters change occurs. Genetic polymorphism inhibitors  reductase inhibitors, including rosuvastatin, transport proteins bind  (organic anion transport polypeptide involved in the capture of statins hepatocytes) and  (efflux transporter). Carriers genotypes  marked increase exposure ( – area under the curve “concentration – time”) rosuvastatin in 1.6 and 2.4 times, respectively, compared .

Special patient populations Age and gender Age and gender identity does not have a clinically significant effect on the pharmacokinetic parameters of rosuvastatin. Ethnic groups Pharmacological studies have shown approximately a two-fold increase in  and C median max of rosuvastatin in patients Mongoloid race  compared with rates in Caucasians; in Hindu patients showed an increase in median approximately 1.3 times. In this analysis of the pharmacokinetics parameters for the entire study population revealed no clinically relevant differences in pharmacokinetics among Caucasian and Negroid races. Renal insufficiency In patients with renal insufficiency of mild to moderate severity value of the plasma concentration of rosuvastatin  does not change significantly. In patients with severe renal failure testosterone enanthate cycle rosuvastatin plasma concentration of 3-fold higher concentration times higher than in healthy volunteers. The concentration of rosuvastatin in the blood plasma of patients on hemodialysis, approximately 50% higher than in healthy volunteers. Hepatic impairment In patients with varying degrees of hepatic failure with a score of 7 or less on the scale h revealed no increase in T 1/2 rosuvastatin . However, 2 patients noted extension of T 1/2 , approximately 2-fold higher than in patients with lower scores . Experience in the use of rosuvastatin in patients with a score of higher than 9 on the scale  is absent.


• Primary Hypercholesterolemia classification Fredrickson (type IIa including familial heterozygous hypercholesterolemia) or mixed hypercholesterolaemia (type IIb) as an adjunct to diet when diet and other non-drug treatments are not sufficient;
• the family homozygous hypercholesterolemia as an adjunct to diet and other lipid-lowering therapy (eg, apheresis), or when such treatment is not effective enough;
• hypertriglyceridemia (IV type classification Fredrickson) as an adjunct to diet;
• to slow the progression of atherosclerosis as an adjunct to diet in patients who have shown therapy to reduce the concentration of total cholesterol and testosterone enanthate cycle.
• primary prevention of major cardiovascular events (stroke, heart attack, unstable angina, arterial revascularization) in adult patients without clinical testosterone enanthate cycle evidence of coronary heart disease, but with an increased risk of its development (age over 50 years in men older than 60 years for women, the increased concentration of C-reactive protein (≥ 2 mg / l) in the presence of at least one additional risk factor, such as hypertension, low concentrations , smoking, family history of early beginning ).