Atorvastatin Thesis

Numerous epidemiological studies and randomized controlled trials have documented the association between elevated LDL-C levels with increased CVD risk in both diabetic and nondiabetic populations [8, 9].Thus reducing LDL-C levels is the primary goal of therapy for diabetic dyslipidemia [5, 10].

Essentially, T2DM lipid profiles consist of elevations in triglyceride (TG) levels (2 mmol/L) and reductions in high-density lipoprotein cholesterol (HDL-C).

While low-density lipoproteins cholesterol (LDL-C) concentration levels are normal, the particles are denser and smaller in size, which is believed to enhance their atherogenic potential [7].

Atorvastatin reduced LDL-C the most at a dose of 40 mg (22.8%), and pravastatin reduced LDL-C the most at a dose of 20 mg (20.3%).

All three statins were safe in relation to muscular and hepatic functions.

The matrix effects of plasma were in the range of 102.7–105.5% for atorvastatin and 90.3–96.6% for atorvastatin lactone.

This method was successfully applied in clinical studies of atorvastatin in coronary artery disease patients.

More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-Co A) Reductase, which catalyzes the conversion of HMG-Co A to mevalonic acid.

This is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as "bad cholesterol"), and very low-density lipoprotein (VLDL).

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