HMG-CoA reductase inhibitors are a class of drugs that are sued to lower lipids. They work by inhibiting the action of Enzyme HMG-CoA reductase that plays a central role in the manufacturing and production of cholesterol in the human body. HMG-CoA reductase inhibitors include Pitavastatin, Rosuvastatin, lovastatin, Fluvastatin, and Simvastatin (Goldstein and Michael 163). These medications are often referred to as Statins. They are used to reduce the amount of cholesterol production in the body. High levels of cholesterol or hypercholesterolemia are linked to coronary heart disease. Statins are the most effective class of drugs that are used to lower the levels of cholesterol in the body. This helps reduce the risk of cardiovascular disease in those who are at high risk like elderly people like the patient in our case. This class of medication is effective in managing early stages of the cardiovascular disease and in those with an elevated risk of having the disease like the patient in our case (Goldstein and Michael 163).
Statins act by inhibiting the action of the Enzyme HMG-CoA reductase. This is done by inhibiting a number of processes that lead to the production of cholesterol in the human body First, the statins inhibit cholesterol biosynthetic pathway. In humans, cholesterol is manufactured from acetyl-CoA through a series of reactions (Würtz et al 1205). The enzyme HMG-CoA reductase is the key to this kind of reactions. Since the statins have the same molecular structure as the enzyme, they, therefore, fit into its pathways and thus compete with the enzyme thus reducing the synthesis of cholesterol. The statins also lower the plasma cholesterol levels due to the regulation of the low-density lipoprotein receptor. The statins also inhibit the activation of small G protein. These proteins are intermediates in the cholesterol synthesis. Thus inhibition of activation of the proteins reduces the amount of cholesterol produced. Statins also work by suppressing the proinflammatory molecules that are also responsible for the activation of the small G protein (Würtz et al 1205). Finally, the statins stimulate the endothelial NOS in patients with atherosclerosis and hypercholesterolemia whose endothelial function is impaired.
Statins work by inhibiting the synthesis of cholesterol in the liver. Therefore the overall effects on the levels of cholesterol in the body will be a reduction in the overall level of cholesterol and LDL in the human body. Since the mode of action of the statins targets the pathway and the action of the key enzyme responsible for the manufacture of cholesterol, the end products of the process will be a reduced amount of cholesterol. LDL is sometimes referred to the bad cholesterol (De Hert et al 114). This is because they lead to blockage of arteries a factor that may lead to heart attacks. Statins increase the LDL uptake and thus an overall reduction of cholesterol in the body.
The most common side effect of the use of Statins is a muscle problem, an increased risk of diabetes mellitus and increased level of level of liver enzymes in the blood. This is because the statins are work by inhibiting the activity of enzyme HMG-CoA reductase that is responsible for the synthesis of cholesterol. The same enzyme is responsible for other processes like the production of CoQ10 that is important in the muscle cell and blood sugar regulation. Other effects include neuropathy, liver and pancreatic dysfunction and sexual dysfunction (Boekholdt et al 1309). But since the patient in our case is an elderly male with diabetes, the application of statins to manage his condition can be the most effective way as diabetes is already managed and his blood sugar level is within normal range. Other scholars argue that statins have been associated with memory loss but the issue has not yet been proofed. No direct link has been found between the use of statin medications and loss of memory.
Goldstein, Joseph L., and Michael S. Brown. “A century of cholesterol and coronaries: from plaques to genes to statins.” Cell 161.1 (2015): 161-172.
Würtz, Peter, et al. “Metabolomic profiling of statin use and genetic inhibition of HMG-CoA reductase.” Journal of the American College of Cardiology 67.10 (2016): 1200-1210.
De Hert, Marc, et al. “Metabolic and cardiovascular adverse effects associated with antipsychotic drugs.” Nature Reviews Endocrinology 8.2 (2012): 114.
Boekholdt, S. Matthijs, et al. “Association of LDL cholesterol, non–HDL cholesterol, and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: a meta-analysis.” Jama 307.12 (2012): 1302-1309.