The reference range provided by student serum data provides a reasonably accurate resemblance to the published reference range for blood cholesterol and triglyceride concentration. As seen in table 2, the reference range for the student serum data is the mean plus/minus one standard deviation, hence the upper range would be 198.87mg/dL which coincides somewhat accurately with the desirable published reference range of 239mg/dL, which is considered ‘high’. Of this total cholesterol count, LDL makes up the significant portion of TC at 329mg/dL which is very alarming as ‘very high’ is considered >190mg/dL. Furthermore, this leaves a HDL cholesterol count of 32mg/dL which is below the recommended reference range of >40mg/dl and rather concerning also. However, contrary to Marcus’s alarming cholesterol levels, his total triglyceride concentration fell within the reference range of 10-150mg/dL at 83.36mg/dL which is perfectly fine and healthy, all of this data can be seen in table one.
The abundance of LDL in Marcus’s serum is symptomatic of coronary heart disease and is the likely cause of his angina. This lipoprotein transports cholesterol to cells in the body via the arteries where it has the potential to build up on artery walls leading to atherosclerosis. With so much LDL in Marcus’s serum the potential for atherosclerosis is greatly increased. On the contrary, the HDL concentration in Marcus’s serum is below average, hence the are less HDL molecules than what is considered healthy and as a result, less cholesterol being transported to the liver to be expelled from the body.
Marcus is a relatively physically healthy man; hence his coronary heart disease cannot be entirely attributed to this. In fact, it was observed in the experimental results that Marcus’s LDL receptor activity was well below normal at 62% as opposed to ;95% reference range. Therefore, due to there being less LDL receptor activity, the uptake of cholesterol from LDL to cells via endocytosis isn’t occurring at a sustainable rate. Therefore, the elimination of LDL from the serum isn’t occurring which is ultimately leading to excess serum LDL which can be seen in Marcus’s altered lipid profile in table 1.
Reduced LDL receptor activity is likely the result of familial hypercholesterolemia and involves the mutation of the LDL receptor gene which encodes the LDL receptor protein which is used to remove LDL from circulation. This diagnosis is also supported by the fact that Marcus has family history of coronary heart disease with his father suffering a heart attack at age 45 and his mother suffering her second at age 69.
Familial hypercholesterolemia is typically treated with statins, a class of lipid lowering medication. These act by inhibiting the enzyme HMG-CoA-reductase in the liver causing the liver to produce more LDL receptors which help to reduce circulating LDL from the blood. These are likely the most appropriate treatment for Marcus and can be combined with additional therapy with other drugs such as bile acid sequestrants if it is required. These disrupt the enterohepatic circulation of bile acids by merging with bile constituents and preventing their reabsorption from the gut, ultimately lowering blood cholesterol.