Hyperlipoproteinemia Research Paper

Hyperlipidemia is the abnormal elevation of any lipoproteins present in the blood. HMG-CoA reductase inhibitors (statins) are commonly used for the treatment of hyperlipidemia, specifically lowering the levels of low-density lipoproteins (LDL) levels. As with most classes of medications, there are many potential side effects. A less common but serious side effect of statins is myopathy. Myopathy is a dose-related side effect that causes skeletal muscle weakness, aching, cramping, pain, stiffness and tightness. The mechanism of this occurrence is unknown, but as will be shown, there is a possible correlation between low vitamin D levels and increased occurrence of statin induced myopathy. The vast numbers of patients on statins results in a high number of patients with statin-induced myopathy throughout the world. This consultation will determine whether vitamin D prophylaxis is safe and effective in the prevention of statin-induced myopathy.

A higher level of fats in the body puts the patient at higher risk for Cardiovascular diseases(CAD). The patient's' family has a history of CAD. Her mom and one of her sister have CAD (Lewis et al., 2014, pp. 733-734). The patient states that she has been taking her meds for cholesterol atorvastatin regularly. Her lipase level was 8272 on 11/11/16 and 2829 on 11/12/16 U/L 1069 on 11/13/16 (Ref range 73-393 U/L). Her HDL cholesterol level was 21 ( ref range>49 mg/dl), LDL Cholesterol level 148 ( ref range: <130 mg/dL). Patient statin drug was on hold because it is contradicted on the patient with an elevated level of ALT 80, 61(Ref range 0-50 U/L) and AST 61 on 11/12/16 and 64 on 11/13/16 (ref range 0-45 U/L). The uncontrolled level of could be the cause of concern for stroke or acute myocardial

He has never been on any statin therapy. His most recent lipids were done in January showing total cholesterol 213, triglycerides 172, HDL 61, LDL is 118.

According to the Merck Manual (2013), hyperlipidaemia is the increased synthesis of hepatic lipoproteins. Marieb (2012) explains that lipoproteins enable fat, fatty acids and cholesterol to circulate in the blood stream. They cannot do this alone due to their insolubility so they use lipoproteins as a type of transport. Nelson (2013) highlights four different varieties of lipoproteins which are chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL).

In a study conducted in 1985 observing primates, it was determined that the major effect of dietary cholesterol is its LDL raising effects. High intakes of cholesterol increase the number of circulating LDL’s and it can also change its size and composition. [12] It was during this time period that the mechanisms by which SFA are thought to increase blood cholesterol concentrations came about. One mechanism for the increase in LDL cholesterol levels is the suppression of LDL receptor activity. Studies in tissue cultures have shown that increasing the cholesterol content of a cell will down-regulate synthesis of LDL receptors. [13] This will lead to an increase in concentration of blood cholesterol. Another cause for an increase in blood cholesterol concentration through intake of dietary SFA is the composition of the newly secreted lipoproteins. With a high saturated fat intake, the LDL’s become rich in cholesterol esters, leaving the triglycerides in the blood. [14] The use of non-human primates in

MR. David likewise takes atorvastatin (Lipitor); 10 mg every day, for hypercholesterolemia (hoisted LDL cholesterol, low HDL cholesterol, and raised triglycerides). He has endured this medicine and holds fast to the day by day plan. Amid the previous 6 months, he has likewise taken chromium picolinate,

Heterozygous familial hypercholesterolemia current drug therapy statins, bile acid sequestrates, or other lipid lowering agents that lower cholesterol levels with relative success. Homozygous familial hypercholesterolemia (HoFH) is not treated well with standard lipid-lowering medications and needs costly methods to lower LDL-like apheresis or a liver transplant. HoFH occurs approximately 1 in 1 million births, creating a small population to gather data about treatments for this rare disease state. 1 Studies have shown that the best role of Juxtapid in familial hypercholesterolemia is as adjunctive therapy

Atherosclerotic research has recently concentrated on inflammatory cytokines involved in vascular inflammation and how they stimulate the production of endothelial adhesion molecules, which could enter circulation in soluble form, and have the cytokines stimulate the production of messenger cytokine interleukin-6, which incites the liver production of acute-phase reactants such as C-reactive protein to increase. (Packard et al., 2007) In short, cytokines released into the bloodstream have a tendency to bring about an inflammatory response. Researchers have also found that that treatment with lipid-reducing agents is correlated with reduced morbidity and mortality from coronary heart disease and it seems to work near the atherosclerotic lesion, causing stabilization, slowed progression and, in some cases, regression of lesions. (Blankenhorn, 1989) In research it is well know that one human risk factor for atherosclerosis is hypercholesterolemia, which is when total cholesterol and low-density lipoprotein cholesterol are elevated. (Genis et al., 2000) There are more contributors and characteristics of hypercholesterolemia, which include inflammatory responses to oxidative stress,

NAFLD is the hepatic manifestation of the metabolic syndrome (MetS). However, little is known about the natural history of NAFLD. Furthermore, the pathophysiological relationships between MetS and hepatic steatosis is not fully understood. The diagnosis of the MetS involves the presence of three of the following five risk factors: 1) hyperglycemia (fasting glucose ≥ 100 mg/dL), 2) low concentrations of high-density lipoprotein (HDL) cholesterol ( (-- removed HTML --) than 150 mg/dL), 4) increased waist circumference (102 cm for men and 89

So based on my family history it is mostly likely that I myself will have it someday, unless I do things to prevent high cholesterol such as exercising and eating fruits and vegetables. The last main cause of high cholesterol is that it could be because of your gender and age an example would be that elderly men have a tendency of having a high cholesterol. There seems to be no history of high cholesterol or discovery of it in the past time due to my research. According to Dr Paulysney Guerrero the symptoms of high cholesterol involve "Dizziness, weakness, nauseas. However, some patients do not show any symptoms at all" Guerrero explains. Basically the only main way to tell is by having the person go through a blood examination. For example when the doctor had sent me to get a blood examination to see what my cholesterol level was (basically to see if I was healthy) I was sent to Labcorp and so they took some blood and so as a result my it was confirmed based on my blood examination that my blood was so far normal and that my cholesterol level was fine as well .Usually when the blood pressure is really high the treatment that is used immediately is medication in order to have the cholesterol at a well and balanced level. An example would be Alfonso Sanchez "when the doctor had discovered how severe my cholesterol was

Statins lower the concentration of low-density lipoprotein cholesterol and very-low-density lipoprotein cholesterol in people with elevated triglycerides. Many

What is the probable genetic causation of excessive cardiovascular disease in the Family pedigree presented? Are any lifestyle issues causing an exacerbation or alleviation of this disease?

This gene instructs the body to make lecithin-cholesterol acyltransferase enzyme (LCAT enzyme) which has a function of removing cholesterol from body and tissues and carrying them to the liver by the help of lipoprotein molecules. The cholesterol molecules will then be redistributed to other body tissues or removed from body by the liver. The activity of LCAT enzymes which adds cholesterol molecules to high-density lipoprotein (HDL) is called Alpha-LCAT activity. When LCAT enzymes add cholesterol molecules to very low-density lipoprotein (VLDL) and low-density lipoprotein, the activity is called Beta-LCAT activity. The mutation in gene LCAT leads to the reducing of Alpha-LCAT activity in the LCAT enzyme. This results in body lacking cholesterol and cornea opacities cholesterol. There is so far no known reason why this mutation only causes cholesterol opacities in cornea (Fish-eye

Statins (also known as 3-hydroxy-3-methylgutaryl coenzyme A reductase inhibitors) are widely prescribed cholesterol-lowering drugs for the treatment of dyslipidemia and cardiovascular disease. Although they are considered to be drugs with a very good safety profile, there are many concerns that their adverse effects might compromise their proven beneficial effects due to their extensive usage.

Goldstein also studied that the level of LDL in the blood is inversely related to the LDLR activity. The LDL binds to the receptor via its principal surface protein called apolipoprotein B-100. The receptor, with it’s acquired LDL, then enters the call. This process is called Receptor-Mediated Endocytosis. When the number of functioning receptors is diminished because of a receptor mutation, LDL with its load of cholesterol