Pharmacologic Treatment of Metabolic Syndrome - Essay Example

? Pharmacologic Treatment of Metabolic Syndrome Introduction The conception of metabolic syndrome has subsisted for the past eightdecades. Metabolic syndrome is a frequent metabolic disease that is a result of increased obesity (Blaha & Tota-Maharaj, 2012). The pathophysiology of the disease is largely credited to insulin opposition with extreme instability of fatty acids incriminated. This assemblage of metabolic uproars and risk factors associated with cardiovascular disease were identified in 1920’s. In the past two decades, there has been an increase in cases of metabolic syndrome due to rising cases of obesity and diabetes (Codario, 2011). In essence, the existence of the metabolic syndrome exposes an individual to the risk of type2 diabetes and cardiovascular disease (Ehrman, 2009). In the first ten years, the disease may expose an individual to high risk of cardiovascular disease while it may expose others to low risk cardiovascular disease events. Needless to say, the individuals exposed to low short term cardiovascular effects always experience high risk long term effects. For an individual to be detected with metabolic syndrome, they should have middle obesity, reduced HDL cholesterol, high blood pressure, high TG, and high fasting plasma glucose (Hansen & Bray, 2008). Because of the growing concern in the contemporary world, there have been recommendations on treatment and management of metabolic syndrome. Stern et al (2005) proposes that the different components that constitute metabolic syndrome are appropriate targets for treatment. These components of metabolic syndrome include insulin resistance, hypertension, glucose intolerance, dyslipidemia, and cardiovascular heart disease. Hansen and Bray (2008) note that cardiovascular disease risks are lowered through lowering LDL-C and total glucose levels. LDL can be lowered through the use of statin drugs. Statins Statins are drugs that act as agents that lower effective cholesterol. These drugs are classified as inhibitors of HMG-CoA reductase when in their active hydrolyzed form (Holmqvist, 2009). HMG-CoA reductase is an enzyme that catalyzes the alteration of HMG-CoA to an early rate restricting phase in cholesterol biosynthesis pathway (Marvasti & Adeli, 2010). The reticence of HMG-CoA reductase by statins reduces the apoB-containing lipoproteins and plasma levels of cholesterol. Wong (2006) asserts that this is attained through augmented levels of hepatic cholesterol absorption because of modulation of the LDL receptor in addition to methods of deeds on apoB, such as decreased translocation through the endoplasmic reticulum tissue layer, decreased lipoprotein fabrication and augmented intercellular dilapidation. In essence, HMG-CoA reductase plays an imperative role in the synthesis of cholesterol in the liver. Arguably, statins influence the secretion of VLDL and LDL in individuals with hyperlipidemia. Recently, statins were also identified as effective reducers of plasma TG levels which hinder intercellular cholesterol bio-production and modulation of LDL receptor look (Reaven, 2005). Needless to say, researchers and scholars have typified statins as highly effectual hypolopidemic agents that alleviate lipid irregularities in individuals with metabolic syndrome (Landsberg, 2005). Since increased levels of cholesterol increase cases of cardiovascular heart disease, statins area used to reduce its prevalence (Reaven, 2005). For this reason, it is one of the widely selected drugs to treat and manage metabolic syndrome. Some of the statins that are used in clinics include atorvastatin, simvastatin, and rosuvastatin. Statins should be prescribed by a doctor according to the levels of cholesterol in the blood stream. The average dosage according to studies by Marvasti and Adeli (2010) ranges from 20 to 80 mg. The table below indicates the dosage to a patient according the percentage reduction of LDL. % LDL diminution Atorvastatin Simvastatin Rosuvastatin 25 - 32 20mg 20mg 10mg 32- 39 40mg 40mg 20mg 37- 45 80mg 80mg 40mg 48-52 80mg Atorvastatin This is a member of the statin drugs that reduce the levels of LDL-C and improve hepatic lipoprotein over-making. In addition, research indicates that atorvastatin inhibits apoB over manufacturing triggered by the improvement of insulin resistance. The research by Lewis et al (2005) on the action of atorvastatin in animal insulin resistance identified that there is a molecular substantiation of ameliorated hepatic insulin sensitivity with atorvastatin management grounded on the evaluation of the phosphorylation condition of the insulin receptor and the appearance of protein tyrosine phosphatase-1B. In essence, atorvastatin not only alleviates LDL-C levels but also enhance hepatic insulin sensitivity. Simvastatin Recent researchers and scholars have noted that statin treatment can increase HDL cholesterol plasma assiduousness in individuals with hyperlipidemia and the anti-atherogenic association of this cholesterol in the bloodstream. High levels of LDL cholesterol and low levels of HDL are the primary risk factors for the growth of coronary heart disease and atherosclerosis (Marvasti & Adeli, 2010). Epidemiological research indicates that high levels of HDL cholesterol do not result to the development of coronary heart disease. Debatably, the modulation of blood HDL cholesterol assiduousness is controlled partly by the rate of break down and secretion of apoA1 by the hepatocytes. In this regard, a study conducted by Bonn et al (2002) revealed that the use of simvastatin increase the breakdown and emission of apoA1. In addition, simvastatin can increase blood HDL assiduity by 17 percent or more. This effect combined with reduced levels of LDL cholesterol concentration reduces the risk of morbidity in individuals with coronary heart disease by 40 percent. Rosuvastatin This is a new member of the statin drugs that reduces LDL cholesterol. This is done through a high number of reactions with HMG-CoA reductase (Wong, 2006). The increased reactions have an improved inhibition of the enzyme and lead to significant therapeutic efficiency (Marvasti & Adeli, 2010). In addition, this drug has a longer half-time and a higher degree of selective attribute for hepatic cells than all the other statin drugs. A research carried out by Park et al (2010) on Korean patients with non-diabetic metabolic syndrome revealed that rosuvastatin is more effective than atorvastatin and simvastatin. Side Effects and relevant drug to drug interactions Statins have numerous side effects which include headaches, sleep apnea, muscle aches, drowsiness, nausea, diarrhea, rash, constipation and abdominal cramping. Liver damage, muscle problems and increased type2 diabetes are some of the chronic side effects of statins (Wong, 2006). In some occasions, the use of statins results to increased liver enzymes. A low increase in the enzymes has no detrimental effects while a high increase in the enzymes has effects and one is advised to stop its consumption (Holmqvist, 2009). This is because the increased liver enzymes increase vulnerability to liver problems. In case of any problems, a patient should always consult with his or her doctor. The use of statins may lead to muscle pain and softness. This condition is referred to as the statin myopathy by Wong (2006). A high consumption of statin exposes an individual to pains. In some occasions, muscle cells may crumble and secrete myoglobin protein into the plasma. Myoglobin damages a person’s kidney (Holmqvist, 2009). In addition, statin use may result to rhabdomyolysis, a condition where all body muscles become weak and painful. On the other hand, taking statin may increase the levels of blood sugar level leading to the development of type2 diabetes. Mixing a statin with a niacin and fibrate exposes an individual to increased risks of rhabdomyolysis (Wong, 2006). In addition, the uptake of grapefruit and bitter oranges hampers the metabolism of simvastatin and atorvastatin. This causes a high level of statin in the blood resulting to statin dose related effects such as headaches, myopathy, diarrhea, rash, constipation and abdominal cramping. Recently, FDA physicians identified that statin and protease inhibitors consumed together can raise blood levels of statin and increase the risk of myopathy, diarrhea, rhabdomyolisis, rash, constipation and abdominal cramping (Holmqvist, 2009). Follow Up Plan The patients should always be monitored to ensure they do not overdose which is one of the contributing factors to the side effects. The physician should advise patients to report to him or her whenever she experiences anything unusual. However, the patient should visit the doctor occasionally after one month. The doctor should check on the kidney and the liver (Wong, 2006). The patients and family members should be educated on the effects of the form of medication to be administered (Ehrman, 2009). In this regard, the patients and his or family should be enlightened on the effects of statins. References Blaha, M. J., & Tota-Maharaj, R. (2012). Metabolic syndrome: From risk factors to management. Torino: SEEd. Bonn, V., Cheung, R., Chen, B., Taghibiglou, C., & Adeli, K. (2002). Simvastatin, an HMG-CoA reductase inhibitor, induces the synthesis and secretion of apolipoprotein A1 in HepG2 cells and primary hamster hepatocytes. Atherosclerosis, 163, 59-68. Codario, R. A. (2011). Type 2 diabetes, pre-diabetes, and the metabolic syndrome. Totowa, N.J: Humana Press. Ehrman, J. K. (2009). Clinical exercise physiology. Champaign, IL: Human Kinetics. Hansen, B. C., & Bray, G. A. (2008). The metabolic syndrome: Epidemiology, clinical treatment, and underlying mechanisms. Totowa, N.J: Humana Press. Holmqvist, G. N. (2009). Statins: Indications and uses, safety and modes of action. New York: Nova Science Publishers. Landsberg, L. (2005). Insulin resistance and the metabolic syndrome. Diabetologia, 48, 1244-1246. Lewis, G., Uffelman, K., Naples, M., Szeto, L., & Haidari, M. (2005). Intestinal lipoprotein overproduction, a newly recognized component of insulin resistance, is ameliorated by the insulin sensitizer rosiglitazone: Studies in the fructose-fed Syrian golden hamster. Endocrinology, 146, 247-255. Marvasti, B., & Adeli, K. (2010). Pharmacological management of metabolic syndrome and its lipid complications. Clinical biochemistry, 1, 146-156. Natali, A., & Ferrannini, E. (2004). Hypertension, Insulin resistance and the metabolic syndrome. Endocrinal Metab Clin N Am, 33, 417-429. Park, J. S., Kim, Y. J., Choi, J. Y., & Hong, T. J. (2010). Comparative study of low doses of rosuvastatin and Atorvastatin on lipid and glycemic control in Patients with Metabolic syndrome and hypercholesterolemia. Korean Intern Med, 25, 27-35. Reaven, G. (2005). The insulin resistance syndrome: Definition and dietary approaches to treatment. Annual nutrition review, 25, 391-406. Stern, S. E., Williams, K., Ferrannini, E., & Defrronzo, R. A. (2005). Identification of Individuals with insulin resistance using routine clinical measurements. Diabetes, 54, 333-339. Wong, B. A. (2006). Focus on statin research. New York: Nova Biomedical Books. Read More