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Cholesterol/Hypercholesterolemia/Hyperlipidemia
Published in Charles Theisler, Adjuvant Medical Care, 2023
Statins (e.g., Lipitor or Crestor) and niacin (the nicotinic acid form of vitamin B3) are medications used to treat high cholesterol. Both medications lower LDL (bad) cholesterol and raise HDL (good) cholesterol.6,7
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Factors that influence plasma cholesterol levels include age, gender, weight, genetics, diseases, and lifestyle factors. High cholesterol is mostly caused by diet, but heredity is also implicated. A lack of sufficient exercise can result in heart disease since LDL cholesterol levels are increased. Measuring the plasma cholesterol is a very important component of the clinical management of dyslipidemia and atherosclerosis. High plasma LDL cholesterol worsens left ventricular function in people with type 2 diabetes mellitus.
The vascular risk factors of ischemic stroke in young adults
Published in Ade Gafar Abdullah, Isma Widiaty, Cep Ubad Abdullah, Medical Technology and Environmental Health, 2020
A. Tursina, R.A. Indrianti, W. Nurruhyuliawati
This happens because cholesterol levels in normal circumstances increase in young adults at an average of 200 mg. Hypercholesterolemia is a disease that is chronic or prolonged while hypocholesterolemia in young adults is less frequent. Patients who have a history of hypercholesterolemia suffer from stroke because their cholesterol levels increase due to their unhealthy lifestyle choices such as consuming foods high in cholesterol and saturated fat. High cholesterol levels can cause atherosclerosis, which results in narrowing of the walls of blood vessels, disrupting the blood supply to the brain. This is what will cause strokes (Alchuriyah & Wahjuni 2016; Burhanuddin 2013; Eshak et al. 2017; Sitorus 2008; Syifa et al. 2017).
Is there a correlation between dyslipidemia and cognitive impairment in patients with multiple sclerosis?
Published in International Journal of Neuroscience, 2021
Adriana Andaloro, Margherita Russo, Concetta Pastura, Edoardo Sessa, Patrizia Calatozzo, Maria Grazia Maggio, Placido Bramanti
Our study aimed to evaluate the correlation between the components of the lipid profile and cognitive dysfunctions in patients affected by various forms of MS. In our sample, cholesterol was correlated with the outcome of overall cognitive functioning, as shown in MoCA score. This findings is in line with recent studies in both other neurological populations, such as dementia, and in MS [9,10]. Noori et al. have found a correlation between cholesterol and cognitive impairment in MSRR patient populations, underlining how this aspect is useful to consider for preventive patient monitoring [18]. In fact, high cholesterol levels could lead to a higher risk of developing cognitive symptoms and could increase the degree of disability of the subjects [19]. The novelty of our study is to assessed this correlation in patients with MS affected by various type of disease. Moreover, in our sample, we showed that the serum levels of triglycerides could lead to cognitive dysfunctions in all forms of MS. In our sample, we observed greater improvement in the subgroup without dyslipidemia, especially as regards the visuospatial components. According to this data, various studies performed on rats have shown that a high level of triglycerides in the blood, following an incorrect diet, alters cognitive functions, in particular the deterioration of visuo-spatial memory and working memory [20–22]. Furthermore, Thirumangalakudi et al. have shown that the condition of hyperlipidemia leads to significant memory deficits following the execution of specific experimental tasks [23].
Awareness, treatment rates, and compliance to treatment in patients with serum LDL cholesterol higher than 250 mg/dL, and possible, probable, or definite familial hypercholesterolemia
Published in Postgraduate Medicine, 2021
Samet Yaman, Didem Ozdemir, Busra Tugce Akman, Bekir Cakir, Osman Ersoy
Although FH is associated with premature atherosclerosis, coronary heart disease (CHD), and increased mortality at a young age, cardiovascular morbidity and mortality can markedly be decreased by early diagnosis and treatment [3]. Screening for hypercholesterolemia is recommended in all adults over 20 years old and in children over 2 years old when there is a familial history of premature cardiovascular disease (CVD) or high cholesterol levels [4]. FH should be considered in adults with LDL-C levels ≥190 mg/dl or nonhigh-density lipoprotein cholesterol (non-HDL-C) ≥220 mg/dl. Below 20 years of age, LDL-C ≥ 160 mg/dL or non-HDL-C ≥ 190 mg/dL requires evaluation for FH. A universally accepted diagnostic criteria is not available for FH. Make Early Diagnosis to Prevent Early Death (MEDPED) criteria in the United States, Simon Broome criteria in United Kingdom, and Dutch Lipid Clinical Network Criteria (DLCNC) in Netherlands were developed for the diagnosis of FH [4–6]. Among these, the most commonly used one is DLCNC which is based on the scoring of a number of parameters including genetic, clinical, and laboratory features. According to the final score, the diagnosis of possible, probable or definite FH can be made. With the use of these criteria, based on the estimated prevalance of 1/500, the diagnosis rate of FH has increased to 71% in Netherlands, while it is less than 1% in many countries [7].
Statins interfere with the attachment of S. cerevisiae mtDNA to the inner mitochondrial membrane
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2020
Angela Cirigliano, Antonia Amelina, Beatrice Biferali, Alberto Macone, Chiara Mozzetta, Michele Maria Bianchi, Mattia Mori, Bruno Botta, Elah Pick, Rodolfo Negri, Teresa Rinaldi
Cholesterol is a vital component of cell membranes, essential for the synthesis of steroid hormones, bile acids, and vitamin D, but high cholesterol levels are associated with an elevated risk of cardiovascular diseases. Cholesterol (ergosterol in yeast) is the end-product of the mevalonate pathway1. The enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase is the rate-limiting step in the synthesis of cholesterol and it catalyses the conversion of HMG-CoA to mevalonate; the mevalonate pathway and the HMG-CoA enzyme, as well as its regulation are conserved from yeast to humans2,3. HMG-CoA is the target of statins4, the most prescribed drug class for lowering elevated LDL-cholesterol, generally effective and well tolerated; however, patients can experience muscle adverse effects such as myopathy5,6. Genetic factors7 and drug-drug interactions8 also contribute as risk factors for the development of muscle side effects in patients9,10.