UMHS Guideline Screening and Management of Lipids
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Lipid Lowering Agents, Cognitive Decline, and Dementia: the Three-City Study
Lipid lowering agents, cognitive decline, and dementia: the three-city study. Marie-Laure Ancelin, Isabelle Carrière, Pascale Barberger-Gateau, Sophie Auriacombe, Olivier Rouaud, Spiros Fourlanos, Claudine Berr, Anne-Marie Dupuy, Karen Ritchie To cite this version: Marie-Laure Ancelin, Isabelle Carrière, Pascale Barberger-Gateau, Sophie Auriacombe, Olivier Rouaud, et al.. Lipid lowering agents, cognitive decline, and dementia: the three-city study.: Lipid Lowering Agents and Cognitive Decline. Journal of Alzheimer’s Disease, IOS Press, 2012, 30 (3), pp.629-37. 10.3233/JAD-2012-120064. inserm-00707350 HAL Id: inserm-00707350 https://www.hal.inserm.fr/inserm-00707350 Submitted on 12 Jun 2012 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Lipid lowering agents, cognitive decline, and dementia: the three-city study Marie-Laure Ancelin 1 * , Isabelle Carrière 1 , Pascale Barberger-Gateau 2 , Sophie Auriacombe 2 , Olivier Rouaud 3 , Spiros Fourlanos 4 , Claudine Berr 1 , Anne-Marie Dupuy 1 5 , Karen Ritchie 1 6 1 Neuropsychiatrie : Recherche Epidémiologique -
An Educational Booklet for Patients with Familial Hypercholesterolemia
Illustrations > Jean Lambert Illustrations graphic design > www.mine-de-rien.net graphic Chol/29/P030/01-01/10 NLA An educational booklet for patients with familial hypercholesterolemia This brochure was provided by Genzyme Corporation for use by the Foundation of the National Lipid Association. DR. LEIV OSE www.learnyourlipids.com CONTENTS PART 1 What will you learn from this booklet? 02 FAMILIAL HYPERCHOLESTEROLEMIA PART 1: FAMILIAL HYPERCHOLESTEROLEMIA 03 1 - What is Familial Hypercholesterolemia? 03 WHAT WILL YOU 2 - What is LDL-Cholesterol? 04 3 - What are the causes of FH? 05 LEARN FROM THIS GREAT GRANDMOTHER GREAT GRANDFATHER 4 - When should FH be suspected? 07 FH NON FH BOOKLET? 5 - How is FH diagnosed? 09 6 - How early can FH be diagnosed? 09 Woman You will learn about Familial PART 2: TREATMENT 10 GRANDMOTHER GRANDFATHER Hypercholesterolemia, NON FH FH Woman with FH 1 - How can LDL-Cholesterol be reduced? 10 its cause, and the potential 2 - Step 1: Dietary management of FH 11 Man consequences of this a) How does diet affect LDL-Cholesterol? 11 disease. You will learn b) What sort of diet? 11 Man with FH about high cholesterol 3 - Step 2: Using medication 12 AUNT MOTHER FATHER UNCLE and what this might mean a) How does medication affect LDL-Cholesterol? 12 NON FH FH NON FH FH for your heart and blood b) Which drug treatments reduce LDL-Cholesterol and how? 13 FIGURE 1: 4 - Why is lifelong treatment important? vessels. Most importantly 15 FH is an inherited disease, you will learn how to find PART 3: CARDIOVASCULAR DISEASE AND LIPOPROTEINS 16 which can usually be traced out whether someone in 1 - What is cardiovascular disease? 16 DAUGTER SON over several generations. -
Core Laboratory
Performance of the vast majority of Hematology, Coagulation, Urinalysis, Clinical Chemistry and Toxicology testing procedures is conducted in the CORE LABORATORY - an advanced, highly automated area where whole blood, serum, plasma, urine and other biological fluid specimens are tested for a comprehensive menu of state-of-the-art laboratory procedures. Significant testing procedures for Clinical Chemistry and Toxicology includes panels currently approved by the Centers for Medicare and Medicaid Services: Basic Metabolic Panel; Comprehensive Metabolic Panel; Liver Function Panel; Renal Function Panel; and Electrolyte Panel. Other key tests include the Lipid Profile (Cholesterol, Triglyceride, HDL- Cholesterol and LDL-Cholesterol), major markers of cardiovascular disease and risk [such as Troponin I, Myoglobin and Beta-type natriuretic peptide (commonly referred to as BNAT or BNP)], critical care analytes, beta-HCG, and significant therapeutic drug levels. Urinary toxicology screens for major drugs of abuse (and/or key metabolites) are also performed. The cornerstones of Hematology testing are analyses of the complete blood count (CBC) and the differential (DIFF). These include evaluation of: (1) white blood cell count and differential with percentage and absolute value given for the leukocyte components; (2) circulating erythrocytes by means of hemoglobin, hematocrit, red blood cell count, and red blood cell indices; and (3) measurement of platelet concentration by count and/or estimation. Morphological variations and changes of cellular constituents are reported. Alteration of any aspect of the hemostatic mechanism may cause abnormal bleeding in a wide variety of familial and acquired disorders. These defects may be differentiated by a profile of significant Coagulation laboratory tests that includes PT, PTT, Fibrinogen, FDP, and D-Dimer for monitoring anticoagulant therapy. -
Genetic Testing for Familial Hypercholesterolemia AHS – M2137
Corporate Medical Policy Genetic Testing for Familial Hypercholesterolemia AHS – M2137 File Name: genetic_testing_for_familial_hypercholesterolemia Origination: 01/01/2019 Last CAP Review: 07/2021 Next CAP Review: 07/2022 Last Review: 07/2021 Description of Procedure or Service Definitions Familial hypercholesterolemia (FH) is a genetic condition that results in premature atherosclerotic cardiovascular disease due to lifelong exposure to elevated low-density lipoprotein cholesterol (LDL-C) levels (Sturm et al., 2018). FH encompasses multiple clinical phenotypes associated with distinct molecular etiologies. The most common is an autosomal dominant disorder caused by mutations in one of three genes, low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB), and proprotein convertase subtilisin-like kexin type 9 (PCSK9) (Ahmad et al., 2016; Goldberg et al., 2011). Rare autosomal recessive disease results from mutation in low-density lipoprotein receptor adaptor protein (LDLRAP) (Garcia et al., 2001). Related Policies Cardiovascular Disease Risk Assessment AHS – G2050 ***Note: This Medical Policy is complex and technical. For questions concerning the technical language and/or specific clinical indications for its use, please consult your physician. Policy BCBSNC will provide coverage for genetic testing for familial hypercholesterolemia when it is determined the medical criteria or reimbursement guidelines below are met. Benefits Application This medical policy relates only to the services or supplies described herein. Please refer to the Member's Benefit Booklet for availability of benefits. Member's benefits may vary according to benefit design; therefore member benefit language should be reviewed before applying the terms of this medical policy. When Genetic Testing for Familial Hypercholesterolemia is covered 1. Genetic testing to establish a molecular diagnosis of Familial Hypercholesterolemia is considered medically necessary when BOTH of the following criteria are met: A. -
Inflammatory Mechanisms Affecting the Lipid Profile in Patients with Systemic Lupus Erythematosus CECILIA P
Inflammatory Mechanisms Affecting the Lipid Profile in Patients with Systemic Lupus Erythematosus CECILIA P. CHUNG, ANNETTE OESER, JOSEPH SOLUS, INGRID AVALOS, TEBEB GEBRETSADIK, AYUMI SHINTANI, MacRAE F. LINTON, SERGIO FAZIO, and C. MICHAEL STEIN ABSTRACT. Objective. Increased low density lipoprotein (LDL) cholesterol and triglycerides, and decreased high density lipoprotein (HDL) cholesterol concentrations are associated with adverse cardiovascular risk in the general population. Patients with systemic lupus erythematosus (SLE) have an altered lipid profile characterized by increased triglycerides and decreased HDL cholesterol concentrations. We examined the relationships between lipid concentrations, cytokines, and inflammatory markers in patients with SLE. Methods. Fasting lipid concentrations, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were measured in 110 patients with SLE. Disease activity was quantified by the SLE Disease Activity Index (SLEDAI), and disease damage by the Systemic Lupus International Collaborating Clinics (SLICC) score. Concentrations of circulating tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and insulin were measured and insulin sensitivity calculated. Results. Lower concentrations of HDL cholesterol were independently associated with higher ESR (p < 0.001), IL-6 (p = 0.02), SLEDAI (p = 0.04), and TNF-α (p = 0.04) after adjustment for age, sex, race, body mass index, insulin sensitivity, and current use of corticosteroids or hydroxychloroquine. Triglyceride concentrations were -
Stems for Nonproprietary Drug Names
USAN STEM LIST STEM DEFINITION EXAMPLES -abine (see -arabine, -citabine) -ac anti-inflammatory agents (acetic acid derivatives) bromfenac dexpemedolac -acetam (see -racetam) -adol or analgesics (mixed opiate receptor agonists/ tazadolene -adol- antagonists) spiradolene levonantradol -adox antibacterials (quinoline dioxide derivatives) carbadox -afenone antiarrhythmics (propafenone derivatives) alprafenone diprafenonex -afil PDE5 inhibitors tadalafil -aj- antiarrhythmics (ajmaline derivatives) lorajmine -aldrate antacid aluminum salts magaldrate -algron alpha1 - and alpha2 - adrenoreceptor agonists dabuzalgron -alol combined alpha and beta blockers labetalol medroxalol -amidis antimyloidotics tafamidis -amivir (see -vir) -ampa ionotropic non-NMDA glutamate receptors (AMPA and/or KA receptors) subgroup: -ampanel antagonists becampanel -ampator modulators forampator -anib angiogenesis inhibitors pegaptanib cediranib 1 subgroup: -siranib siRNA bevasiranib -andr- androgens nandrolone -anserin serotonin 5-HT2 receptor antagonists altanserin tropanserin adatanserin -antel anthelmintics (undefined group) carbantel subgroup: -quantel 2-deoxoparaherquamide A derivatives derquantel -antrone antineoplastics; anthraquinone derivatives pixantrone -apsel P-selectin antagonists torapsel -arabine antineoplastics (arabinofuranosyl derivatives) fazarabine fludarabine aril-, -aril, -aril- antiviral (arildone derivatives) pleconaril arildone fosarilate -arit antirheumatics (lobenzarit type) lobenzarit clobuzarit -arol anticoagulants (dicumarol type) dicumarol -
Lipid Profile and Its Relationship with Blood
Onkar Singh et al. Lipid profile and blood glucose levels in MetS National Journal of Physiology, DOI: 10.5455/njppp.2015.5.051120141 NJPPP Pharmacy & Pharmacology http://www.njppp.com/ RESEARCH ARTICLE Correspondence LIPID PROFILE AND ITS RELATIONSHIP Onkar Singh ([email protected]) WITH BLOOD GLUCOSE LEVELS IN Received 27.08.2014 METABOLIC SYNDROME Accepted 09.09.2014 1 1 2 Onkar Singh , Mrityunjay Gupta , Vijay Khajuria Key Words Metabolic Syndrome; 1 Department of Physiology, Government Medical College, Jammu, India Dyslipidemia; Lipid Pattern; 2 Department of Pharmacology, Government Medical College, Jammu, India Type 2 Diabetes Mellitus Background: Metabolic syndrome (MetS) and its associated factors such as dyslipidemia and hyperglycemia are associated with increased risk of cardiovascular disease (CVD). Aims and Objective: To assess lipid profile and its relation with blood glucose levels in patients with MetS. Materials and Methods: This cross-sectional study included 72 male patients with MetS. Anthropometry, lipid profile, blood glucose, and presence of MetS (JIS criteria) were determined. Results: High triglyceride (TG) level (>200 mg/dL, 44.4%) was the most common dyslipidemia followed by low levels of high-density lipoprotein cholesterol (<40 mg/dL, 19.4%). High total cholesterol levels (>240 mg/dL, 13.8%) and high low- density lipoprotein cholesterol levels (>160 mg/dL, 9.7%) were observed. On comparison, no significant differences in lipid levels of MetS patients with normal fasting glucose, impaired fasting glucose, and type 2 diabetes mellitus were observed. Conclusions: Dyslipidemia was frequent in patients with MetS. High TG was the most common lipid abnormality, and a large number of patients had more than one abnormal lipid parameter. -
Community Lab Costs
Sickle Cell This tests for the genetic trait which may lead to sickle cell anemia. Osteoporosis Screening This uses ultrasound to screen people for low bone density or osteoporosis and is completed by painlessly scanning the heel. Because osteoporosis rarely causes signs or symptoms until it’s advanced, the National Osteoporosis Foundation recommends a bone density test if you are: • A woman older than age 65 or a man older than age 70 • A postmenopausal woman with at least one risk factor for osteoporosis Community Lab Costs • A man between age 50 and 70 who has at least one osteoporosis (greatly reduced rates) risk factor • Older than age 50 with a history of a broken bone • Taking medications, such as prednisone, aromatase inhibitors or Wellness Panel........................................................................ $20 Fasting anti-seizure drugs, that are associated with osteoporosis Includes screening for glucose, electrolytes, kidney, liver and • A postmenopausal woman who has recently stopped taking thyroid, plus complete blood count and lipid profile hormone therapy • A woman who experienced early menopause Diabetic Screening (A1c)...................................................... $5 The results of this test will indicate if you have or at risk for osteoporosis. Sickle Cell................................................................................ $6 If so, your doctor can offer treatment. PSA (Prostate Screening)...................................................... $8 Breathing Test This measures airflow and lung -
Commonly Used Lipidcentric ICD-10 (ICD-9) Codes
Commonly Used Lipidcentric ICD-10 (ICD-9) Codes *This is not an all inclusive list of ICD-10 codes R.LaForge 11/2015 E78.0 (272.0) Pure hypercholesterolemia E78.3 (272.3) Hyperchylomicronemia (Group A) (Group D) Familial hypercholesterolemia Grütz syndrome Fredrickson Type IIa Chylomicronemia (fasting) (with hyperlipoproteinemia hyperprebetalipoproteinemia) Hyperbetalipoproteinemia Fredrickson type I or V Hyperlipidemia, Group A hyperlipoproteinemia Low-density-lipoid-type [LDL] Lipemia hyperlipoproteinemia Mixed hyperglyceridemia E78.4 (272.4) Other hyperlipidemia E78.1 (272.1) Pure hyperglyceridemia Type 1 Diabetes Mellitus (DM) with (Group B) hyperlipidemia Elevated fasting triglycerides Type 1 DM w diabetic hyperlipidemia Endogenous hyperglyceridemia Familial hyperalphalipoproteinemia Fredrickson Type IV Hyperalphalipoproteinemia, familial hyperlipoproteinemia Hyperlipidemia due to type 1 DM Hyperlipidemia, Group B Hyperprebetalipoproteinemia Hypertriglyceridemia, essential E78.5 (272.5) Hyperlipidemia, unspecified Very-low-density-lipoid-type [VLDL] Complex dyslipidemia hyperlipoproteinemia Elevated fasting lipid profile Elevated lipid profile fasting Hyperlipidemia E78.2 (272.2) Mixed hyperlipidemia (Group C) Hyperlipidemia (high blood fats) Broad- or floating-betalipoproteinemia Hyperlipidemia due to steroid Combined hyperlipidemia NOS Hyperlipidemia due to type 2 diabetes Elevated cholesterol with elevated mellitus triglycerides NEC Fredrickson Type IIb or III hyperlipoproteinemia with E78.6 (272.6) -
The Effects of Statin and Fibrate Drugs on Cholesterol Metabolism And
The effects of statin and fibrate drugs on cholesterol metabolism and steroid production in two fish species. By Aziz Al-Habsi Thesis submitted to the Faculty of Graduate and Postdoctoral Studies University of Ottawa In partial fulfillment of the requirements for the PhD degree in the Ottawa-Carleton Institute of Biology Thèse soumise à la Faculté des Études Supérieurs et Postdoctorales Université d’Ottawa En vue de la réalisation partielle du doctorat à L’Institut de Biologie Ottawa-Carleton ©Aziz Al-Habsi, Ottawa, Canada, 2014 This thesis is dedicated to my wife and children who have always stood by me and dealt with all my absence from many family occasions with a smile. ii Acknowledgments Completing a PhD is truly a marathon event, and I would not have able to complete this journey without the aid and support of countless people over the past seven years. First and foremost I would like to gratefully and sincerely thank my supervisor Dr. Thomas W. Moon for his guidance, understanding, friendship, and most importantly, his patience during my graduate studies at University of Ottawa. His mentorship was paramount in providing a well-rounded experience consistent my long-term career goals. He encouraged me not only to be a biologist but also be an instructor and independent thinker. I am not sure many graduate students are given the opportunity to develop their own individuality and self- sufficiency by being allowed to work with such independence. For everything you’ve done for me, Dr. Moon, I thank you. I would like to extend my thanks the Department of Biology at University of Ottawa, especially those members of my doctoral committee for their input, valuable discussions and accessibility. -
Lipid Profile Abnormalities Seen in T2DM Patients in Primary Healthcare in Turkey: a Cross-Sectional Study Aclan Ozder
Ozder Lipids in Health and Disease 2014, 13:183 http://www.lipidworld.com/content/13/1/183 RESEARCH Open Access Lipid profile abnormalities seen in T2DM patients in primary healthcare in Turkey: a cross-sectional study Aclan Ozder Abstract Background: Diabetes is characterized by chronic hyperglycemia and disturbances of carbohydrate, lipid and protein metabolism. We aimed to research association between serum lipid profile and blood glucose, hypothesizing that early detection and treatment of lipid abnormalities can minimize the risk for atherogenic cardiovascular disorder and cerebrovascular accident in patients with type 2 diabetes mellitus. Methods: Fasting blood glucose (FBG), total cholesterol (TC), high density lipoprotein (HDL), low density lipoprotein (LDL), triglyceride (TG) and glycated haemoglobin (HbA1c) levels were evaluated. A hepatic ultrasound was performed for every diabetic to evaluate hepatosteatosis. The study was done from January 2014 to June 2014 among 132 patients with T2DM who were admitted to outpatient clinic of Family Medicine department in a university hospital. The patients whose taking multi-vitamin supplementation or having hepatic, renal or metabolic bone disorders (including parathyroid related problems) were excluded from the study for the reason that those conditions might affect the carbohydrate and lipid metabolism in diabetes. Test of significance was calculated by unpaired student’s t test between cases and controls. Correlation studies (Pearson’s correlation) were performed between the variables of blood glucose and serum lipid profile. Significance was set at p<0.05. Results: Results of serum lipid profile showed that the mean values for TC, TG, HDL and LDL in female patients were 227.6 ± 57.7 mg/dl, 221.6 ± 101.1 mg/dl, 31.5 ± 6.7 mg/dl and 136.5 ± 43.7 mg/dl, respectively. -
Hyperlipidemia
Hyperlipidemia Overview Hyperlipidemia (HLP) is a condition in which there are high levels of lipid (or fat) in the blood. The two main types of fat that are found in the blood are cholesterol and triglycerides. Nutrition and lifestyle factors such as maintaining a healthy weight, limiting alcohol consumption, avoiding tobacco, and adequate physical activity play a role in both the prevention and treatment of hyperlipidemia. Hyperlipidemia is the most common risk factor for the development of cardiovascular disease, which is why it is important to manage your blood lipid levels by implementing a heart healthy lifestyle. LDL Cholesterol Cholesterol is an essential component found in all human cell membranes and is required for healthy bodily functions. Your body makes all the cholesterol it needs to function and therefore the amount consumed in the diet should be limited. High levels of cholesterol in the blood increases your risk for heart disease by sticking to the walls of your arteries and causing plaque to build-up. Over time, this plaque can narrow your arteries and prevent adequate blood flow. This condition is called atherosclerosis and it is one of the primary causes of heart attack and stroke. There are two types of cholesterol, low-density lipoprotein (LDL) or “bad” cholesterol, and high-density lipoprotein (HDL) or “good” cholesterol. High levels of LDL are associated with the formation of atherosclerotic plaque. High levels of HDL have been shown to decrease the risk for heart disease and stroke by removing excess cholesterol from the bloodstream. Triglycerides Triglycerides are the most common type of fat in the body.