Hypercholesterolemia. Medical search

A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.

A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).

The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.

Substances used to lower plasma CHOLESTEROL levels.

Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.

Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.

Cholesterol present in food, especially in animal products.

A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.

Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.

A condition marked by the development of widespread xanthomas, yellow tumor-like structures filled with lipid deposits. Xanthomas can be found in a variety of tissues including the SKIN; TENDONS; joints of KNEES and ELBOWS. Xanthomatosis is associated with disturbance of LIPID METABOLISM and formation of FOAM CELLS.

Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.

A chlorinated epoxy compound used as an industrial solvent. It is a strong skin irritant and carcinogen.

Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.

A diet that contributes to the development and acceleration of ATHEROGENESIS.

A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)

Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.

A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.

A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.

An individual having different alleles at one or more loci regarding a specific character.

A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.

An individual in which both alleles at a given locus are identical.

Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.

7-carbon saturated monocarboxylic acids.

Conditions with excess LIPIDS in the blood.

Any procedure in which blood is withdrawn from a donor, a portion is separated and retained and the remainder is returned to the donor.

Proteolytic enzymes that are involved in the conversion of protein precursors such as peptide prohormones into PEPTIDE HORMONES. Some are ENDOPEPTIDASES, some are EXOPEPTIDASES.

An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).

A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).

The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.

Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

High-molecular-weight insoluble polymers that contain functional cationic groups capable of undergoing exchange reactions with anions.

Polymers of high molecular weight which at some stage are capable of being molded and then harden to form useful components.

A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.

Dried, ripe seeds of PLANTAGO PSYLLIUM; PLANTAGO INDICA; and PLANTAGO OVATA. Plantain seeds swell in water and are used as demulcents and bulk laxatives.

Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.

A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.

The main trunk of the systemic arteries.

Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.

A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.

A condition of elevated levels of TRIGLYCERIDES in the blood.

The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.

A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.

Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels.

Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.

Nutrient blood vessels which supply the walls of large arteries or veins.

A corneal disease in which there is a deposition of phospholipid and cholesterol in the corneal stroma and anterior sclera.

Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.

The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.

An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.

An abnormal lipoprotein present in large amounts in patients with obstructive liver diseases such as INTRAHEPATIC CHOLESTASIS. LP-X derives from the reflux of BILE lipoproteins into the bloodstream. LP-X is a low-density lipoprotein rich in free CHOLESTEROL and PHOSPHOLIPIDS but poor in TRIGLYCERIDES; CHOLESTEROL ESTERS; and protein.

Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.

Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.

A family of sterols commonly found in plants and plant oils. Alpha-, beta-, and gamma-isomers have been characterized.

A class of organic compounds known as STEROLS or STEROIDS derived from plants.

A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.

Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.

A membrane-bound cytochrome P450 enzyme that catalyzes the 7-alpha-hydroxylation of CHOLESTEROL in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP7, converts cholesterol to 7-alpha-hydroxycholesterol which is the first and rate-limiting step in the synthesis of BILE ACIDS.

A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.

A genus in the family ROSACEAE of shrubs and small trees native to the North Temperate Zone. It is best known for a traditional medication for the heart.

Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.

Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).

Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.

Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.

A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.

The veins and arteries of the HEART.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

Genetically developed small pigs for use in biomedical research. There are several strains - Yucatan miniature, Sinclair miniature, and Minnesota miniature.

A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.

A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.

Drugs used to cause dilation of the blood vessels.

Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.

A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.

A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.

Elements of limited time intervals, contributing to particular results or situations.

The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.

Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.

Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones.

The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.

Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.

Fatty acids which are unsaturated in only one position.

Steroids with a hydroxyl group at C-3 and most of the skeleton of cholestane. Additional carbon atoms may be present in the side chain. (IUPAC Steroid Nomenclature, 1987)

A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.

Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.

The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.

Regular course of eating and drinking adopted by a person or animal.

A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).

The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.

The transmission of traits encoded in GENES from parent to offspring.

The total number of cases of a given disease in a specified population at a designated time. It is differentiated from INCIDENCE, which refers to the number of new cases in the population at a given time.

Pathological processes involving any part of the AORTA.

The vessels carrying blood away from the heart.

A diet that contains limited amounts of fat with less than 30% of calories from all fats and less than 10% from saturated fat. Such a diet is used in control of HYPERLIPIDEMIAS. (From Bondy et al, Metabolic Control and Disease, 8th ed, pp468-70; Dorland, 27th ed)

Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.

Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.

A plant genus of the family ROSACEAE. The common names of chokeberry or chokecherry are also used for some species of PRUNUS.

The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.

Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.

Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.

A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).

An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.

Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.

A fibrous cord that connects the muscles in the back of the calf to the HEEL BONE.

Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.

Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.

An island republic in the eastern Mediterranean Sea. Its capital is Nicosia. It was colonized by the Phoenicians and ancient Greeks and ruled successively by the Assyrian, Persian, Ptolemaic, Roman, and Byzantine Empires. It was under various countries from the 12th to the 20th century but became independent in 1960. The name comes from the Greek Kupros, probably representing the Sumerian kabar or gabar, copper, famous in historic times for its copper mines. The cypress tree is also named after the island. (From Webster's New Geographical Dictionary, 1988, p308 & Room, Brewer's Dictionary of Names, 1992, p134)

An essential amino acid that is physiologically active in the L-form.

Therapy with two or more separate preparations given for a combined effect.

The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.

Inhaling and exhaling the smoke of burning TOBACCO.

Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.

A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.

Genes that influence the PHENOTYPE only in the homozygous state.

Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)

Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Lipid-laden macrophages originating from monocytes or from smooth muscle cells.

Proteins which are present in or isolated from vegetables or vegetable products used as food. The concept is distinguished from PLANT PROTEINS which refers to non-dietary proteins from plants.

Maleness or femaleness as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or effect of a circumstance. It is used with human or animal concepts but should be differentiated from SEX CHARACTERISTICS, anatomical or physiological manifestations of sex, and from SEX DISTRIBUTION, the number of males and females in given circumstances.

PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.

Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.

The minute vessels that collect blood from the capillary plexuses and join together to form veins.

Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.

An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.

Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.

A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.

A competitive inhibitor of nitric oxide synthetase.

The two principal arteries supplying the structures of the head and neck. They ascend in the neck, one on each side, and at the level of the upper border of the thyroid cartilage, each divides into two branches, the external (CAROTID ARTERY, EXTERNAL) and internal (CAROTID ARTERY, INTERNAL) carotid arteries.

Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.

Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.

Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with LONGITUDINAL STUDIES which are followed over a period of time.

A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.

An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.

An indicator of body density as determined by the relationship of BODY WEIGHT to BODY HEIGHT. BMI=weight (kg)/height squared (m2). BMI correlates with body fat (ADIPOSE TISSUE). Their relationship varies with age and gender. For adults, BMI falls into these categories: below 18.5 (underweight); 18.5-24.9 (normal); 25.0-29.9 (overweight); 30.0 and above (obese). (National Center for Health Statistics, Centers for Disease Control and Prevention)

Part of the arm in humans and primates extending from the ELBOW to the WRIST.

A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.

Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.

The relationship between the dose of an administered drug and the response of the organism to the drug.

Uptake of substances through the lining of the INTESTINES.

Variation in a population's DNA sequence that is detected by determining alterations in the conformation of denatured DNA fragments. Denatured DNA fragments are allowed to renature under conditions that prevent the formation of double-stranded DNA and allow secondary structure to form in single stranded fragments. These fragments are then run through polyacrylamide gels to detect variations in the secondary structure that is manifested as an alteration in migration through the gels.

Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects. (1/3532)

Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Total (resting-stress-recovery phases) cardiovascular (blood pressure [BP] and heart rate [HR]) and regional hemodynamic (FBF and FVR) reactivity to stressful stimuli were calculated as area-under-the-curve (auc) (valuextime). Compared with baseline levels, simvastatin reduced total (TOT-C) and LDL cholesterol (LDL-C) (1.27 mmol/L, P<0.001 and 1.33 mmol/L, P<0.001, respectively). Enalapril also reduced TOT-C and LDL-C (0.6 mmol/L, P<0.001 and 0.58 mmol/L, P<0.05, respectively). MFBF was increased substantially by both treatments (P<0.001). Enalapril had a greater effect (-1.7 arbitrary units (AU), P<0.001) than simvastatin (-0.6 AU, P<0.05) on mFVR. During stress, FBF increased more with enalapril (4.4 FBFxminutes, P<0.001) than with simvastatin (1.8 FBFxminutes, P<0.01). Conversely, FVR stress response was reduced more with enalapril (9.1 FVRxminutes, P<0.001) than with simvastatin (2.9 FVRxminutes, P<0.01). During combination treatment, a significant (0.001>P<0.05) additive effect on hypercholesterolemia, structural vascular damage, BP, and FVR was shown. The findings suggest that angiotensin-converting enzyme (ACE) inhibition induces a larger reduction than HMG-CoA reductase blockade in vascular reactivity and structural damage in hypercholesterolemic hypertensive subjects. (+info)

Protective effect of dietary tomato against endothelial dysfunction in hypercholesterolemic mice. (2/3532)

The effects of dietary ingestion of tomato were studied in mice that had been made hypercholesterolemic by feeding atherogenic diets. Mice which had been fed on the atherogenic diet without tomato for 4 months had significantly increased plasma lipid peroxide, and the vaso-relaxing activity in the aorta induced by acetylcholine (ACh) was harmed when compared with mice fed on a common commercial diet. On the other hand, mice which had been fed on the atherogenic diet containing 20% (w/w) lyophilized powder of tomato showed less increase in the plasma lipid peroxide level, and ACh-induced vaso-relaxation was maintained at the same level as that in normal mice. These results indicate that tomato has a preventive effect on atherosclerosis by protecting plasma lipids from oxidation. (+info)

Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. (3/3532)

Exogenously hypercholesterolemic (ExHC) rats were fed on an atherogenic diet supplemented with 1% each of either ethyl ester docosahexaenoic acid [EE-DHA, 22:6(n-3)], ethyl ester eicosapentaenoic acid [EE-EPA, 20:5(n-3)] or safflower oil (SO) for 6 months. The rats fed on the diets containing EE-EPA or EE-DHA, compared with those fed on SO, had lower serum cholesterol and triacylglycerol levels, less aggregation of platelets and slower progress of intimal thickening in the ascending aorta. Relative to the SO-fed rats, both of the (n-3) fatty acid-fed rats had a significantly reduced proportion of arachidonic acid in the platelet and aortic phospholipids, and lower production of thromboxane A2 by platelets and of prostacyclin by the aorta. These results suggest that EPA and DHA are similarly involved in preventing atherosclerosis development by reducing hypercholesterolemia and modifying the platelet functions. (+info)

Comparative hypocholesterolemic effects of five animal oils in cholesterol-fed rats. (4/3532)

The hypocholesterolemic efficacy of various animal oils was compared in rats given a cholesterol-enriched diet. After acclimatization for one week, male F344 DuCrj rats (8 weeks of age) that had been fed with a conventional diet were assigned to diets containing 5% of oil from emu (Dromaius), Japanese Sika deer (Cervus nippon yesoensis, Heude), sardine, beef tallow, or lard with 0.5% cholesterol for 6 weeks. After this feeding period, the concentrations of serum total cholesterol and of very-low-density lipoprotein + intermediate-density lipoprotein + low-density lipoprotein-cholesterol in the sardine oil group were significantly lower than those in the other groups. The serum high-density lipoprotein-cholesterol concentration in the Japanese Sika deer oil group was significantly higher than that in the other groups. The atherosclerotic index and liver cholesterol concentration in the sardine oil and Japanese Sika deer oil groups were significantly lower than those in the other groups. The fecal cholesterol excretion by the Japanese Sika deer oil group was significantly higher than that of the other groups, except for the sardine oil group, and the fecal bile acid excretion by the sardine oil group was significantly higher than that of the other groups, except for the lard group. These results suggest that Japanese Sika deer oil reduced the atherosclerotic index and liver cholesterol concentration in the presence of excess cholesterol in the diet as well as sardine oil did by increasing the excretion of cholesterol from the intestines of rats. (+info)

Comparison of synthetic saponin cholesterol absorption inhibitors in rabbits: evidence for a non-stoichiometric, intestinal mechanism of action. (5/3532)

The hypocholesterolemic activities of pamaqueside and tiqueside, two structurally similar saponins, were evaluated in cholesterol-fed rabbits. The pharmacological profiles of the saponins were virtually identical: both dose-dependently decreased the intestinal absorption of labeled cholesterol 25-75%, increased fecal neutral sterol excretion up to 2.5-fold, and decreased hepatic cholesterol content 10-55%. High doses of pamaqueside (>5 mg/kg) or tiqueside (>125 mg/kg) completely prevented hypercholesterolemia. Decreases in plasma and hepatic cholesterol levels were strongly correlated with increased neutral sterol excretion. Ratios of neutral sterol excreted to pamaqueside administered were greater than 1:1 at all doses, in opposition to the formation of a stoichiometric complex previously suggested for tiqueside and other saponins. Ratios in tiqueside-treated rabbits were less than unity, a reflection of its lower potency. Pamaqueside-treated rabbits exhibited a more rapid decline in plasma cholesterol concentrations than control animals fed a cholesterol-free diet, indicating that the compound also inhibited the absorption of biliary cholesterol. Intravenous administration of pamaqueside had no effect on plasma cholesterol levels despite plasma levels twice those observed in rabbits given pamaqueside orally. These data indicate that pamaqueside and tiqueside induce hypocholesterolemia by blocking lumenal cholesterol absorption via a mechanism that apparently differs from the stoichiometric complexation of cholesterol hypothesized for other saponins. (+info)

Identification of a novel Arg-->Cys mutation in the LDL receptor that contributes to spontaneous hypercholesterolemia in pigs. (6/3532)

We previously carried out genetic and metabolic studies in a partially inbred herd of pigs carrying cholesterol-elevating mutations. Quantitative pedigree analysis indicated that apolipoprotein (apo)B and a second major gene were responsible for the hypercholesterolemia in these animals. In this study, we assessed LDL receptor function by three different methods: ligand blots of liver membranes using beta-very low density lipoprotein (VLDL) as a ligand; low density lipoprotein (LDL)-dependent proliferation of T-lymphocytes; and direct binding of 125I-labeled LDL to cultured skin fibroblasts. All three methods demonstrated that LDL receptor ligands bound with decreased affinity to the LDL receptor in these animals. In skin fibroblasts from the hypercholesterolemic pigs, the Kd of binding was about 4-fold higher than in cells from normal pigs. The cDNA of the pig LDL receptor from normal and hypercholesterolemic pigs was isolated and sequenced. We identified a missense mutation that results in an Arg'Cys substitution at the position corresponding to Arg94 of the human LDL receptor. The mutation is in the third repeat of the ligand binding domain of the receptor. By single-stranded conformational polymorphism (SSCP) analysis, we studied the relationship between LDL receptor genotype and plasma cholesterol phenotype. In contrast to humans, the hypercholesterolemia associated with the LDL receptor mutation in pigs was expressed as a recessive trait. The LDL receptor mutation made a far more significant contribution to hypercholesterolemia than did the apoB mutation, consistent with observations made in human subjects with apoB mutations. Within each genotypic group (mutated apoB or mutated receptor), there was a wide range in plasma cholesterol. As the animals were on a well-controlled low-fat diet, this suggests that there are additional genetic factors that influence the penetrance of cholesterol-elevating mutations. (+info)

Macroscopic distribution of coronary atherosclerotic lesions in cholesterol-fed rabbits. (7/3532)

In the present study we macroscopically examined a change in the distribution of coronary atherosclerosis in cholesterol-fed rabbits. Rabbits were fed a cholesterol-enriched diet for 15 weeks, then replaced by a normal diet, and were sacrificed at 15, 24, 32 and 42 weeks after the start of the experiment. The coronary atherosclerosis in the cholesterol-fed rabbits was distributed more densely in the proximal portion than in the middle and distal portions, and the lesions were severe at 24 and 32 weeks after the start of the experiment. comparison of lesions in the three portions at these time points showed that the percentages of lesion areas in the proximal portion, the middle portion and the distal portion were approximately 51%, 21 to 25% and 0.2 to 3.7%, respectively. Macroscopic observation of the coronary atherosclerotic lesions showed that the lesions formed over the vessel lumen in the proximal portion within the range of approximately 5 mm from the orifice of the left coronary artery. In the middle portion, the lesions formed predominantly around the orifices of branches as small patchy lesions from 1 to 3 mm in diameter. These findings support previous histopathological reports that suggested that the incidence of stenosis in the proximal portion was high, and the incidence of lesion occurrence in the middle and the distal portions varied. The method, macroscopical investigation of the coronary artery, is useful for analyzing coronary atherosclerosis in the rabbit. (+info)

Variability in meta-analytic results concerning the value of cholesterol reduction in coronary heart disease: a meta-meta-analysis. (8/3532)

Despite official support for the efficacy of cholesterol reduction, considerable controversy exists, and meta-analyses of this topic have produced conflicting results. The authors assessed the variability of meta-analyses, evaluating the cardiovascular value of cholesterol reduction while attempting to explain the variability. Metaanalyses were identified by electronic search and citation tracking. Included were those conducted prior to 1995 that dealt with cholesterol reduction and total mortality, cardiovascular mortality, or nonfatal cardiovascular disease. In addition to extracting odds ratios for total mortality, cardiovascular mortality, and nonfatal cardiovascular disease, the authors encoded methodological variables, publication variables, and data concerning investigators' backgrounds. Twenty-three meta-analyses were reviewed, and 15 concluded that cholesterol reduction was beneficial. Summary odds ratios for total mortality were heterogeneous, generally failing to support the value of cholesterol reduction. Odds ratios depended on inclusion criteria and investigator variables. Odds ratios for cardiovascular mortality and for nonfatal cardiovascular disease were more homogeneous and supported the value of cholesterol reduction. Methodologically better meta-analyses tended to report more beneficial odds ratios. Although "supportiveness" of the value of cholesterol reduction was associated with inclusion/exclusion criteria and publication variables, the primary outcome variable related to supportiveness was the statistical significance of the odds ratios for cardiovascular mortality. (+info)

There are several types of hypercholesterolemia, including:

1. Familial hypercholesterolemia: This is an inherited condition that causes high levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood.
2. Non-familial hypercholesterolemia: This type of hypercholesterolemia is not inherited and can be caused by a variety of factors, such as a high-fat diet, lack of exercise, obesity, and certain medical conditions, such as hypothyroidism or polycystic ovary syndrome (PCOS).
3. Mixed hypercholesterolemia: This type of hypercholesterolemia is characterized by high levels of both LDL and high-density lipoprotein (HDL) cholesterol in the blood.

The diagnosis of hypercholesterolemia is typically made based on a physical examination, medical history, and laboratory tests, such as a lipid profile, which measures the levels of different types of cholesterol and triglycerides in the blood. Treatment for hypercholesterolemia usually involves lifestyle changes, such as a healthy diet and regular exercise, and may also include medication, such as statins, to lower cholesterol levels.

The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, such as the low-density lipoprotein receptor gene (LDLR) or the PCSK9 gene. These mutations lead to a decrease in the ability of the liver to remove excess cholesterol from the bloodstream, resulting in high levels of LDL cholesterol and low levels of HDL cholesterol.

Hyperlipoproteinemia type II is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases can be caused by spontaneous mutations or incomplete penetrance, where not all individuals with the mutated gene develop the condition.

Symptoms of hyperlipoproteinemia type II can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white, waxy deposit on the iris of the eye), and tendon xanthomas (small, soft deposits of cholesterol under the skin). Treatment typically involves a combination of dietary changes and medication to lower LDL cholesterol levels and increase HDL cholesterol levels. In severe cases, liver transplantation may be necessary.

Hyperlipoproteinemia type II is a serious condition that can lead to cardiovascular disease, including heart attacks, strokes, and peripheral artery disease. Early diagnosis and treatment are important to prevent or delay the progression of the disease and reduce the risk of complications.

The most common form of xanthomatosis is called familial hypercholesterolemia, which is caused by a deficiency of low-density lipoprotein (LDL) receptors in the body. This results in high levels of LDL cholesterol in the blood, which can lead to the accumulation of cholesterol and other lipids in the skin, eyes, and other tissues.

Other forms of xanthomatosis include:

* Familial apo A-1 deficiency: This is a rare disorder caused by a deficiency of apolipoprotein A-1 (apoA-1), a protein that plays a critical role in the transportation of triglycerides and cholesterol in the blood.
* familial hyperlipidemia: This is a group of rare genetic disorders that are characterized by high levels of lipids in the blood, including cholesterol and triglycerides.
* Chylomicronemia: This is a rare disorder caused by a deficiency of lipoprotein lipase, an enzyme that breaks down triglycerides in the blood.

The symptoms of xanthomatosis vary depending on the specific form of the condition and the organs affected. They may include:

* Yellowish deposits (xanthomas) on the skin, particularly on the elbows, knees, and buttocks
* Deposits in the eyes (corneal arcus)
* Fatty liver disease
* High levels of cholesterol and triglycerides in the blood
* Abdominal pain
* Weight loss

Treatment for xanthomatosis typically involves managing the underlying genetic disorder, which may involve dietary changes, medication, or other therapies. In some cases, surgery may be necessary to remove affected tissue.

In summary, xanthomatosis is a group of rare genetic disorders that are characterized by deposits of lipids in the skin and other organs. The symptoms and treatment vary depending on the specific form of the condition.

Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.

There are several types of arteriosclerosis, including:

1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.

Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.

There are several types of hyperlipidemia, including:

1. High cholesterol: This is the most common type of hyperlipidemia and is characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol.
2. High triglycerides: This type of hyperlipidemia is characterized by elevated levels of triglycerides in the blood. Triglycerides are a type of fat found in the blood that is used for energy.
3. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol is known as "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for excretion. Low levels of HDL cholesterol can contribute to hyperlipidemia.

Symptoms of hyperlipidemia may include xanthomas (fatty deposits on the skin), corneal arcus (a cloudy ring around the iris of the eye), and tendon xanthomas (tender lumps under the skin). However, many people with hyperlipidemia have no symptoms at all.

Hyperlipidemia can be diagnosed through a series of blood tests that measure the levels of different types of cholesterol and triglycerides in the blood. Treatment for hyperlipidemia typically involves dietary changes, such as reducing intake of saturated fats and cholesterol, and increasing physical activity. Medications such as statins, fibric acid derivatives, and bile acid sequestrants may also be prescribed to lower cholesterol levels.

In severe cases of hyperlipidemia, atherosclerosis (hardening of the arteries) can occur, which can lead to cardiovascular disease, including heart attacks and strokes. Therefore, it is important to diagnose and treat hyperlipidemia early on to prevent these complications.

The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.

The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.

Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.

Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.

In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.

There are several causes of hypertriglyceridemia, including:

* Genetics: Some people may inherit a tendency to have high triglyceride levels due to genetic mutations that affect the genes involved in triglyceride metabolism.
* Obesity: Excess body weight is associated with higher triglyceride levels, as there is more fat available for energy.
* Diabetes: Both type 1 and type 2 diabetes can lead to high triglyceride levels due to insulin resistance and altered glucose metabolism.
* High-carbohydrate diet: Consuming high amounts of carbohydrates, particularly refined or simple carbohydrates, can cause a spike in blood triglycerides.
* Alcohol consumption: Drinking too much alcohol can increase triglyceride levels in the blood.
* Certain medications: Some drugs, such as anabolic steroids and some antidepressants, can raise triglyceride levels.
* Underlying medical conditions: Certain medical conditions, such as hypothyroidism, kidney disease, and polycystic ovary syndrome (PCOS), can also contribute to high triglyceride levels.

Hypertriglyceridemia is typically diagnosed with a blood test that measures the level of triglycerides in the blood. Treatment options for hypertriglyceridemia depend on the underlying cause of the condition, but may include lifestyle modifications such as weight loss, dietary changes, and medications to lower triglyceride levels.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

The cause of arcus senilis is not well understood, but it may be related to aging, sun exposure, smoking, or systemic diseases such as high blood pressure or diabetes. The condition does not impair vision and is usually asymptomatic, but it can be an early sign of other eye disorders, such as cataracts or age-related macular degeneration (AMD).

Arcus senilis is typically diagnosed through a comprehensive eye exam, which includes visual acuity testing, refraction, and retinoscopy to determine the curvature of the cornea. The presence of arcus senilis is confirmed by observing the deposits on the rim of the cornea with a slit-lamp biomicroscope.

There is no specific treatment for arcus senilis, but monitoring the condition regularly can help detect any progression or associated eye disorders early. Management of underlying systemic conditions, such as high blood pressure or diabetes, may also be beneficial in slowing the progression of the condition. In some cases, arcus senilis may resolve spontaneously over time.

In summary, arcus senilis is a harmless age-related condition characterized by white deposits on the rim of the cornea that can be an early sign of other eye disorders. Regular monitoring and management of underlying systemic conditions can help detect any progression or associated eye disorders early.

Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.

The symptoms of coronary disease can vary depending on the severity of the condition, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back

Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Preventative measures for coronary disease include:

* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.

1. Coronary artery disease: The narrowing or blockage of the coronary arteries, which supply blood to the heart.
2. Heart failure: A condition in which the heart is unable to pump enough blood to meet the body's needs.
3. Arrhythmias: Abnormal heart rhythms that can be too fast, too slow, or irregular.
4. Heart valve disease: Problems with the heart valves that control blood flow through the heart.
5. Heart muscle disease (cardiomyopathy): Disease of the heart muscle that can lead to heart failure.
6. Congenital heart disease: Defects in the heart's structure and function that are present at birth.
7. Peripheral artery disease: The narrowing or blockage of blood vessels that supply oxygen and nutrients to the arms, legs, and other organs.
8. Deep vein thrombosis (DVT): A blood clot that forms in a deep vein, usually in the leg.
9. Pulmonary embolism: A blockage in one of the arteries in the lungs, which can be caused by a blood clot or other debris.
10. Stroke: A condition in which there is a lack of oxygen to the brain due to a blockage or rupture of blood vessels.

The condition is caused by mutations in genes that code for proteins involved in lipid metabolism, such as the low-density lipoprotein receptor gene (LDLR), apolipoprotein A-1 gene (APOA1), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. These mutations can lead to the overproduction or underexpression of certain lipids, leading to the characteristic lipid abnormalities seen in HeFH.

HeFH is usually inherited in an autosomal dominant manner, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by recessive inheritance or de novo mutations. The condition can affect both children and adults, and it is important for individuals with HeFH to be monitored closely by a healthcare provider to manage their lipid levels and reduce the risk of cardiovascular disease.

Treatment for HeFH typically involves a combination of dietary modifications, such as reducing saturated fat intake and increasing fiber and omega-3 fatty acid intake, and medications, such as statins, to lower cholesterol levels. In some cases, apheresis or liver transplantation may be necessary to reduce lipid levels. Early detection and management of HeFH can help prevent or delay the development of cardiovascular disease, which is the leading cause of death worldwide.

The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.

CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:

* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Diabetes
* Smoking
* Obesity
* Lack of exercise

Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:

* Electrocardiogram (ECG or EKG)
* Stress test
* Echocardiogram
* Coronary angiography

Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.

Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.

There are several types of dyslipidemias, including:

1. Hyperlipidemia: Elevated levels of lipids and lipoproteins in the blood, which can increase the risk of CVD.
2. Hypolipidemia: Low levels of lipids and lipoproteins in the blood, which can also increase the risk of CVD.
3. Mixed dyslipidemia: A combination of hyperlipidemia and hypolipidemia.
4. Familial dyslipidemia: An inherited condition that affects the levels of lipids and lipoproteins in the blood.
5. Acquired dyslipidemia: A condition caused by other factors, such as poor diet or medication side effects.

Dyslipidemias can be diagnosed through a variety of tests, including fasting blood sugar (FBS), lipid profile, and apolipoprotein testing. Treatment for dyslipidemias often involves lifestyle changes, such as dietary modifications and increased physical activity, as well as medications to lower cholesterol and triglycerides.

In conclusion, dyslipidemias are abnormalities in the levels or composition of lipids and lipoproteins in the blood that can increase the risk of CVD. They can be caused by a variety of factors and diagnosed through several tests. Treatment often involves lifestyle changes and medications to lower cholesterol and triglycerides.

There are several types of diabetes mellitus, including:

1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.

The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds

If left untreated, diabetes mellitus can lead to a range of complications, including:

1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.

It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.

There are several types of hyperlipoproteinemias, each with distinct clinical features and laboratory findings. The most common forms include:

1. Familial hypercholesterolemia (FH): This is the most common type of hyperlipoproteinemia, caused by mutations in the LDLR gene that codes for the low-density lipoprotein receptor. FH is characterized by extremely high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to premature cardiovascular disease, including heart attacks and strokes.
2. Familial hypobetalipoproteinemia (FHBL): This rare disorder is caused by mutations in the APOB100 gene that codes for a protein involved in lipid metabolism. FHBL is characterized by very low levels of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, as well as a deficiency of Apolipoprotein B-100, a protein that helps transport lipids in the blood.
3. Hypertriglyceridemia: This condition is caused by mutations in genes that regulate triglyceride metabolism, leading to extremely high levels of triglycerides in the blood. Hypertriglyceridemia can increase the risk of pancreatitis and other health problems.
4. Lipoprotein lipase deficiency: This rare disorder is caused by mutations in the LPL gene that codes for the enzyme lipoprotein lipase, which helps break down triglycerides in the blood. Lipoprotein lipase deficiency can lead to very high levels of triglycerides and cholesterol in the blood, increasing the risk of pancreatitis and other health problems.
5. Familial dyslipidemia: This is a group of rare inherited disorders that affect lipid metabolism and can cause extremely high or low levels of various types of cholesterol and triglycerides in the blood. Some forms of familial dyslipidemia are caused by mutations in genes that code for enzymes involved in lipid metabolism, while others may be caused by unknown factors.
6. Chylomicronemia: This rare disorder is characterized by extremely high levels of chylomicrons (type of triglyceride-rich lipoprotein) in the blood, which can increase the risk of pancreatitis and other health problems. The exact cause of chylomicronemia is not fully understood, but it may be related to genetic mutations or other factors that affect lipid metabolism.
7. Hyperchylomicronemia: This rare disorder is similar to chylomicronemia, but it is characterized by extremely high levels of chylomicrons in the blood, as well as very low levels of HDL (good) cholesterol. Hyperchylomicronemia can increase the risk of pancreatitis and other health problems.
8. Hypoalphalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein A-I (ApoA-I), a protein that plays a key role in lipid metabolism and helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypoalphalipoproteinemia can increase the risk of pancreatitis and other health problems.
9. Hypobetalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein B (ApoB), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypobetalipoproteinemia can increase the risk of pancreatitis and other health problems.
10. Sitosterolemia: This rare genetic disorder is caused by mutations in the gene that codes for sterol-CoA-desmethylase (SCD), an enzyme involved in the metabolism of plant sterols. Sitosterolemia can cause elevated levels of plant sterols and sitosterol in the blood, which can increase the risk of pancreatitis and other health problems.
11. Familial hyperchylomicronemia type 1 (FHMC1): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC1 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
12. Familial hyperchylomicronemia type 2 (FHMC2): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein A-IV (APOA4), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC2 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
13. Lipoprotein (a) deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein (a), a protein that helps to regulate the levels of lipoproteins in the blood. Lipoprotein (a) deficiency can cause low levels of lipoprotein (a) and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
14. Chylomicron retention disease: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of chylomicrons in the blood. Chylomicron retention disease can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
15. Hypertriglyceridemia-apolipoprotein C-II deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of triglycerides in the blood. Hypertriglyceridemia-apolipoprotein C-II deficiency can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
16. Familial partial lipodystrophy (FPLD): This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the arms, legs, and buttocks. FPLD can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
17. Lipodystrophy: This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the face, arms, and legs. Lipodystrophy can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
18. Abetalipoproteinemia: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein B, a protein that helps to regulate the levels of lipids in the blood. Abetalipoproteinemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
19. Chylomicronemia: This rare genetic disorder is characterized by the presence of excessively large amounts of chylomicrons (type of lipid particles) in the blood. Chylomicronemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
20. Hyperlipidemia due to medications: Certain medications, such as corticosteroids and some anticonvulsants, can cause elevated levels of lipids in the blood.

It's important to note that many of these disorders are rare and may not be common causes of high triglycerides. Additionally, there may be other causes of high triglycerides that are not listed here. It's important to talk to a healthcare provider for proper evaluation and diagnosis if you have concerns about your triglyceride levels.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

1. Aneurysms: A bulge or ballooning in the wall of the aorta that can lead to rupture and life-threatening bleeding.
2. Atherosclerosis: The buildup of plaque in the inner lining of the aorta, which can narrow the artery and restrict blood flow.
3. Dissections: A tear in the inner layer of the aortic wall that can cause bleeding and lead to an aneurysm.
4. Thoracic aortic disease: Conditions that affect the thoracic portion of the aorta, such as atherosclerosis or dissections.
5. Abdominal aortic aneurysms: Enlargement of the abdominal aorta that can lead to rupture and life-threatening bleeding.
6. Aortic stenosis: Narrowing of the aortic valve, which can impede blood flow from the heart into the aorta.
7. Aortic regurgitation: Backflow of blood from the aorta into the heart due to a faulty aortic valve.
8. Marfan syndrome: A genetic disorder that affects the body's connective tissue, including the aorta.
9. Ehlers-Danlos syndrome: A group of genetic disorders that affect the body's connective tissue, including the aorta.
10. Turner syndrome: A genetic disorder that affects females and can cause aortic diseases.

Aortic diseases can be diagnosed through imaging tests such as ultrasound, CT scan, or MRI. Treatment options vary depending on the specific condition and may include medication, surgery, or endovascular procedures.

There are several different types of obesity, including:

1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.

Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.

Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:

1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.

The main symptom of abetalipoproteinemia is a complete absence of chylomicrons, which are small particles that carry triglycerides and other lipids in the bloodstream. This results in low levels of triglycerides and other lipids in the blood, as well as an impaired ability to absorb vitamins and other nutrients from food.

Abetalipoproteinemia is usually diagnosed during infancy or early childhood, when symptoms such as fatigue, weakness, and poor growth become apparent. The disorder can be identified through blood tests that measure lipid levels and genetic analysis.

Treatment for abetalipoproteinemia typically involves a combination of dietary changes and supplements to ensure adequate nutrition and prevent complications such as malnutrition and liver disease. In some cases, medications may be prescribed to lower triglyceride levels or improve the absorption of fat-soluble vitamins.

The prognosis for abetalipoproteinemia varies depending on the severity of the disorder and the presence of any complications. In general, early diagnosis and appropriate treatment can help to manage symptoms and prevent long-term health problems. However, some individuals with abetalipoproteinemia may experience ongoing health issues throughout their lives.

These diseases can cause a wide range of symptoms such as fatigue, weight changes, and poor wound healing. Treatment options vary depending on the specific condition but may include lifestyle changes, medications, or surgery.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

Some types of hypercholesterolemia lead to specific physical findings. For example, familial hypercholesterolemia (Type IIa ... If the hypercholesterolemia is hereditary (familial hypercholesterolemia), more often a family history of premature, earlier ... Genetic screening is now advised if a form of familial hypercholesterolemia is suspected. Classically, hypercholesterolemia was ... Hypercholesterolemia, also called high cholesterol, is the presence of high levels of cholesterol in the blood. It is a form of ...

https://en.wikipedia.org/wiki/Hypercholesterolemia

Hypercholesterolemia. (June 2011). "Familial hypercholesterolemia: screening, diagnosis and management of pediatric and adult ... Familial hypercholesterolemia (FH) is a genetic disorder characterized by high cholesterol levels, specifically very high ... MedicinePlus: Familial Hypercholesterolemia (CS1 maint: multiple names: authors list, CS1: long volume value, Articles with ... 2006). "Diagnosing familial hypercholesterolaemia: the relevance of genetic testing". Eur. Heart J. 27 (18): 2240-6. doi: ...

https://en.wikipedia.org/wiki/Familial_hypercholesterolemia

Varghese MJ (May 2014). "Familial hypercholesterolemia: A review". Annals of Pediatric Cardiology. 7 (2): 107-117. doi:10.4103/ ... Familial Hypercholesterolemia). Recognizing an increased genetic burden earlier can allow clinicians to intervene earlier and ...

https://en.wikipedia.org/wiki/Polygenic_score

APOB Hypercholesterolemia, familial; 143890; LDLR Hypercholesterolemia, familial, 3; 603776; PCSK9 Hypercholesterolemia, ... TJP2 Hypercholesterolemia, due to ligand-defective apo B; 144010; ... familial, autosomal recessive; 603813; LDLRAP1 Hypercholesterolemia, familial, modification of; 143890; APOA2 ...

https://en.wikipedia.org/wiki/List_of_OMIM_disorder_codes

"Familial Hypercholesterolemia (FH)". www.heart.org. Retrieved 2 August 2019. "How Can I Lower High Cholesterol" (PDF). American ... Mannu GS, Zaman MJ, Gupta A, Rehman HU, Myint PK (October 2012). "Update on guidelines for management of hypercholesterolemia ... There are several international guidelines on the treatment of hypercholesterolaemia. Human trials using HMG-CoA reductase ... November 1995). "Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland ...

https://en.wikipedia.org/wiki/Cholesterol

... such as familial hypercholesterolemia. Treatment may include, niacin or statin or ezetimibe.: 534 It is also known as " ... "normotriglyceridemic hypobetalipoproteinemia". Familial hypercholesterolemia Braunwald, Eugene; Hauser, Stephen L.; et al. ( ...

https://en.wikipedia.org/wiki/Apolipoprotein_B_deficiency

December 2005). "Severe hypercholesterolemia in four British families with the D374Y mutation in the PCSK9 gene: long-term ... February 2014). "The hypercholesterolemia-risk gene SORT1 facilitates PCSK9 secretion". Cell Metabolism. 19 (2): 310-318. doi: ... PCSK9 inhibitor drugs are now approved by the FDA to treat familial hypercholesterolemia. Drugs can inhibit PCSK9, leading to ... September 2014). "Living the PCSK9 adventure: from the identification of a new gene in familial hypercholesterolemia towards a ...

https://en.wikipedia.org/wiki/PCSK9

In familial hypercholesterolemia, a mutation in the LDLR, PCSK9, or APOB is usually the reason for this and these mutations ... Some common genetic disorders associated with primary dyslipidemias are homozygous or heterozygous hypercholesterolemia, ... "Familial hypercholesterolemia in adults: Overview". UpToDate. Retrieved April 22, 2021.{{cite web}}: CS1 maint: url-status ( ... "Inherited disorders of LDL-cholesterol metabolism other than familial hypercholesterolemia". UpToDate. Retrieved April 22, 2021 ...

https://en.wikipedia.org/wiki/Dyslipidemia

Familial hypercholesterolemia Ileojejunal bypass Buchwald H, Stoller DK, Campos CT, Matts JP, Varco RL (September 1990). " ... Chalstrey LJ, Winder AF, Galton DJ (November 1982). "Partial ileal bypass in treatment of familial hypercholesterolaemia". J R ... "Partial ileal bypass for hypercholesterolemia. 20- to 26-year follow-up of the first 57 consecutive cases". Ann. Surg. 212 (3 ... the procedure is used to treat a number of hyperlipidemias including familial hypercholesterolemia. The only randomized ...

https://en.wikipedia.org/wiki/Partial_ileal_bypass_surgery

In children statins are effective at reducing cholesterol levels in those with familial hypercholesterolemia. Their long term ... Statins may be less effective in reducing LDL cholesterol in people with familial hypercholesterolemia, especially those with ... Braamskamp MJ, Wijburg FA, Wiegman A (April 2012). "Drug therapy of hypercholesterolaemia in children and adolescents". Drugs. ... Rader DJ, Cohen J, Hobbs HH (June 2003). "Monogenic hypercholesterolemia: new insights in pathogenesis and treatment". The ...

https://en.wikipedia.org/wiki/Statin

"Chinese herbal medicines for hypercholesterolemia". Cochrane Database of Systematic Reviews (7): CD008305. doi:10.1002/14651858 ... Cochrane review found inconclusive evidence to support the use of TCM herbal medicines for treatment of hypercholesterolemia. A ...

https://en.wikipedia.org/wiki/Traditional_Chinese_medicine

The presence of palmar xanthomata, like the presence of tendinous xanthomata, is indicative of hypercholesterolaemia.[citation ... Achilles'-tendon xanthoma in familial hypercholesterolemia". The New England Journal of Medicine. 338 (22): 1591. doi:10.1056/ ... "Acute myocardial infarction in an 18 year old South Indian girl with familial hypercholesterolemia: a case report". Cases ... 531 Also associated with familial hypercholesterolemia (FH). Eruptive xanthoma (ILDS E78.220) is clinically characterized by ...

https://en.wikipedia.org/wiki/Xanthoma

"OMIM Entry #144010 - HYPERCHOLESTEROLEMIA, FAMILIAL, 2; FCHL2". www.omim.org. Retrieved 2019-07-01. "OMIM Entry #162200 - ...

https://en.wikipedia.org/wiki/Genetic_disorder

It is associated with hypercholesterolemia (typically 8-12 mmol/L), hypertriglyceridemia (typically 5-20 mmol/L), a normal ApoB ... Hyperlipidemia represents a subset of dyslipidemia and a superset of hypercholesterolemia. Hyperlipidemia is usually chronic ... These unclassified forms are extremely rare: Hyperalphalipoproteinemia Polygenic hypercholesterolemia Acquired hyperlipidemias ... that is hypercholesterolemia, hypertriglyceridemia or both in combined hyperlipidemia. Elevated levels of Lipoprotein(a) may ...

https://en.wikipedia.org/wiki/Hyperlipidemia

"Sitosterolemia Presenting as Pseudohomozygous Familial Hypercholesterolemia". Clin Med Res. 14 (2): 103-8. doi:10.3121/cmr. ...

https://en.wikipedia.org/wiki/Metab-L

Familial hypercholesterolemia: this disorder is characterized by the absence of functional receptors for LDL. Deficiencies in ... "Novel Therapies for Treating Familial Hypercholesterolemia". Current Atherosclerosis Reports. 16 (1): 382. doi:10.1007/s11883- ...

https://en.wikipedia.org/wiki/Biosynthesis

Desai NR, Sabatine MS (Feb 2015). "PCSK9 inhibition in patients with hypercholesterolemia". Trends in Cardiovascular Medicine. ... its role in causing some cases of familial hypercholesterolaemia when some mutations are present, and its role in causing very ... from the identification of a new gene in familial hypercholesterolemia towards a potential new class of anticholesterol drugs ... added an indication for alirocumab to treat adults with homozygous familial hypercholesterolemia (HoFH), a genetic condition ...

https://en.wikipedia.org/wiki/Alirocumab

January 2007). "Inhibition of microsomal triglyceride transfer protein in familial hypercholesterolemia". The New England ... "FDA Approves Aegerion Pharmaceuticals' Juxtapid (lomitapide) Capsules for Homozygous Familial Hypercholesterolemia (HoFH)" ( ... is a medication used as a lipid-lowering agent for the treatment of familial hypercholesterolemia, developed by Aegerion ... in patients with homozygous familial hypercholesterolemia (HoFH)." In a Phase III study, lomitapide led to elevated ...

https://en.wikipedia.org/wiki/Lomitapide

2003). "Autosomal recessive hypercholesterolemia in a Sicilian kindred harboring the 432insA mutation of the ARH gene". ... 2002). "Autosomal recessive hypercholesterolaemia in Sardinia, Italy, and mutations in ARH: a clinical and molecular genetic ... 2001). "Autosomal recessive hypercholesterolemia caused by mutations in a putative LDL receptor adaptor protein". Science. 292 ... 2005). "A novel ARH splice site mutation in a Mexican kindred with autosomal recessive hypercholesterolemia". Hum. Genet. 116 ( ...

https://en.wikipedia.org/wiki/Low-density_lipoprotein_receptor_adapter_protein_1

Yamamoto, Akira; Sudo, Hiroshi; Endo, Akira (March 1980). "Therapeutic effects of ML-236B in primary hypercholesterolemia". ...

https://en.wikipedia.org/wiki/Akira_Endo_(biochemist)

"27-Hydroxycholesterol links hypercholesterolemia and breast cancer pathophysiology". Science. 342 (6162): 1094-8. doi:10.1126/ ...

https://en.wikipedia.org/wiki/27-Hydroxycholesterol

Endocrinology Hypercholesterolemia is associated with significant retinal microvascular dysfunction as evidenced in a study ... Nägele MP et al.: Retinal microvascular dysfunction in hypercholesterolemia.J Clin Lipidol. 2018;12:1523-1531 Hanssen, H; et al ... based on 67 patients with hypercholesterolemia without known cardiovascular disease by a reduction in flicker-induced ...

https://en.wikipedia.org/wiki/Retinal_vessel_analysis

Zech LA, Hoeg JM (March 2008). "Correlating corneal arcus with atherosclerosis in familial hypercholesterolemia". Lipids in ...

https://en.wikipedia.org/wiki/Arcus_senilis

Hypercholesterolemia is not a risk factor for mortality in persons older than 70 years and risks from statin drugs are more ... Cicero, Arrigo F. G.; Fogacci, Federica; Zambon, Alberto (9 February 2021). "Red Yeast Rice for Hypercholesterolemia: JACC ... Apoprotein-B inhibitor mipomersen (approved by the FDA in 2013 homozygous familial hypercholesterolemia.). Bempedoic acid, an ...

https://en.wikipedia.org/wiki/Lipid-lowering_agent

Qin Y, Niu K, Zeng Y, Liu P, Yi L, Zhang T, Zhang QY, Zhu JD, Mi MT (2013). "Isoflavones for hypercholesterolaemia in adults". ...

https://en.wikipedia.org/wiki/Soybean

Heterozygous familial hypercholesterolemia in children Homozygous familial hypercholesterolemia Hypertriglyceridemia ( ... May 1995). "Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG ... August 2006). "The anti-atherosclerotic effects of lipid lowering with atorvastatin in patients with hypercholesterolemia". ... Hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson types IIa and IIb) to reduce ...

https://en.wikipedia.org/wiki/Atorvastatin

Past nine months of age, hypercholesterolemia may be seen. In the final stages of the disease, at around 15 months of age for ...

https://en.wikipedia.org/wiki/Samoyed_hereditary_glomerulopathy

"Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia". The New England Journal of Medicine. 356 ( ...

https://en.wikipedia.org/wiki/Cholesteryl_ester_transfer_protein

INMEGEN also works on identifying the biomarkers for hypercholesterolemia. INMEGEN has established collaborations with both ...

https://en.wikipedia.org/wiki/Instituto_Nacional_de_Medicina_Genómica

Paillard F (May 1999). "A novel soluble chimera for the treatment of familial hypercholesterolemia". Human Gene Therapy. 10 (7 ...

https://en.wikipedia.org/wiki/SFRS6

Genetics of Familial Hypercholesterolemia. Familial hypercholesterolemia (FH) can be caused by inherited changes (mutations) in ... How do I know if I have familial hypercholesterolemia?. One of the main signs of FH is LDL cholesterol levels over 190 mg/dL in ... Familial hypercholesterolemia (FH) is a genetic disorder that affects about 1 in 250 people and increases the likelihood of ... If you are concerned that you could have familial hypercholesterolemia or hereditary heart disease, the first step is to ...

https://www.cdc.gov/genomics/disease/fh/FH.htm

Familial hypercholesterolemia is a disorder that is passed down through families. It causes LDL (bad) cholesterol level to be ... Familial hypercholesterolemia is a disorder that is passed down through families. It causes LDL (bad) cholesterol level to be ... Familial hypercholesterolemia is a genetic disorder. It is caused by a defect on chromosome 19. ... A strong family history of familial hypercholesterolemia or early heart attacks. *High level of LDL cholesterol in either or ...

https://medlineplus.gov/ency/article/000392.htm

Familial hypercholesterolemia is an inherited condition characterized by very high levels of cholesterol in the blood. Explore ... Genetic Testing Registry: Hypercholesterolemia, autosomal dominant, type B *Genetic Testing Registry: Hypercholesterolemia, ... Familial hypercholesterolemia resulting from mutations in the LDLR, APOB, or PCSK9 gene have an autosomal dominant pattern. of ... Mutations in the APOB, LDLR, LDLRAP1, or PCSK9 gene cause familial hypercholesterolemia. Changes in the LDLR gene are the most ...

https://ghr.nlm.nih.gov/condition/familial-hypercholesterolemia

Tags familial hypercholesterolemia How Common is Familial Hypercholesterolemia?. Familial Hypercholesterolemia (FH) is a ... Tags familial hypercholesterolemia, public health Familial Hypercholesterolemia as a Prototype for Precision Public Health. In ... Tags familial hypercholesterolemia Reducing the Global Public Health Burden of Familial Hypercholesterolemia: More Work Ahead. ... Tags familial hypercholesterolemia Many Adults with Familial Hypercholesterolemia Are Not Meeting Goal LDL-Cholesterol Level. ...

https://blogs.cdc.gov/genomics/tag/familial-hypercholesterolemia/

Tags familial hypercholesterolemia, genetics, genomics, public health A Public Health Genomic State-by-State Clickable Map: ... Tags familial hypercholesterolemia Public Health Genomics in Action: Reducing Morbidity and Mortality from Familial ... What Gets Measured Gets Done: Public Health Progress in Familial Hypercholesterolemia. Just 4 years ago, one of us (MJK) co- ... Tags familial hypercholesterolemia, genetic counseling, genetic testing, genetics, genomics, hereditary breast and ovarian ...

https://blogs.cdc.gov/genomics/tag/familial-hypercholesterolemia/page/2/

Efficacy and Safety of Lomitapide in Hypercholesterolemia Xin Liu 1 2 , Peng Men 3 , Yuhui Wang 2 , Suodi Zhai 3 , Zhigang Zhao ... Efficacy and Safety of Lomitapide in Hypercholesterolemia Xin Liu et al. Am J Cardiovasc Drugs. 2017 Aug. ... Lomitapide: A novel agent for the treatment of homozygous familial hypercholesterolemia. Davis KA, Miyares MA. Davis KA, et al. ... Lomitapide for the treatment of hypercholesterolemia. Berberich AJ, Hegele RA. Berberich AJ, et al. Expert Opin Pharmacother. ...

https://www.ncbi.nlm.nih.gov/pubmed/28255870

Familial hypercholesterolaemia (FH) is a dominantly inherited disorder present from birth that markedly elevates plasma low- ... Integrated guidance on the care of familial hypercholesterolaemia from the International FH Foundation Int J Cardiol. 2014 Feb ... Familial hypercholesterolaemia (FH) is a dominantly inherited disorder present from birth that markedly elevates plasma low- ...

https://pubmed.ncbi.nlm.nih.gov/24418289/?dopt=Abstract

... and Treatment for Familial Hypercholesterolemia (FH) (R61/R33 Clinical Trial Required) RFA-HL-22-006. NHLBI ... Familial Hypercholesterolemia (FH) is a common genetic disorder, affecting 1 in 250 people in the U.S., that causes high levels ... Implementation Research to Improve Case Finding, Cascade Screening, and Treatment for Familial Hypercholesterolemia (FH) (R61/ ... blood relatives of familial hypercholesterolemia (FH) index cases are systematically contacted based on their risk according to ...

https://grants.nih.gov/grants/guide/rfa-files/RFA-HL-22-006.html

... and fatty acid concentration in individuals with familial hypercholesterolemia (FH). Plasma and MP samples were collected from ... Lipoprotein-apheresis reduces circulating microparticles in individuals with familial hypercholesterolemia. This is some text ... and fatty acid concentration in individuals with familial hypercholesterolemia (FH). Plasma and MP samples were collected from ... and fatty acid concentration in individuals with familial hypercholesterolemia (FH). Plasma and MP samples were collected from ...

https://www.izon.com/publications/60fa0f255bfd9fa21612097c-1609

Jassim, W.E. (‏2012)‏. Association of ABO blood group in Iraqis with hypercholesterolaemia, hypertension and diabetes mellitus ... Association of ABO blood group in Iraqis with hypercholesterolaemia, hypertension and diabetes mellitus. ... This study in Baghdad, Iraq investigated the possible association of diabetes mellitus, hypercholesterolaemia and hypertension ... The data were derived from 920 patients with diabetes mellitus, hypertension and hypercholesterolaemia attending hospitals, ...

https://extranet.who.int/iris/restricted/handle/10665/118552?locale-attribute=ar&

... , an example of a thesis we printed. Visit ... Home / Cases / Management of pediatric familial hypercholesterolemia; growing older, getting wiser. Management of pediatric ...

https://www.gildeprint.nl/en/case/management-of-pediatric-familial-hypercholesterolemia-growing-older-getting-wiser/

The purpose of the study is to establish the proportion of patients on lipid-lowering pharmacological treatment reaching the LDL-C goals according to the All-Russian Scientific Cardiology Society guidelines/ the 4th Joint European Task Force guidelines.

https://www.astrazenecaclinicaltrials.com/study/NIS-CRU-DUM-2010%2F1/

Angiotensinogen, Coronary heart disease, Familial hypercholesterolemia, Haplotype, Polymorphism Persistent URL doi.org/10.1097/ ... OBJECTIVE: Familial hypercholesterolemia is characterized by high plasma low-density lipoprotein cholesterol levels and ... Haplotype of the angiotensinogen gene is associated with coronary heart disease in familial hypercholesterolemia. Publication. ... METHODS: In a cohort of 1785 familial hypercholesterolemia patients, we reconstructed five frequent haplotypes of the ...

https://repub.eur.nl/pub/29523

A man with a history of heterozygous familial hypercholesterolemia and premature coronary heart disease has an LDL-C level of ... A 43-year-old man in the United States with a history of heterozygous familial hypercholesterolemia (FH) presents for a ... Skill Checkup: A Man With History of Heterozygous Familial Hypercholesterolemia and Premature Coronary Heart Disease - Medscape ... Skill Checkup: A Man With History of Heterozygous Familial Hypercholesterolemia and Premature Coronary Heart Disease. ...

https://reference.medscape.com/viewarticle/963430

Association of ABO blood group in Iraqis with hypercholesterolaemia, hypertension and diabetes mellitus ... Association of ABO blood group in Iraqis with hypercholesterolaemia, hypertension and diabetes mellitus ... The differences were more marked in patients with diabetes mellitus, hypercholesterolaemia and hypertension than in the healthy ... This study in Baghdad, Iraq investigated the possible association of diabetes mellitus, hypercholesterolaemia and hypertension ...

http://www.emro.who.int/emhj-volume-18-2012/issue-8/article-14.html

Inclusion Criteria: Includes only relevant concepts associated with diagnoses of hypercholesterolemia. Exclusion Criteria: No ... of hypercholesterolemia. Data Element Scope: This value set may use the Quality Data Model (QDM) category or attributes related ... Clinical Focus: This value set contains concepts that represent a diagnosis, past or present, of hypercholesterolemia.. Data ... Inclusion Criteria: Includes only relevant concepts associated with diagnoses of hypercholesterolemia.. Exclusion Criteria: No ...

https://ecqi.healthit.gov/mcw/2021/ecqm-dataelement/diagnosishypercholesterolemia.html

... Experts Conclude Heritable Human Genome Editing Not Ready for Clinical Applications Posted on ... Tags: clinical germline gene editing, CRISPR, designer babies, DNA, DNA editing, embryos, ethics, familial hypercholesterolemia ... A possible example is familial hypercholesterolemia (FH), in which people carrying a mutation in the LDL receptor gene have ...

https://directorsblog.nih.gov/tag/familial-hypercholesterolemia/

Familial hypercholesterolaemia; Markov model; Cost effectiveness; Cascade testing; General practice; Secondary care registers. ... Background and aims: The cost effectiveness of cascade testing for familial hypercholesterolaemia (FH) is well recognised. Less ... analysis of searching electronic health records and cascade testing to identify and diagnose familial hypercholesterolaemia in ... analysis of searching electronic health records and cascade testing to identify and diagnose familial hypercholesterolaemia in ...

http://eprints.nottingham.ac.uk/52108/

... can be considered as the common link between hypertension and hypercholesterolemia. In particular, hypercholesterolemia seems ... can be considered as the common link between hypertension and hypercholesterolemia. In particular, hypercholesterolemia seems ... Probably, hypercholesterolemia is also a risk factor for the development of hypertension. On the other side, it is also ... Probably, hypercholesterolemia is also a risk factor for the development of hypertension. On the other side, it is also ...

https://cris.unibo.it/handle/11585/596176

Health and Aging in Africa: A Longitudinal Study of an INDEPTH Community in South Africa [HAALSI] Baseline Survey: Agincourt, South Africa, 2015 (ICPSR 36633 ...

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Posts about hypercholesterolemia written by Robert O. Young, CPT, MS, D.SC., PH.D. Naturopathic Practitioner ... Tag Archives: hypercholesterolemia Diabetes, Dr. Robert O. Young, Heart, Hypercholesterolemia, Nutrition, pHorever Young, ... Robert O. Younggood cholesterolheart diseasehypercholesterolemiaResearchsclerotic plaquewhat causes high cholesterol. ... Alkaline Lifestyle and Diet, arterosclerosis, Case Studies, Dietary Acidosis, Heart, Hypercholesterolemia, Medicine, Natural ...

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https://www.medscape.com/answers/1950759-196057/what-is-the-role-of-blood-glucose-and-ha1c-in-the-workup-of-noncoronary-atherosclerosis

Familial hypercholesterolemia: news * Genetics of familial hypercholesterolemia: updated criteria for LDLR gene variant ... Genetics of familial hypercholesterolemia: updated criteria for LDLR gene variant interpretation Czech version ... Familial hypercholesterolemia is one of the most common metabolic diseases. It is mostly associated with pathogenic variants in ... A case of autosomal recessive hypercholesterolemia caused by a new variant in the LDL receptor adaptor protein 1 gene. J Clin ...

https://www.atheroreview.eu/en/journals/athero-review/2021-3-23/genetics-of-familial-hypercholesterolemia-updated-criteria-for-ldlr-gene-variant-interpretation-128525

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Information on getting active. Activities such as walking, cycling - and more vigorous exercise such as running and energetic dancing - can help lower your cholesterol levels.

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https://g-2-c-2.org/search/Familial%20hypercholesterolemia

Background and aims: The cost effectiveness of cascade testing for familial hypercholesterolaemia (FH) is well recognised. (nottingham.ac.uk)
Prevalence and management of familial hypercholesterolaemia in patients with acute coronary syndromes. (ox.ac.uk)
AIMS: We aimed to assess the prevalence and management of clinical familial hypercholesterolaemia (FH) among patients with acute coronary syndrome (ACS). (ox.ac.uk)
ODYSSEY FH I and FH II: 78 week results with alirocumab treatment in 735 patients with heterozygous familial hypercholesterolaemia. (exchangecme.com)
Inhibition of PCSK9 with evolocumab in homozygous familial hypercholesterolaemia (TESLA Part B): a randomised, double-blind, placebo-controlled trial. (exchangecme.com)
Familial hypercholesterolaemia (FH) is an autosomal dominant genetic disorder, associated with elevated levels of low-density lipoprotein-cholesterol (LDL-C), which can lead to premature cardiovascular disease. (blogspot.com)

Despite extensive use of statins, patients with hypercholesterolemia, especially homozygous familial hypercholesterolemia (HoFH), do not achieve recommended targets of low-density lipoprotein cholesterol (LDL-C). There is an urgent need for novel options that could reduce proatherogenic lipoprotein cholesterol levels. (nih.gov)
The lifelong burden of homozygous familial hypercholesterolemia. (exchangecme.com)
Efficacy and safety of alirocumab in adults with homozygous familial hypercholesterolemia: The ODYSSEY HoFH trial. (exchangecme.com)
Challenges in the diagnosis and treatment of homozygous familial hypercholesterolemia. (exchangecme.com)
Evinacumab for homozygous familial hypercholesterolemia. (exchangecme.com)
Homozygous familial hypercholesterolemia is a rare inherited disease of metabolism. (nih.gov)
Researchers plan to evaluate patients with homozygous familial hypercholesterolemia using new and standard methods for detecting atherosclerosis. (nih.gov)

[ 2 ] The revisions and update have reflected the results of randomized placebo controlled clinical trials that have demonstrated reduced morbidity and mortality in subjects with moderate hypercholesterolemia treated with cholesterol-lowering agents, particularly (though not exclusively) statins. (medscape.com)

Metacarpophalangeal joint tendon xanthomas in a 45-year-old man with heterozygous familial hypercholesterolemia. (medscape.com)
PCSK9 inhibition with alirocumab in pediatric patients with heterozygous familial hypercholesterolemia: The ODYSSEY KIDS study. (exchangecme.com)
Long-term safety, tolerability, and efficacy of evolocumab in patients with heterozygous familial hypercholesterolemia. (exchangecme.com)
Cascade screening and treatment initiation in young adults with heterozygous familial hypercholesterolemia. (exchangecme.com)
Inclisiran for the treatment of heterozygous familial hypercholesterolemia. (exchangecme.com)

Genetics of familial hypercholesterolemia: updated. (atheroreview.eu)

Familial hypercholesterolemia (FH) is a genetic disorder that affects about 1 in 250 people and increases the likelihood of having coronary heart disease at a younger age. (cdc.gov)
Familial hypercholesterolemia is a genetic disorder. (medlineplus.gov)
Familial Hypercholesterolemia (FH) is a common genetic disorder, affecting more than 1 million people in the United States. (cdc.gov)
People with the genetic disorder familial hypercholesterolemia (FH) have increased blood levels of low-density lipoprotein (LDL) cholesterol, which increases their risk for developing coronary artery disease or having a heart attack. (cdc.gov)
Host Dr. Alan Brown discusses management issues and practical advice with certified registered nurse practitioner and clinical lipid specialist Joyce Ross, who says that familial hypercholesterolemia (FH) is the most common genetic disorder, and many who have it are totally unaware of their condition until a cardiovascular event occurs. (reachmd.com)
Familial Hypercholesterolemia (FH) is a common genetic disorder, affecting 1 in 250 people in the U.S., that causes high levels of low-density lipoprotein cholesterol (LDL-C) leading to premature coronary heart disease. (nih.gov)
Familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder characterized by premature mortal cardiovascular complications . (bvsalud.org)

Familial hypercholesterolemia (FH) can be caused by inherited changes (mutations) in the LDLR , APOB , and PCSK9 genes, which affect how your body regulates and removes cholesterol from your blood. (cdc.gov)
Mutations in the APOB , LDLR , LDLRAP1 , or PCSK9 gene cause familial hypercholesterolemia. (nih.gov)
Less commonly, familial hypercholesterolemia is caused by mutations in the APOB , LDLRAP1 , or PCSK9 gene. (nih.gov)
Elevated levels of non-HDL cholesterol and LDL in the blood may be a consequence of diet, obesity, inherited (genetic) diseases (such as LDL receptor mutations in familial hypercholesterolemia), or the presence of other diseases such as type 2 diabetes and an underactive thyroid. (findzebra.com)

Molecular genetic background of an autosomal dominant hypercholesterolemia in the Czech Republic. (atheroreview.eu)

Familial hypercholesterolemia affects an estimated 1 in 200 to 1 in 250 people in most countries and is thought to be the most common inherited condition affecting the heart and blood vessels (cardiovascular disease). (nih.gov)
Data synthesis Hypertension and hypercholesterolemia are highly prevalent in the general population and their coexistence in the same subjects additively increases the risk of cardiovascular disease. (unibo.it)
Why patients with familial hypercholesterolemia are at high cardiovascular risk? (exchangecme.com)
Prevention of atherosclerotic cardiovascular disease in children with familial hypercholesterolemia. (exchangecme.com)
Family history of hypercholesterolemia and/or cardiovascular disease before the age of 60 years. (nih.gov)

The Clinical Genome Resource (ClinGen) Familial Hypercholesterolemia Variant Curation Expert Panel consensus guidelines for LDLR variant classification. (atheroreview.eu)
Familial hypercholesterolemia: screening, diagnosis and management of pediatric and adult patients: clinical guidance from the National Lipid Association Expert Panel on Familial Hypercholesterolemia. (exchangecme.com)

Polygenic hypercholesterolemia is the most common cause of elevated serum cholesterol concentrations. (medscape.com)
Polygenic hypercholesterolemia is caused by a susceptible genotype aggravated by one or more factors, including atherogenic diet (excessive intake of saturated fat, trans fat, and, to a lesser extent, cholesterol), obesity , and sedentary lifestyle. (medscape.com)
Polygenic hypercholesterolemia is associated with an increased risk for coronary heart disease (CHD), as displayed in the image below. (medscape.com)
Familial hypercholesterolemia (FH) is sometimes clinically difficult to distinguish from polygenic hypercholesterolemia unless genetic testing is performed. (medscape.com)
A case-controlled study was done in the UK to determine if LDL cholesterol gene score can help differentiate patients with polygenic and monogenic familial hypercholesterolemia. (medscape.com)
Some patients with mixed dyslipidemias (elevations of both LDL-C and triglycerides) may have polygenic hypercholesterolemia along with some other condition such as insulin resistance or obesity that causes high triglyceride values. (medscape.com)
Familial hypercholesterolemia: is it time to separate monogenic from polygenic familial hypercholesterolemia? (exchangecme.com)

This study in Baghdad, Iraq investigated the possible association of diabetes mellitus, hypercholesterolaemia and hypertension with ABO type. (who.int)
The data were derived from 920 patients with diabetes mellitus, hypertension and hypercholesterolaemia attending hospitals, clinics and laboratories in Baghdad, and 200 healthy control individuals. (who.int)
Aim The aim of this study is to discuss the reliable scientific evidence of an interactive link between hypertension and hypercholesterolemia considering the metabolic pathways and the pathogenetic mechanisms connecting the two risk factors. (unibo.it)
Probably, hypercholesterolemia is also a risk factor for the development of hypertension. (unibo.it)
Although the mechanisms of interaction between these two risk factors have not been completely elucidated thus far, there is rapidly growing evidence that the involvement of the renin-angiotensin system (RAS) can be considered as the common link between hypertension and hypercholesterolemia. (unibo.it)
Conclusions Hypertension and hypercholesterolemia are highly coprevalent and strongly related from a pathophysiological point of view. (unibo.it)

Bempedoic acid plus ezetimibe fixed-dose combination in patients with hypercholesterolemia and high CVD risk treated with maximally tolerated statin therapy. (exchangecme.com)

Two years of pravastatin therapy induced a significant regression of carotid atherosclerosis in children with familial hypercholesterolemia, with no adverse effects on growth, sexual maturation, hormone levels, or liver or muscle tissue. (nih.gov)
Although hypercholesterolemia itself is asymptomatic, longstanding elevation of serum cholesterol can lead to atherosclerosis (hardening of arteries). (findzebra.com)

This post is a summary of our recently published paper in JAMA and outlines the public health impact and challenges for cascade screening for Familial Hypercholesterolemia (FH) in the United States. (cdc.gov)
A randomized controlled trial of genetic testing and cascade screening in familial hypercholesterolemia. (exchangecme.com)

In our previous blog, we discussed familial hypercholesterolemia as a prototype for "precision public health" and how the combination of public health and genetic approaches can contribute to raising awareness, diagnosis, and treatment of more than 1 million individuals in the United States with this relatively common genetic condition. (cdc.gov)

However, one parent will have severe hypercholesterolemia and will also probably have either a personal or family history for premature coronary artery disease (CAD). (medscape.com)
The diagnosis of both homozygous and heterozygous FH is based primarily on the finding of severe LDLc elevations in the absence of secondary causes of hypercholesterolemia. (medscape.com)
If necessary, other treatments such as LDL apheresis or even surgery (for particularly severe subtypes of familial hypercholesterolemia) are performed. (findzebra.com)
Ten further patients with severe hypercholesterolaemia ingested daily for 3 weeks, in random order, activated charcoal 16 g, cholestyramine 16 g, activated charcoal 8 g + cholestyramine 8 g, or bran. (diff.org)

A possible example is familial hypercholesterolemia (FH), in which people carrying a mutation in the LDL receptor gene have unusually high levels of cholesterol in their blood. (nih.gov)
In particular, hypercholesterolemia seems to promote the upregulation of type 1 angiotensin II (AT1) receptor genes because of an increase in the stability of mRNA followed by structural overexpression of vascular AT1 receptors for angiotensin II. (unibo.it)
A case of autosomal recessive hypercholesterolemia caused by a new variant in the LDL receptor adaptor protein 1 gene. (atheroreview.eu)

OBJECTIVE: Familial hypercholesterolemia is characterized by high plasma low-density lipoprotein cholesterol levels and premature coronary heart disease. (eur.nl)
Despite the monogenetic origin of familial hypercholesterolemia, the incidence of coronary heart disease varies considerably among patients, which is only partly explained by classical risk factors. (eur.nl)
Therefore, we analyzed the angiotensinogen gene as a modifier gene for coronary heart disease risk in patients with familial hypercholesterolemia. (eur.nl)
CONCLUSIONS: We conclude that genetic variation in the angiotensinogen gene contributes to coronary heart disease risk in patients with familial hypercholesterolemia. (eur.nl)

Worldwide Prevalence of Familial Hypercholesterolemia: Meta-Analyses of 11 Million Subjects. (atheroreview.eu)

If you are concerned that you could have familial hypercholesterolemia or hereditary heart disease, the first step is to collect your family health history of heart disease and share this information with your doctor. (cdc.gov)

Hypercholesterolemia results when low-density lipoprotein receptors are unable to remove cholesterol from the blood effectively. (nih.gov)
Familial Hypercholesterolemia (FH) is a genetic condition that results in elevated levels of low-density lipoprotein cholesterol (LDL-C) from birth, resulting in increased risk of heart disease and myocardial infarction. (cdc.gov)
Familial Hypercholesterolemia (FH) is a genetic condition that leads to high blood levels of low-density lipoprotein cholesterol, also known as LDL-C or "bad cholesterol. (cdc.gov)

One of Dr. Young's research clients Maren Hale was diagnosed with familial hypercholesterolemia and hypertriglycerides with LDL's over 400 mg/dl and triglycerides over 200 mg/dl. (wordpress.com)

Children with familial hypercholesterolemia have endothelial dysfunction and increased carotid intima-media thickness (IMT), which herald the premature atherosclerotic disease they develop later in life. (nih.gov)
Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. (drugs.com)

METHODS: In a cohort of 1785 familial hypercholesterolemia patients, we reconstructed five frequent haplotypes of the angiotensinogen gene, based on four polymorphisms. (eur.nl)
Les données ont été recueillies à partir des dossiers de 920 patients atteints de diabète, d'hypertension et d'hypercholestérolémie en consultation dans des hôpitaux, des cliniques et des laboratoires d'analyses de Bagdad, et de 200 témoins en bonne santé. (who.int)
Its ability to restrain molecules in the gastrointestinal tract can used to treat patients with hypercholesterolemia. (diff.org)
The dose-response relationship of activated charcoal in reducing serum cholesterol was determined and the effects of charcoal and cholestyramine were compared in patients with hypercholesterolaemia. (diff.org)
Montreal-FH-SCORE predicts coronary artery calcium score in patients with familial hypercholesterolemia. (exchangecme.com)

Just 4 years ago, one of us (MJK) co-chaired the Familial Hypercholesterolemia (FH) Foundation's first FH Global Summit: Awareness to Action held in Annapolis, Maryland. (cdc.gov)
In October 2019, the 7th annual FH Foundation global summit on familial hypercholesterolemia (FH) took place in Atlanta, Georgia. (cdc.gov)

Familial hypercholesterolemia is one of the most common metabolic diseases. (atheroreview.eu)

Some people with familial hypercholesterolemia do not have a mutation in one of these genes. (nih.gov)

The curative treatment of familial hypercholesterolemia: Liver transplantation. (bvsalud.org)
A second study conducted by the same research team showed the effects of different a.c. doses and the combination with cholestyramine in reducing serum Cholesterol ( Activated charcoal in the treatment of hypercholesterolaemia: dose-response relationships and comparison with cholestyramine, 1989 . (diff.org)

Familial hypercholesterolemia is an inherited condition characterized by very high levels of cholesterol in the blood. (nih.gov)
People with familial hypercholesterolemia have a high risk of developing a form of heart disease called coronary artery disease at a young age. (nih.gov)
Familial hypercholesterolemia accounts for only a small percentage of all cases of high cholesterol. (nih.gov)
Hypercholesterolemia , also called high cholesterol , is the presence of high levels of cholesterol in the blood. (findzebra.com)
In people with very high cholesterol (e.g., familial hypercholesterolemia), diet is often not sufficient to achieve the desired lowering of LDL, and lipid-lowering medications are usually required. (findzebra.com)

To determine the 2-year efficacy and safety of pravastatin therapy in children with familial hypercholesterolemia. (nih.gov)

Economic evaluation of drug therapy for hypercholesterolaemia in the United Kingdom / by Michael F. Drummond, Alistair L. McGuire and Astrid E. Fletcher. (who.int)

Both genetic and environmental risk factors play roles in familial hypercholesterolemia. (nih.gov)
Researchers are working to identify and characterize additional genes that may influence cholesterol levels and the risk of heart disease in people with other forms of hypercholesterolemia. (nih.gov)

How Common is Familial Hypercholesterolemia? (cdc.gov)

Familial Hypercholesterolemia Screening in Children and Adolescents in the United States: Where Are We Heading? (cdc.gov)
Two hundred fourteen children with familial hypercholesterolemia, aged 8 to 18 years and recruited from an academic medical referral center in the Netherlands. (nih.gov)

Anatomy16

Organisms7

Diseases23

Chemicals and Drugs69

Analytical, Diagnostic and Therapeutic Techniques and Equipment20

Psychiatry and Psychology1

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Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects. (1/3532)

Protective effect of dietary tomato against endothelial dysfunction in hypercholesterolemic mice. (2/3532)

Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. (3/3532)

Comparative hypocholesterolemic effects of five animal oils in cholesterol-fed rats. (4/3532)

Comparison of synthetic saponin cholesterol absorption inhibitors in rabbits: evidence for a non-stoichiometric, intestinal mechanism of action. (5/3532)

Identification of a novel Arg-->Cys mutation in the LDL receptor that contributes to spontaneous hypercholesterolemia in pigs. (6/3532)

Macroscopic distribution of coronary atherosclerotic lesions in cholesterol-fed rabbits. (7/3532)

Variability in meta-analytic results concerning the value of cholesterol reduction in coronary heart disease: a meta-meta-analysis. (8/3532)

Hypercholesterolemia

Hyperlipoproteinemia Type II

Cholesterol

Anticholesteremic Agents

Receptors, LDL

Cholesterol, LDL

Cholesterol, Dietary

Lipoproteins, LDL

Hydroxymethylglutaryl-CoA Reductase Inhibitors

Xanthomatosis

Apolipoproteins B

Epichlorohydrin

Azetidines

Arteriosclerosis

Diet, Atherogenic

Lipids

Lipoproteins

Triglycerides

Simvastatin

Apolipoproteins E

Heterozygote

Lovastatin

Homozygote

Cholesterol, HDL

Heptanoic Acids

Hyperlipidemias

Blood Component Removal

Proprotein Convertases

Pravastatin

Probucol

Rabbits

Pyrroles

Risk Factors

Anion Exchange Resins

Resins, Synthetic

Atherosclerosis

Psyllium

Endothelium, Vascular

Apolipoprotein B-100

Aorta

Hypolipidemic Agents

Cholestyramine Resin

Hypertriglyceridemia

Pedigree

Lipoproteins, IDL

Liver

Lipoproteins, VLDL

Fluorobenzenes

Colestipol

Disease Models, Animal

Hypertension

Vasa Vasorum

Arcus Senilis

Hydroxymethylglutaryl CoA Reductases

Vasodilation

Coronary Disease

Lipoprotein-X

Cardiovascular Diseases

Apolipoproteins

Sitosterols

Phytosterols

Lipoproteins, HDL

Dietary Fats

Cholesterol 7-alpha-Hydroxylase

Hyperlipidemia, Familial Combined

Crataegus

Lipid Metabolism

Swine

Cholesterol, VLDL

Coronary Artery Disease

Lipoprotein(a)

Coronary Vessels

Mice, Knockout

Portugal

Japan

Mice, Inbred C57BL

Swine, Miniature

Nitroprusside

Mutation

Cholesterol Esters