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Familial Hypercholesterolemia: more books (15)

Familial Hypercholesterolemia - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References by ICON Health Publications, 2004-10-01
Familial Hypercholesterolemia by Frederic P. Miller, Agnes F. Vandome, et all 2010-01-19
Complex Genetics of Monogenic Familial Hypercholesterolemia by K. C. M. C. Koeijvoets, 2007
Statin reverses atherogenesis in highest-risk kids familial hypercholesterolemia.(Children's Health): An article from: Family Practice News by Bruce Jancin, 2004-02-01
Towards Genetic Prediction of Coronary Heart Disease in Familial Hypercholesterolemia by Jeroen Van Der Net, 2009
Familial hypercholesterolemia: genetic predisposition to atherosclerosis.(Advanced Practice): An article from: MedSurg Nursing by Mary B. Engler, 2004-08-01
Statin reverses atherogenesis in highest-risk children: familial hypercholesterolemia.: An article from: Pediatric News by Bruce Jancin, 2004-02-01
Lipid Disorders: Low-Density Lipoprotein, Cholesterol, High-Density Lipoprotein, Triglyceride, Familial Hypercholesterolemia, Lipoprotein(a)
Screening of APOB gene mutations in subjects with clinical diagnosis of familial hypercholesterolemia.: An article from: Human Biology by Erardo Merino-Ibarra, Sergio Castillo, et all 2005-10-01
ACAT Inhibition and Progression of Carotid Atherosclerosis in Patients With Familial Hypercholesterolemia: The CAPTIVATE Randomized Trial / Religious Coping and Use of Intensive Life-Prolonging Care Near Death in Patients With Advanced Cancer (JAMA: The Journal of the American Mediacl Association, Volume 301, Number 11, March 18, 2009) by M. C. Meuwese, 2009
Ultrasound Measurement of Intima-media Thickness and Atherosclerotic Plaques in Carotid and Femoral Arteries (Methodological Studies & a Five-year Observational Study in Familial Hypercholesterolemia) by Inger Wendelhag, 1995
Familial hypercholesterolemia and other disorders of lipoprotein metabolism (Medical Grand Rounds) by Joseph L Goldstein, 1979
A familial-racial analysis of serum cholesterol and triglyceride levels by Jess David Curb, 1973
Lowering plasma cholesterol by raising LDL receptors (Medical Grand Rounds) by Michael S Brown, 1981

lists with details

Familiar Hypercholesterolemia - West Virginia
familiar hypercholesterolemia, West Virginia, 1800-982-8242 Extension 4816.WV DHHR BPH OEHP HP. Addressing familial hypercholesterolemia
http://www.wvdhhr.org/bph/oehp/hp/cardio/fh.htm

Extractions: WV DHHR BPH OEHP ... HP What is FH? FH or Familial Hypercholesterolemia is an inherited disorder which causes cholesterol levels to be elevated. One in every 250-500 people have FH. People with this inherited disorder lack LDL (low density lipoproteins) receptors or molecules which can identify cholesterol. LDL receptors on the cell membrane take cholesterol into the cell and break it down, so that the HDL (high density lipoproteins) can carry the cholesterol to the liver to be excreted from the body People with FH have fewer receptors on their cell membranes and therefore have elevated cholesterol in their blood, because the cholesterol cannot get into the cell to be carried to the liver. Thus, fewer receptors lead to elevated cholesterol which causes plaque formation and coronary artery disease. The elevated cholesterol levels in the blood cause an increased risk of early death secondary to heart disease. For example, people with FH have an increased chance of having a heart attack at an extremely early age. Even without other risk factors such as obesity, men may have a heart attack when they are 40-55 years old and women may have a heart attack when they are 50-65 years old.
ACLS -- Sign In Page
familial hypercholesterolemia (FH) is the most common genetic disorder leading to Patients with familial hypercholesterolemia (FH) have elevated
http://www.annclinlabsci.org/cgi/content/full/32/1/50

Extractions: This Article Abstract Full Text (PDF) Alert me when this article is cited ... Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager PubMed PubMed Citation Articles by Miltiadous, G. Articles by Elisaf, M. To view this item, select one of the options below: Sign In User Name Sign in without cookies. Purchase Short-Term Access Pay per Article - You may access this article (from the computer you are currently using) for 7 days for US$7.00 Pay for Admission - You may access all content in Annals of Clinical and Laboratory Science Online (from the computer you are currently using) for 7 days for US$25.00.
HDL Cholesterol Levels In Patients With Molecularly Defined Familial Hypercholes
familial hypercholesterolemia (FH) is the most common genetic disorder leading Keywords HDL cholesterol, familial hypercholesterolemia, apoE genotype,
http://www.annclinlabsci.org/cgi/content/abstract/32/1/50

Extractions: This Article Full Text Full Text (PDF) Alert me when this article is cited ... Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager PubMed PubMed Citation Articles by Miltiadous, G. Articles by Elisaf, M. Molecular Genetics Department,The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus Address correspondence to Moses Elisaf, M.D., F.R.S.H., Department of Internal Medicine, Medical School, University of Ioannina, GR 451 10, Ioannina, Greece; tel 306 519 7509; fax 306 514 5944; e-mail Familial hypercholesterolemia (FH) is the most common genetic disorder leading to premature atherosclerosis. Typically, it
Biochip For The Diagnosis Of Familial Hypercholesterolemia
Hypercholesterolemia patients now have a new method of diagnosis that enablesthem to know for sure if they are suffering from Familial Hypercholesteloremia
http://www.innovations-report.de/html/berichte/medizin_gesundheit/bericht-25652.

Extractions: Hypercholesterolemia patients now have a new method of diagnosis that enables them to know for sure if they are suffering from Familial Hypercholesteloremia (FH) or not. The new tool, known as Lipochip, is the first biochip for the diagnosis of Familial Hypercholesteloremia (a pathology that affects some 100,000 persons in Spain). The majority of those currently suffering from FH are not diagnosed as such. It is calculated that less than 30% of them have received a correct diagnosis with the majority receiving inadequate or inappropriate treatment. Moreover, when the illness is diagnosed, it is often too late as the patient a premature cardiovascular event which may be life-threatening. Lipochip enables the early diagnosis of a large number of patients in a short space of time. In this way, cardiovascular illnesses can be prevented, these pathologies appearing in more than half of the patients affected by FH before 55 years of age. Amongst those between 20 and 39 years of age who suffer from Familial Hypercholesterolemia, mortality due to a coronary pathology is 100 times greater than amongst those without FH. The importance of early diagnosis of FH with Lipochip lies in this high incidence of level of premature cardiovascular illnesses amongst FH patients. Without the correct diagnosis and treatment, many patients die between 35 and 65 years of age, and seven out of ten will suffer myocardiac attack before their sixtieth birthday. However, with early diagnosis and treatment, the survival rate and quality of life of patients improves, as these coronary events are greatly diminished. This also reduces hospital costs as there are less cardiovascular events amongst patients being suitably diagnosed and treated.
Familial Hypercholesterolemia
familial hypercholesterolemia. Treating FH. Treatment options now exist for FH,based on the accumulated knowledge of cholesterol metabolism.
http://www.hhmi.org/biointeractive/museum/exhibit98/content/d7info.html

Extractions: Treating FH Treatment options now exist for FH, based on the accumulated knowledge of cholesterol metabolism. Heterozygous people can take preventive measures, such as choosing a low-fat, low-cholesterol diet. Drugs are also available to lower blood cholesterol. Treatment for FH homozygous people may include regular apheresis, a process that removes LDL from blood. Can gene therapy help patients with FH? Some researchers are working to treat diseases by correcting defective genes. James Wilson, a former HHMI investigator, developed such a procedure called gene therapy for people with FH. In the first clinical trial, Wilson removed cells from the patient's liver, grew them on 800 culture plates, and "infected" them with a virus containing the gene for normal LDL receptors. Some of the cultured liver cells accepted the new gene. The "transgenic" cells were injected directly back into the patient's liver, where they produced LDL receptors. The LDL levels in the patient's blood dropped 15 to 30 percent and stayed down for 6 months. Since then, at least four more patients have undergone the experimental procedure. So far, the approach appears promising, but more research is needed to develop a broadly practical treatment and achieve a permanent cure.
Homozygous Familial Hypercholesterolemia - Evaluation, Treatment And Research At
The National Heart, Lung and Blood Institute is actively seeking patients withHomozygous familial hypercholesterolemia to receive free evaluation and/or
http://patientrecruitment.nhlbi.nih.gov/LDL500.aspx

Extractions: LDL > 500 mg/dL Research Study If you have homozygous familial hypercholesterolemia (FH), you are invited to participate in a study that will evaluate the development and follow the natural history of atherosclerosis in your disorder. A variety of clinical and research techniques will be used to assess and follow the development of atherosclerosis. Recommendations for treatments will be provided based upon these findings. Persons with homozygous familial hypercholesterolemia typically have a total and low density lipoprotein (LDL) cholesterol concentration greater than 700 mg/dL with normal triglycerides. Cholesterol deposits called xanthomas are frequently present in the first few years of life and are located on the elbows, knees, between the webs of the fingers and on the Achilles tendons. Eligible persons will undergo a comprehensive cardiac evaluation. All patients will remain under the care of their own physician who will receive results of the laboratory and diagnostic tests. In most cases, you will be invited back for yearly evaluations. There is no cost to you for travel or medical testing.
Departement Of Cardiology Faculty Of Medicine, University Of Indonesia
familial hypercholesterolemia AND COMPLICATIONS. Andria Priyana. Introduction.familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder
http://www.kardiologi-ui.com/newsread.php?id=121
IngentaConnect High Risk/high Priority: Familial Hypercholesterolemia - A Paradi
familial hypercholesterolemia provides an excellent model for Familialhypercholesterolemia should serve as a paradigm of molecular medicine we
http://www.ingentaconnect.com/content/els/15675688/2002/00000002/00000004/art000

Extractions: For Researchers For Librarians Author: Schuster H. Source: Atherosclerosis, Supplements , Volume 2, Number 4, 1 April 2002, pp. 27-32(6) Publisher: Elsevier Science View Table of Contents full text options Keywords: Familial hypercholesterolemia Molecular characterization Disease prevention Language: English Document Type: Research article DOI: Affiliations: Infogen GmbH and Max Delbruck Center, Humboldt University, , Berlin, Germany Access to this article is through a website external to IngentaConnect You may be required to register and activate access/purchase before you can obtain the full text.
HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA IS ASSOCIATED WITH LARGER LDL SIZE FO
OBJECTIVES familial hypercholesterolemia (FH) is a genetic disorder associatedwith raised plasma LDLcholesterol levels and premature coronary heart
http://www.ccs.ca/society/congress2002/abstracts/abs/a157.htm

Extractions: OBJECTIVES: Familial hypercholesterolemia (FH) is a genetic disorder associated with raised plasma LDL-cholesterol levels and premature coronary heart disease (CHD). Although it has been suggested that LDL size could further increase the CHD risk resulting from an elevated LDL concentration, factors controlling LDL size in FH patients are not fully understood. Therefore, the objectives of the present study were to compare LDL size in FH vs nonFH patients and to study its relationship with known correlates of LDL size such as abdominal obesity (waist girth) and triglyceride (TG) levels. METHODS: After exclusion of patients with fasting TG and glucose levels greater than 4.5 mmol/L and 7.0 mmol/L respectively, a sample of 112 male patients (46.7 ± 12.6 years of age) with a clinical and/or molecular diagnosis of heterozygous FH was compared to a group of 305 nonFH men (42.3 ± 11.9 years). LDL size was assessed by 2-16% polyacrylamide gel electrophoresis. RESULTS: FH patients were characterized by the expected differences in their plasma lipid profile including substantially higher cholesterol (+65.8%), LDL-cholesterol (+88.9%) and apo B (+30.6%) levels than non FH men despite the fact that they had lower body mass index (-8.1%) and waist circumference (-5.4%) values than nonFH controls (p
Entrez PubMed
Fibroblasts from patients with homozygous familial hypercholesterolemia (FH), adisease characterized by accelerated atherogenesis, are known to lack
http://www.immunityageing.com/pubmed/2963664

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Oligonucleotide Ligation Assay (OLA) For The Diagnosis Of Familial Hypercholeste
Molecular genetics of the LDL receptor gene in familial hypercholesterolemia . explain one third of familial hypercholesterolemia in a German sample.
http://www.nature.com/nbt/journal/v14/n10/abs/nbt1096-1279.html

Extractions: @import "/nbt/style.css"; NATURE.COM NEWS@NATURE.COM NATUREJOBS NATUREEVENTS ... Help E-MAIL: PASSWORD: Save password Forgotten password? SEARCH JOURNAL Advanced search Journal home Archive Table of Contents ... For librarians NPG Resources Bioentrepreneur The Nature Biotechnology Directory Nature Reviews Drug Discovery Nature ... Browse all publications Research Article Nature Biotechnology doi:10.1038/nbt1096-1279 Heike Baron , Steven Fung , Atakan Aydin , Friedrich C. Luft Applied Biosystems Division of Perkin Elmer, Foster City, CA 94404. Corresponding author. REFERENCES Kannel, W.B., Castelli, W.P., Gordon, T., and McNamara, P.M. 1971. Serum cholesterol, lipoproteins, and the risk of coronary heart disease. Ann. Intern. Med PubMed ISI ChemPort Scandinavian Simvastatin Survival Study Group. 1994. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet PubMed ISI Shepherd, J., Cobbe, S.M., Ford, I., Isles, C.G., Lorimer, A.R., Macfarlane, P.W., et al. 1996. Prevention of coronary heart disease with pravastatin in men with hyper-cholesterolemia. N. Engl. J. Med
Familial Hypercholesterolemia
Federally Funded Research on familial hypercholesterolemia. EJournals PubMedCentral Finding Nutrition Studies on familial hypercholesterolemia
http://www.icongrouponline.com/health/Familial_Hypercholesterolemia_Ph.html

Extractions: E B O O K Electronic File * E-Book version sent via e-mail in 2 business days Pages Price $34.95(USD) ISBN Published Synopsis In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading." Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with familial hypercholesterolemia is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to conduct medical research using the most advanced tools available and spending the least amount of time doing so. Related Conditions/Synonyms hypercholesterolemic xanthomatosis; type II hyperlipoproteinemia
LIPOSORBER® LDL Apheresis - Treatment Option For Familial Hypercholesterolemia
familial hypercholesterolemia) for whom diet has been ineffective and maximum University of Michigan Treating familial hypercholesterolemia with LDL
http://www.liposorber.com/

Extractions: The Liposorber LA-15 LDL Apheresis System is approved by the FDA and indicated for use to acutely remove LDL-C from the plasma of the following high-risk patient populations (ex. Familial Hypercholesterolemia) for whom diet has been ineffective and maximum drug therapy (such as Statins) has either been ineffective or not tolerated: Examples of Current Liposorber Treatment Sites Near You (alphabetical order by state, city) Cedars-Sinai Medical Center Los Angeles, CA Emory University Atlanta, GA Evanston Hospital: LDL Apheresis Evanston, IL University of Kansas Medical Center Kansas City, KS University of Michigan: Treating Familial Hypercholesterolemia with LDL Apheresis Ann Arbor, MI Mayo Clinic Rochester, MN University of North Carolina: Only Lipid Clinic in NC to offer LDL Apheresis Chapel Hill, NC
Familial Hypercholesterolemia Probed - MIT News Office
Bostonarea scientists, including two at the Whitehead Institute for BiomedicalResearch, have found why defects occur in the receptors for the low-density
http://web.mit.edu/newsoffice/1996/hypercholesterolemia-0911.html

Extractions: September 11, 1996 Familial hypercholesterolemia (FH), a genetic disease characterized by high levels of cholesterol and early mortality, is caused by defects in the receptor for the low-density lipoprotein (LDL)the "bad" cholesterol. Now, Boston-area scientists including two at the Whitehead Institute for Biomedical Research have found that this occurs because mutations in the LDL receptor prevent the protein from folding into its normal shape. This in turn impedes the receptor's ability to bind bad cholesterol and remove it from the bloodstream, causing the hypercholesterolemia. FH is an autosomal dominant trait, meaning that a child born to an affected parent has a 50 percent chance of inheriting the gene. About 1 in 500 people are heterozygous for FH-they have one abnormal and one normal copy of the LDL receptor gene-making FH one of the most common inborn errors of metabolism. At birth, FH-heterozygous people have a twofold increase in cholesterol levels, and they develop coronary heart disease in middle age. Homozygotes (people who have two abnormal copies of the LDL receptor gene) number about one in a million and have a severe form of the disease in which coronary heart disease begins during childhood and causes death by age 20.
Lipid Digestion And Lipoproteins
Type II (familial hypercholesterolemia, FH), 4 classes of LDL receptor defect,reduced LDL clearance leads to hypercholesterolemia, resulting in
http://www.dentistry.leeds.ac.uk/biochem/thcme/lipoproteins.html

Extractions: Return to Medical Biochemistry Home Page Intestinal Uptake of Lipids In order for the body to make use of dietary lipids, they must first be absorbed from the small intestine. Since these molecules are oils, they are essentially insoluble in the aqueous environment of the intestine. The solubilization (or emulsification) of dietary lipids is thereforeaccomplished by means of bile salts, which are synthesized from cholesterol in the liver and then stored in the gallbladder; they are secreted following the ingestion of fat. The emulsification of dietary fats renders them accessible to pancreatic lipases (primarily lipase and phospholipase A ). These enzymes, secreted into the intestine from the pancreas, generate free fatty acids and a mixtures of mono- and diacylglycerols from dietary triacylglycerols. Pancreatic lipase degrades triacylglycerols at the 1 and 3 positions sequentially to generate 1,2-diacylglycerols and 2-acylglycerols. Phospholipids are degraded at the 2 position by pancreatic phospholipase A releasing a free fatty acid and the lysophospholipid. The products of pancreatic lipases then diffuse into the intestinal epithelial cells, where the re-synthesis of triacyglycerols occurs.
Hypercholesterolemia, Familial
Clinical Outcome of Patients with familial hypercholesterolemia and CoronaryArtery Disease Undergoing Partial Ileal Bypass Surgery Clinical Outcome of
http://www.gfmer.ch/genetic_diseases_v2/gendis_detail_list.php?cat3=124
Familial Hypercholesterolemia
A dominantly inherited genetic condition that results in markedly elevated (lowdensitylipoprotein) cholesterol levels beginning at birth, and resulting in
http://www.ehendrick.org/healthy/000392.htm

Extractions: Injury Disease Nutrition Poison ... Prevention A dominantly inherited genetic condition that results in markedly elevated LDL (low-density lipoprotein) cholesterol levels beginning at birth, and resulting in heart attacks at an early age. Type II hyperlipoproteinemia; Hypercholesterolemic xanthomatosis; Low density lipoprotein receptor mutation Affected people have consistently high levels of low-density lipoprotein, which leads to premature atherosclerosis of the coronary arteries. Typically in affected men, heart attacks occur in their 40s to 50s, and 85% of men with this disorder have experienced a heart attack by age 60. The incidence of heart attacks in women with this disorder is also increased, but delayed 10 years later than in men.
Arquivos Brasileiros De Cardiologia -
familial hypercholesterolemia is characterized by high serum levels of total The clinical presentation of familial hypercholesterolemia is through
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2000000700005
Familial Hypercholesterolemia - Definition Of Familial Hypercholesterolemia In T
Definition of familial hypercholesterolemia in the Medical Dictionary and Thesaurus.familial hypercholesterolemia explanation. Information about familial
http://medical-dictionary.thefreedictionary.com/familial hypercholesterolemia
Familial Hypercholesterolemia Lahiri Koushik, Lahiri Bhabesh Chandra - Indian J
Lahiri K, Lahiri B. familial hypercholesterolemia. Homozygous familialhypercholesterolemia. Indian J Dermatol Venereol Leprol 2000;66331332.
http://www.ijdvl.com/article.asp?issn=0378-6323;year=2001;volume=67;issue=4;spag

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