Hyperhomocysteinemia Elevation of the plasma homocysteine concentration (hyperhomocysteinemia) is a common and important risk factor for http://www.tigc.org/eguidelines/hyperhomocysteinemia.htm
Extractions: November 2002 Background Elevation of the plasma homocysteine concentration (hyperhomocysteinemia) is a common and important risk factor for atherosclerotic arterial disease (Boushey CJ et al., JAMA 274:1049-1057, 1995) and for venous thromboembolism (Ray JG, Arch. Intern. Med. 158:2101-2106, 1998). The risk conferred by homocysteine adds to or even multiplies the risk conferred by factors such as smoking, hypertension, diabetes, and lipid disorders (for arterial disease) and Factor V Leiden (for venous thromboembolism). Even mild elevations of plasma homocysteine confer risk. Homocysteine levels are influenced by diet, as homocysteine is produced from metabolism of methionine, and cleared by metabolic pathways that require folic acid, vitamin B , and vitamin B as cofactors. Low levels of these vitamins are therefore associated with hyperhomocysteinemia. Congenital deficiencies of enzymes in these metabolic pathways, and renal failure, also are important causes of hyperhomocysteinemia. Screening Fasting plasma or serum homocysteine concentrations should be measured as a part of the investigation of selected patients with venous thromboembolism, particularly those with idiopathic thrombosis, recurrent thrombosis, and thrombosis at a young age or at an unusual site (see guideline on Investigation of Suspected Hypercoagulable States). Measurement of a homocysteine level should be considered in patients with arterial disease.
HYPERHOMOCYSTEINEMIA, HYPERFIBRINOGENEMIA, AND LIPOPROTEIN(A) EXCESS IN MAINTENA Arch Intern Med. 161;26282629, November 26, 2001, Is hyperhomocysteinemia a Risk Factor or a Consequence of Coronary Heart Disease?, Marco Cattaneo, MD Paul Knekt, PhD; Antti Reunanen, MD, PhD; Georg http://www.nal.usda.gov/ttic/tektran/data/000007/59/0000075926.html
Extractions: High blood levels of the amino acid homocysteine, the clotting factor fibrinogen and the cholesterol-carrying particle lipoprotein(a)[Lp(a)] appear to increase the risk for development of heart attacks and strokes in the general population. Kidney failure patients have been shown to have high blood levels of homocysteine or fibrinogen or Lp(a), but the occurrence of simultaneous elevations of homocysteine, fibrinogen, and Lp(a) in these patients had never been evaluated. We demonstrated that nearly one-fourth of kidney failure patients maintained on dialysis have simultaneous elevations in homocysteine, fibrinogen and Lp(a), which was 35-fold greater than in persons with normal kidney function. The combined elevated levels of homocysteine, fibrinogen, and Lp(a) in kidney failure patients on dialysis may contribute to their increased risk for heart attacks and strokes. Keywords:
Hyperhomocysteinemia hyperhomocysteinemia. A patient who is heterozygous for this mutation has no evidenceof hyperhomocysteinemia or increased risk of thrombotic disorders. http://www-admin.med.uiuc.edu/hematology/PtHomocysteinemia.htm
Extractions: University of Illinois - Urbana/Champaign Carle Cancer Center Hematology Resource Page Patient Resources Hyperhomocysteinemia Home Factor V Leiden Antiphospholipid Syndrome General Clotting Information ... Protein S deficiency Homocystinuria (homocystine excreted in the urine) was first reported in 1962. Homocystinuria is associated with a syndrome of mental retardation, skeletal and visual problems and arterial as well as venous thrombosis. There are two primary enzymes that, when a defect is present, can result in either homocystinuria or hyperhomocysteinemia (hyper=high) as discussed below. Mechanism of Hyperhomocysteinemia: Homocysteine is a naturally occurring molecule in the body and it is required in several reactions that occur within the cells that comprise the human body. The reactions are detailed in the figure above; they result in the formation of cysteine and methionine, which can be further used by the body. If the pathways to either cysteine or methionine are blocked, then homocysteine levels may rise. Three enzymes in the above diagram will be focused on, as they are associated with elevated levels of homocysteine. These enzymes are methylenetetrahydrofolate reductase (MTHFR), cystathionine beta-synthase (CBS) and methionine synthase (MS).
Member Sign In hyperhomocysteinemia. Folic acid deficiency or methylenetetrahydrofolatereductase (MTHFR) deficiency are also causes of hyperhomocysteinemia. http://www.medscape.com/viewarticle/415086_7
HYPERHOMOCYSTEINEMIA IN CHRONIC ALCOHOLISM: CORRELATION WITH FOLATE, VITAMIN B-1 University of Illinois Urbana/Champaign Carle Cancer Center Hematology Resource Page Homocystinuria (homocystine excreted in the urine) was first reported in 1962. Mechanism of hyperhomocysteinemia Homocysteine is a naturally occurring molecule in the body and it is required in http://www.nal.usda.gov/ttic/tektran/data/000007/86/0000078615.html
Extractions: Homocysteine is an amino acid which plays an important function in the body but becomes harmful when its level in the blood becomes excessive. A high homocysteine in the blood is also indication that the individual is not taking some other B vitamins including folic acid, vitamin B12 or vitamin B6. It is known that heavy alcohol drinkers often manifest vitamin deficiencies. In this study we have shown that heavy drinkers have high levels of homocysteine in their blood and that this high homocysteine is due in part to deficiency in B6, folate and B12. Keywords:
Member Sign In hyperhomocysteinemia. Patients thromboses. Such severe inherited forms of hyperhomocysteinemiaare rarely encountered in daily practice, however. http://www.medscape.com/viewarticle/439361_4
The Chiropractic Resource Organization when a defect is present, can result in either homocystinuria or hyperhomocysteinemia. (hyper=high) as discussed below. http://chiro.org/
Extractions: The Chiropractic Resource Organization (CHIRO.ORG) has existed since 1995 as a non-profit Internet site developed by a group of chiropractic volunteers dedicated to supplying useful information to chiropractors. Whether you're a new DC , or a student whether you're looking for an associate or you want to learn some Chiropractic History we think we have a site you will enjoy. To navigate to these and other areas of CHIRO.ORG click on the menu bar above, use the site map or find exactly what you're looking for using our search tool. If you'd like to contribute to the content of our site, or perhaps create your own new section, please subscribe to the mailing list for our "Projects" group. Just go to the projects list page and follow the directions. Once you join our list, you will be able to post to our list (as a member) and advise us what your interests are. We are all volunteers here and welcome everyone with a positive, non-partisan spirit. Search Chiro.Org:
Hyperhomocysteinemia hyperhomocysteinemia Slide 31 of 33. http://meds.queensu.ca/medicine/deptmed/hemonc/macro/slide31.html
CTF Selected References: Hyperhomocysteinemia Selected References. Preventive Health Care, 2000 Update Screening and Managementof hyperhomocysteinemia for the Prevention of Coronary Artery Disease Events. http://www.ctfphc.org/References/Homocyst_bib.html
Extractions: Prepared by Gillian L. Booth, MD, Departments of Medicine, Clinical Epidemiology and Health Care Research Program, University of Toronto, Elaine E. L. Wang, MD, Departments of Pediatrics, Clinical Epidemiology and Health Care Research Program, University of Toronto These recommendations were finalized by the Task Force in July 1999 Statistics Canada. Causes of death, 1995 (Catalogue 84-208-XPB). 1997. Ottawa, Minister of Industry. Brophy JM. The epidemiology of acute myocardial infarction and ischemic heart disease in Canada. data from 1976 to 1991. Can J Cardiol 1997;13:474-478. Skovby F. Inborn errors of metabolism causing homocysteinemia and related vascular involvement. Haemostasis 1989;19(suppl 1):4-9. Mudd SH, Skovby F, Levy HL, Pettigrew KD, Wilcken B, Pyeritz RE, Andria G, Boers GHJ, Bromberg IL, Cerone R, Fowler B, Gröbe H, Schmidt H, Schweitzer L. The natural history of homocystinuria due to cystathione-synthase deficiency. Am J Hum Genet 1985;37:1-31. Moghadasian MH, McManus BM, Frohlich JJ. Homocyst(e)ine and coronary artery disease. Clinical evidence and genetic and metabolic background. Arch Intern Med 1997;157:2299-2308.
CTF Structured Abstract: Hyperhomocysteinemia Structured Abstract. Preventive Health Care, 2000 Update Screening and Managementof hyperhomocysteinemia for the Prevention of Coronary Artery Disease Events. http://www.ctfphc.org/Abstracts/Homocyst_abs.html
Extractions: Prepared by Gillian L. Booth, MD, Departments of Medicine, Clinical Epidemiology and Health Care Research Program, University of Toronto, Elaine E. L. Wang, MD, Departments of Pediatrics, Clinical Epidemiology and Health Care Research Program, University of Toronto These recommendations were finalized by the Task Force in July 1999 To evaluate the quality of evidence pertaining to homocysteine and coronary artery disease (CAD) and make recommendations regarding screening and treatment of hyperhomocysteinemia. Cardiovascular disease is the leading cause of death in Canada, accounting for almost 40% of all deaths. While mortality rates for ischemic heart disease are declining, the costs to society remain high. Since a number of cardiovascular deaths may be preventable, the search for novel risk factors continues. Homocysteine is an intermediate that is generated in the metabolism of methionine. Therefore, altered homocysteine metabolism has become the focus of increasing attention based on its potential role in the pathogenesis of atherosclerosis and other conditions, such as venous thrombosis and neural tube defects. The prevalence of hyperhomocysteinemia in the general population is between 5 and 10%, based on a threshold set at the 90
Extractions: Heart disease is the number one killer in this country, claiming 500,000 lives every year. Factors such as cigarette smoking, high blood pressure and cholesterol, physical inactivity, age, stress, hereditary factors, diabetes, and being a male all contribute to an increased risk of heart disease. However, many heart attacks occur in people without any of these risk factors. Recently studies point to a new risk factor. Homocysteine, an amino acid and a basic unit of protein, appears to be implicated in 10-15 percent of vascular (heart) disease cases. A 1992 study of over 14,000 male physicians found that those with the highest levels of homocysteine had more than three times the risk of heart disease. Foods rich in B vitamins - folate, B12 and B6 - help keep homocysteine at safe levels. In other words, when B-vitamins are provided, the homocysteine levels may decrease. Conversely, low levels of blood folate are consistently related to high levels of homocysteine. Folate (also known as folic acid) seems to have a greater clearing effect on homocysteine levels that B6, B12, or both vitamins combined. Some people may be more prone to homocysteine buildup and may consequently need more B-vitamins.
JAMA -- Page Not Found Impairment of Endothelial Functions by Acute hyperhomocysteinemia and Reversal byAntioxidant Vitamins Author Information Francesco Nappo, MD, PhD; Nicoletta http://jama.ama-assn.org/issues/v281n22/abs/jci90005.html
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Extractions: Hyperhomocysteinemia May Accelerate the Development of Atherosclerotic Lesions Despite Significantly Lowering Plasma Cholesterol Levels in LDL Receptor Knockout Mice. Rebecca L. Eastgard, Elizabeth A. Kirk, Renee C LeBoeuf, Michael E. Rosenfeld. Department of Pathobiology and Program in Nutritional Sciences, University of Washington, Seattle WA. Hyperhomocysteinemia is an independent risk factor for vascular diseases but the mechanisms by which homocysteine contributes to the disease process are not known. To address this question, we have developed a dietary protocol for induction of homocysteinemia involving stepwise increases in methionine intake from 2% to 4% over 16 and 24 week periods in the LDL receptor knockout mouse (LDLR-/-). This protocol results in a range of plasma homocysteine levels between 14 and 47 umol/l (n=58). Surprisingly, the elevation of plasma homocysteine was highly correlated with a significant reduction in total plasma cholesterol levels at all time points between 4 and 24 weeks in the LDLR-/-mice (r = -0.43) (average 223 +/- 37mg/dl [n=57] in the methionine fed LDLR-/- mice versus m m [n=19] for the chow fed mice vs. 13,721 +/- 6011
Extractions: Home German Journal of Psychiatry ISSN 1433-1055 Moderate hyperhomocysteinemia and neuropsychiatric symptoms in manganese-induced parkinsonism Stefan Bleich, Detlef Degner, Borwin Bandelow, Antje Riegel , Juan M. Maler, Eckart Rüther, and Johannes Kornhuber Department of Psychiatry Department of Neuroradiology Georg-August University of Göttingen, Germany Corresponding author: Stefan Bleich, M.D, Department of Psychiatry, Georg-August University of Göttingen, von-Siebold-Str. 5, D-37075 Göttingen, Germany; e-mail stefan.bleich@t-online.de Abstract Manganese intoxication is a well-known cause of parkinsonism and dementia. Here we present the case of an 80-year-old patient with proven manganese poisoning. We observed no long-term progression of the manganese-induced parkinsonian syndrome. The blood manganese concentration is now reduced to below the normal range (4.8 m g/l), but the manganese concentration in scalp hair (2.79 m g/g) has kept on increasing. Strikingly, even though we found normal cobalamin and even elevated serum folate levels, we observed a moderate hyperhomocysteinemia in two independent samples. We did not find any common known risk factors for this moderate hyperhomocysteinemia The possible role of hyperhomocysteinemia in manganese-induced parkinsonism is discussed (German J Psychiatry 2000;3:14-20) Key words: manganese, homocysteine, parkinsonism
Extractions: Hyperhomocysteinemia has been identified as a major risk factor for both arterial and venous thrombosis disease. Individuals homozygous for the thermolabile variant of the methylene tetrahydrofolate reductase gene (MTHFR) have significantly elevated plasma homocysteine levels. Homozygous thermolabile MTHFR has been described in 5% of normal Caucasians, 19% of patients with arterial disease, 11% of patients with venous thrombosis and 2% of women with recurrent pregnancy loss. Indications for Testing
Extractions: G.B Boncoraglio, G. Bussone, E.A Parati Istituto Nazionale Neurologico Carlo Besta, Milano, Italy Purpose: To describe cerebrovascular events in 20 patients affected by hyperhomocysteinemia. Methods: We evaluated clinical and neuroradiological findings (CT, MR, duplex US or DSA) in 20 patients (7 females, 13 males, 27 to 55 yrs). In all patients biochemical tests, serum folate, cobalamin level, homocysteine level (MEIA), protein C, protein S, antiphospholipid antibodies, FV-Leiden and protrombin mutation (20120A) were performed. Results: Conclusions: Mild hyperhomocysteinemia may be an additional thrombogenic risk factor for stroke. The inclusion of homocysteine determination is useful in stroke patients, besides high levels may be corrected with vitamins therapy.`
Extractions: R Clarke, L Daly, K Robinson, E Naughten, S Cahalane, B Fowler, and I Graham Table of Contents Find Similar Articles in the Journal Notify a friend about this article Add to Personal Archive ... Related Articles in Medline Articles in Medline by Author: Clarke, R. Graham, I. Medline Citation Abstract This article has been cited by other articles: Nappo, F., De Rosa, N., Marfella, R., De Lucia, D., Ingrosso, D., Perna, A. F., Farzati, B., Giugliano, D. (1999). Impairment of Endothelial Functions by Acute Hyperhomocysteinemia and Reversal by Antioxidant Vitamins. JAMA [Abstract] [Full Text] McCully, K. S. (1998). Homocysteine, Folate, Vitamin B6, and Cardiovascular Disease. JAMA [Full Text] Leontiadis, G. I., Sharma, V. K., Howden, C. W. (1999). Non-Gastrointestinal Tract Associations of Helicobacter pylori Infection: What Is the Evidence?. Arch Intern Med [Abstract] [Full Text] Stein, J. H., McBride, P. E. (1998). Hyperhomocysteinemia and Atherosclerotic Vascular Disease: Pathophysiology, Screening, and Treatment.
Extractions: ABSTRACT Background Previous studies have suggested that hyperhomocysteinemia may be a risk factor for venous thrombosis. To assess the risk of venous thrombosis associated with hyperhomocysteinemia, we studied plasma homocysteine levels in patients with a first episode of deep-vein thrombosis and in normal control subjects. Methods We measured plasma homocysteine levels in 269 patients with a first, objectively diagnosed episode of deep-vein thrombosis and in 269 healthy controls matched to the patients according to age and sex. Hyperhomocysteinemia was defined as a plasma homocysteine level above the 95th percentile in the control Results Of the 269 patients, 28 (10 percent) had plasma homocysteine