1. Hyperhomocysteinemia Issue 6, 2003. hyperhomocysteinemia. Andrea Cortese Hassett Ph.D., Although severe hyperhomocysteinemia is rare, mild hyperhomocysteinemia occurs in approximately 5 to 1 2 Patients with mild http://www.itxm.org/tmu2003/issue2003-6.htm

Issue # Hyperhomocysteinemia Andrea Cortese Hassett Ph.D., Chief Science Officer, ITxM Diagnostics INTRODUCTION Homocysteine is a naturally occurring, sulfur containing amino acid formed during the metabolism of methionine, an essential amino acid derived from the diet. The interconversion of methionine and homocysteine depends on the availability of the methyl donor 5-methyltetrahydrofolate, cofactors vitamin B and folate, and the enzyme activity of methionine synthase. Elevated intracellular homocysteine concentrations with corresponding increases in blood levels can result from augmented production or reduced metabolism. Although severe hyperhomocysteinemia is rare, mild hyperhomocysteinemia occurs in approximately 5 to 7 percent of the general population. Patients with mild hyperhomocysteinemia are asymptomatic until the third or fourth decade of life when premature coronary artery disease may develop, as well as recurrent arterial and venous thrombosis. MEASUREMENT SPECIMEN REQUIREMENTS Plasma homocysteine is measured on a morning specimen collected in an EDTA (lavender top) tube after an overnight fast. Because homocysteine is continuously released by blood cells, the specimen must be centrifuged and the plasma separated immediately to avoid falsely elevated values. Alternatively, the specimen can be placed on wet ice until it can be centrifuged. Specimens that are not sent to the lab the same day must be spun down and the plasma frozen until testing is performed.

2. Hyperhomocysteinemia hyperhomocysteinemia. A patient who is heterozygous for this mutation has no evidence of hyperhomocysteinemia or increased risk of thrombotic disorders. http://www-admin.med.uiuc.edu/hematology/PtHomocysteinemia.htm

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).

3. Hyperhomocysteinemia University of Illinois Urbana/Champaign. Carle Cancer Center. Hematology Resource Page. Patient Resources. hyperhomocysteinemia. Home. Factor V Leiden. Antiphospholipid Syndrome. General Clotting http://www.med.uiuc.edu/hematology/PtHomocysteinemia.htm

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).

4. Epidemiology Of Hyperhomocysteinemia Epidemiology of hyperhomocysteinemia. Levels increase with age; higher in men. Population data from the Framingham Heart Study and http://www.abbottdiagnostics.com/Your_Health/Heart_Disease/Homocysteine/Clinical

Abbott Diagnostics Division Although all information remains accessible via Navigator 4.x browsers, we are considering it an obsolete program from the point of view of our interface design. Please visit if you wish to upgrade your browser. Thank you! Jump to: [ content Abbott Diagnostics Home contact glossary ... Worldwide Your Health Information Homocysteine: The New Risk Factor Cardiovascular Risk Stratification Epidemiology of Hyperhomocysteinemia Homocysteine as a risk factor for coronary heart disease, cerebrovascular disease and stroke ... References and Additional Reading Epidemiology of Hyperhomocysteinemia Levels increase with age; higher in men Click on the image to view a larger version. Top of page Dr. Wilson emphasized that there are several measurement considerations to keep in mind when evaluating homocysteine and other emerging CHD risk factors. These include test standardization, assay variability, correlation with currently accepted risk factors, the possibility of nonlinear effects, the potential for improvement in risk prediction, and the cost of the assay. New biological markers for CHD risk should be assayed by standardized techniques, show little interlaboratory variability, and be performed by laboratories that meet the accreditation standards of either the Centers for Disease Control or the College of American Pathologists. In addition, the marker should have little biological variability. For example, while fibrinogen and other acute-phase reactants are useful markers on an individual basis, they have tremendous intersubject variability.

5. Trials And Treatment Trials and Treatment of hyperhomocysteinemia. Supplemental vitamin B 6 will modulate postprandial hyperhomocysteinemia in both groups. http://www.abbottdiagnostics.com/Your_Health/Heart_Disease/Homocysteine/Clinical

Abbott Diagnostics Division Although all information remains accessible via Navigator 4.x browsers, we are considering it an obsolete program from the point of view of our interface design. Please visit if you wish to upgrade your browser. Thank you! Jump to: [ content Abbott Diagnostics Home contact glossary ... Worldwide Your Health Information Homocysteine: The New Risk Factor Cardiovascular Risk Stratification Epidemiology of Hyperhomocysteinemia Homocysteine as a risk factor for coronary heart disease, cerebrovascular disease and stroke ... References and Additional Reading Trials and Treatment of Hyperhomocysteinemia Updated conclusions for therapy. According to Godfried H. Boers, MD, PhD, in 1976 Wilcken et al published one of the first reports of an association of mild hyperhomocysteinemia and premature CHD. The Wilckens' paper described 25 patients under the age of 50 years with angiographically documented coronary artery disease who had elevated levels of cysteine-homocysteine mixed disulfide following methionine loading. These investigators suggested that a reduced ability to metabolize homocysteine may occur when the methionine pathway is stressed in some patients. Subsequent studies by Boers et al and by Clarke and colleagues confirmed the association of hyperhomocysteinemia and premature vascular disease and suggested that the abnormality in these patients represented a heterozygous presentation of cystathionine b-synthase deficiency. Since the standard treatment of homocystinuria at the time was vitamin B

6. Hyperhomocysteinemia hyperhomocysteinemiaHomocystinuria (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. a defect is present, can result in either homocystinuria or hyperhomocysteinemia http://www.med.uiuc.edu/hematology/PDF Files/Hyperhomocysteinemia.pdf

7. ClinicalTrials.gov - Information On Clinical Trials And Human Research Studies: Nutritional and Metabolic Diseases hyperhomocysteinemia. Include trials that are no longer recruiting of Folic Acid Therapy for hyperhomocysteinemia in Patients with End Stage http://clinicaltrials.gov/ct/screen/BrowseAny?path=/browse/by-condition/hier/BC1

8. Hyperhomocysteinemia Issue 8, 2003. Detection of Bacterial Contamination in Platelet Components Blood Bulletin Vol. 6, No. 4, DECEMBER 2003. SUMMARY. http://www.itxm.org/tmu2003/issue2003-8.htm

Issue # Detection of Bacterial Contamination in Platelet Components Blood Bulletin: Vol. 6, No. 4, DECEMBER 2003 SUMMARY Bacterial contamination of platelets represents the most frequent transfusion-associated infectious risk. Bacterial contamination levels of as few as 10 to 10 CFU/mL have been associated with fever and positive blood cultures. The incidence of clinically significant platelet-associated contamination is estimated at 1/15,000 and death due to sepsis or endotoxemia at 1/60,000 platelet transfusions. New measures to limit and detect bacterial contamination in platelet components to be implemented by March 2004 are expected to significantly decrease current risks. Extensive donor selection and testing strategies effectively reduce the transmission of viral agents by asymptomatic volunteer blood donors. Today, the most frequent transfusion-associated infectious risk in the United States is sepsis associated with bacterial contamination of platelet components. Given the frequency, clinical significance, and potential for fatal complications that the presence of bacteria poses for certain patients, two accrediting agencies (the American Association of Blood Banks and the College of American Pathologists) have issued directives requiring the use of methods to detect and limit bacterial contamination of platelets.

9. ClinicalTrials.gov - Information On Clinical Trials And Human Research Studies: Diseases and Abnormalities at or before Birth hyperhomocysteinemia. Include trials that are no of Folic Acid Therapy for hyperhomocysteinemia in Patients with End Stage Renal http://clinicaltrials.gov/ct/screen/BrowseAny?path=/browse/by-condition/hier/BC1

10. Entrez PubMed Click here to read hyperhomocysteinemia increases risk of death, especially in type 2 diabetes 5year follow-up of the Hoorn Study. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1

11. THE MERCK MANUAL, Sec. 11, Ch. 132, Thrombotic Disorders to activated protein C, hyperhomocysteinemia, protein C deficiency, protein S and venous thromboembolism. hyperhomocysteinemia is also strongly correlated with atherosclerotic http://www.merck.com/pubs/mmanual/section11/chapter132/132a.htm

This Publication Is Searchable The Merck Manual of Diagnosis and Therapy Section 11. Hematology And Oncology Chapter 132. Thrombotic Disorders Topics [General] [General] Thrombotic disorders: Diseases characterized by formation of a thrombus that obstructs vascular blood flow locally or detaches and embolizes to occlude blood flow downstream (thromboembolism). Thrombi are mechanical masses that form within the cardiovascular system on denuded endovascular or prosthetic flow surfaces. They are composed of insoluble fibrin, deposited platelets, accumulating WBCs, and entrapped RBCs in variable flow-dependent patterns. Thrombus formation is a multifactorial process involving many mutually interactive genetic and environmental factors. Thrombotic predisposition is usually identified clinically. The most important features are family history, recurrence, young age, severity of provocation, and unusual sites of thrombosis. Suspected arterial or venous thrombosis or thromboembolism requires objective confirmation. Angiography is the diagnostic reference standard. However, ultrasonography performed by skilled personnel is suitable for superficial vessels and for cardiac assessment. Of patients with venographically proven spontaneous deep vein thrombosis, 25 to 50% have a genetic predisposing factor. A genetically impaired anticoagulant mechanism (eg, factor V resistance to activated protein C, hyperhomocysteinemia, protein C deficiency, protein S deficiency, antithrombin deficiency, defective fibrinolysis), when combined with a thrombotic stimulus (eg, surgery, pregnancy, oral contraceptive use, antiphospholipid antibodies), is sufficient to develop a venous thromboembolism. Persons with more than one abnormality experience thrombosis earlier, more frequently, and more severely than those with single defects.

12. Entrez PubMed vegetarians. Normalization of hyperhomocysteinemia with vitamin B(12) and reduction of platelet aggregation with n3 fatty acids. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1

13. Flash Plugin Test 05/12/04 hyperhomocysteinemia Associated with Osteoporotic Fracture (Reuters http://www.acr.org/

14. Clinical Trial: Randomized Study Of Folic Acid Therapy For Hyperhomocysteinemia Randomized Study of Folic Acid Therapy for hyperhomocysteinemia in Patients with End Stage Renal Disease Receiving Hemodialysis. http://www.clinicaltrials.gov/ct/show/NCT00004495?order=4

15. NEJM -- Hyperhomocysteinemia As A Risk Factor For Deep-Vein Thrombosis Original Article from The New England Journal of Medicine hyperhomocysteinemia as a Risk Factor for DeepVein Thrombosis Previous studies have suggested that hyperhomocysteinemiamay be a risk http://www.nejm.org/cgi/content/abstract/334/12/759

HOME SEARCH CURRENT ISSUE PAST ISSUES ... HELP Please sign in for full text and personal services Previous Volume 334:759-762 March 21, 1996 Number 12 Next Hyperhomocysteinemia as a Risk Factor for Deep-Vein Thrombosis Full Text PDF Letters Add to Personal Archive ... Chapters at Harrison's 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 levels above the 95th percentile for the controls, as compared with 13 of the controls (matched odds ratio, 2.5; 95 percent

16. Homocysteine: A New Risk Factor For Atherosclerosis / October 15, 1997, AFP concentrations should be considered in patients with premature atherosclerosis or a strong family history of atherosclerosis, since hyperhomocysteinemia is a http://www.aafp.org/afp/971015ap/fallest.html

Advanced Search Articles Departments Patient Information This article exemplifies the AAFP 1997-98 Annual Clinical Focus on prevention and management of cardiovascular disease. Homocysteine: A New Risk Factor for Atherosclerosis PATRICIA C. FALLEST-STROBL, PH.D., DAVID D. KOCH, PH.D., JAMES H. STEIN, M.D., and PATRICK E. MCBRIDE, M.D., M.P.H. The accumulating evidence for the role of homocysteine as a risk factor for atherosclerosis is persuasive. A high plasma homocysteine concentration induces pathologic changes in the arterial wall and thus is strongly associated with an increased risk of atherosclerosis, manifested as cardiovascular, cerebrovascular and peripheral vascular events. Studies are being conducted to determine whether lowering homocysteine levels prevents occlusive events. At present, testing for elevated homocysteine concentrations should be considered in patients with premature atherosclerosis or a strong family history of atherosclerosis, since hyperhomocysteinemia is a common risk factor in these patients. Treatment of hyperhomocysteinemia is straightforward and associated with minimal risk. This disorder is usually correctable with vitamin supplements containing folic acid. An elevated plasma level of the amino acid homocysteine has been identified as an independent risk factor for atherosclerosis, including coronary artery disease, cerebrovascular disease, peripheral vascular disease and venous thromboembolism.

17. Dekker.com - Hyperhomocysteinemia And Oxidative Stress During Dialysis Treatment The concomitant presence of hyperhomocysteinemia and oxidative stress may represent a determinant to analyze the occurrence of hyperhomocysteinemia and oxidative stress and their http://www.dekker.com/servlet/product/DOI/101081JDI120018721

onunload=closeRefPopup Login/Register Forgot your Password? My Workspace Shopping Cart ... FAQs Dekker is a digital publisher that offers accessible at the article level with linked references. Abstract Editorial Board Author Instructions Continue Shopping ... Advertising Rate Card (PDF) setCatId('art:101081JDI120018721'); To contact Dekker customer service by phone, please call 1-800-228-1160 South America) or 0041-61-260-63-00 (Europe, Far East, CLINICAL STUDY Hyperhomocysteinemia and Oxidative Stress During Dialysis Treatment Published in Renal Failure Volume 25 , Issue 2 Print ISSN: Online ISSN: Purchase Options Online Article World Price: $22.00 Search for documents only within this product. Paula Garcia Chiarello Maria Terezinha I. Vannucchi Corresponding Brazil Journal Article DOI: 10.1081/JDI-120018721 Keywords Homocysteine, Folate, Dialysis, Lipoperoxidation, Antioxidants Abstract Background Aims Methods Results Conclusions Return to Top About Dekker Author Services Site Map , by Marcel Dekker, Inc.

18. Homocysteine Conference 2003 Beside the role of hyperhomocysteinemia as an important risk factor for atherosclerotic vessel diseases, elevated homocysteine levels have been recognised as a http://www.uniklinik-saarland.de/zentrallabor/homocysteine-conference.html

3rd Conference on Hyperhomocysteinemia Second Announcement Author guidelines for poster abstracts Author guidelines for posters register online Historical Aspects and Perspectives of Homocysteine Research The strong rising prevalence of chronic diseases in most of the industrialised countries causes major problems in the health system of these countries. High blood cholesterol by high fat consumption, hypertension, low physical activity, and smoking are the most discussed risk factors responsible for the high rate of heart infarction, stroke or peripheral arterial disease in these countries. Since the mid eighties, many studies and investigations have documented that a moderately elevated plasma homocysteine level is also a strong and independent risk factor for atherosclerotic vessel diseases, like heart infarction, stroke or peripheral vessel disease. Nowadays, the homocysteine literature is rapidly growing. Beside the role of hyperhomocysteinemia as an important risk factor for atherosclerotic vessel diseases, elevated homocysteine levels have been recognised as a risk factor for venous thrombosis. Furthermore, hyperhomocysteinemia is discussed to play an important role in the development of neural tube defects, pregnancy complications, cognitive impairments in the elderly and several neuro-psychiatric disorders. The prevalence of hyperhomocysteinemia as a result of vitamin deficiency is very high in the elderly population and rises strongly with advancing age. In industrialised countries the number of elderly people is rapidly growing and a great portion of this population is effected by this condition. Furthermore, supplementation with vitamins (folate, vitamin B-12, vitamin B-6) is efficient and inexpensive in lowering homocysteine concentrations, even in subjects without overt vitamin deficiencies. Several ongoing and planned multicenter intervention trials will contribute to clarify the causality of hyperhomocysteinemia and the value of homocysteine lowering therapy, especially whether this treatment may effect the progression of the atherosclerotic process.

19. 3rd Conference On Hyperhomocysteinemia SEARCH CRC By Specialty. By Date. By Location. Register for Personal Edition. Contact Doctor's Guide. Submit your Congress/Conference 3rd Conference on hyperhomocysteinemiais finished. Return to http://www.docguide.com/crc.nsf/congresses/4C26AFD3F5A22D2D85256C0E002A6E5F

SEARCH CRC: View Congresses By Specialty By Date By Location Register for Personal Edition ... Submit your Congress/Conference 3rd Conference on Hyperhomocysteinemia is finished. Return to Congress Resource Centre Home Page

20. The International XVII Puijo Symposium Abstracts Line C hyperhomocysteinemia AND OXIDATIVE STRESS ARE ASSOCIATED WITH ISCHEMIC HEART DISEASE IN SLOVAK FEMALES. J. Lietava1, M. Atalay2, M http://ffp.uku.fi/cgi-bin/edueditor/presenter.pl?slideshow_id=103&slide_id=1052&

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