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Hyperhomocysteinemia: more detail

Hyperhomocysteinemia: Webster's Timeline History, 1992 - 2007 by Icon Group International, 2009-02-20

Hyperhomocysteinemia as a result of the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism causes an increased risk of cerebrovascular disease: ... An article from: Original Internist by Robert A., Jr. Duca, 2010-09-01

Hyperhomocysteinemia in end stage renal disease: is treatment necessary? (Continuing Education).: An article from: Nephrology Nursing Journal by Jennifer Snavely, 2002-04-01

lists with details

THE MERCK MANUAL, Sec. 11, Ch. 132, Thrombotic Disorders
hyperhomocysteinemia. hyperhomocysteinemia is also strongly correlated with atheroscleroticthrombosis (including coronary artery diseasesee Ch. 201).
http://www.merck.com/pubs/mmanual/section11/chapter132/132a.htm

Extractions: 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.
Mild Hyperhomocysteinemia Is Associated With Impaired Renal Function But Not Wit
2002 Mild hyperhomocysteinemia is Associated with Impaired Renal Functionbut not with Progression of Small Abdominal Aortic Aneurysms.
http://link.springer-ny.com/link/service/journals/00547/contents/01/0068/s00547-

Extractions: International Journal of Angiology DOI: 10.1007/s00547-001-0068-2 Jes S. Lindholt, M.D., Ph.D. , and Eskild W. Henneberg, M.D., Cand. Scient. Department of Vascular Surgery, Rigshospitalet, University of Copenhagen, Denmark Department of Clinical Biochemistry, Skejby Sygehus, University of Aarhus, Denmark Department of Vascular Surgery, Hospital of Viborg, Viborg, Denmark Abstract P r P Correspondence to: jslindholt@mail.tele.dk
Mild Hyperhomocysteinemia Is Associated With Impaired Renal Function But Not Wit
http://link.springer-ny.com/link/service/journals/00547/contents/01/0068/
Homocysteine Conference 2003
Beside the role of hyperhomocysteinemia as an important risk factor for atheroscleroticvessel diseases, elevated homocysteine levels have been recognised as a
http://www.uniklinik-saarland.de/zentrallabor/homocysteine-conference.html

Extractions: 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.
BioMed Central | Abstract | Diagnosis And Treatment Of Hyperhomocysteinemia
Report Diagnosis and Treatment of hyperhomocysteinemia Mary E Keebler BS, , CyrusDe Souza MD and Vivian Fonseca MD Section of Endocrinology Department of
http://www.biomedcentral.com/1523-3804/3/54/abstract
What Is Considered Hyperhomocysteinemia
What is considered hyperhomocysteinemia? The healthy level is consideredto be 12 micromoles/L in blood plasma. Any concentration
http://students.biology.lsa.umich.edu/bio208_6/homocysteine/3.html

Extractions: What is considered Hyperhomocysteinemia? The healthy level is considered to be 12 micromoles/L in blood plasma. Any concentration exceeding 15 micromoles/L is considered as Hyperhomocysteinemia (American Academy of Family Physicians). A healthy woman's level of homocysteine will usually drop during pregnancy.
ClinicalTrials.gov - Linking Patients To Medical Research: Study Details
Randomized Study of Folic Acid Therapy for hyperhomocysteinemia inPatients with End Stage Renal Disease Receiving Hemodialysis.
http://www.clinicaltrials.gov/ct/gui/show/NCT00004495?order=3
QuestHealthLibrary.com - Full Description
hyperhomocysteinemia. DESCRIPTION Breaking the term hyperhomocysteinemia intoits roots does much to clarify this disease hyper (too much) homocysteine.
http://www.questhealthlibrary.com/full_description.php?ElementID=496
Hyperhomocysteinemia And Risk For Vascular Disease
25May-01 ACE Genotype, CAD and Restenosis After Coronary Stenting
http://www.genetics.wayne.edu/programs/SGS2001/presentations/Crisan.htm
Possible Mechanism Of Hyperhomocysteinemia
Possible Mechanism of hyperhomocysteinemia. Direct toxic effects on endothelialtissue. promote oxidation of LDL. abnormalities in platelet function.
http://www.calstatela.edu/faculty/lcalder/411/tsld070.htm
Possible Mechanism Of Hyperhomocysteinemia
First Previous Next Last Index Text. Slide 70 of 157.
http://www.calstatela.edu/faculty/lcalder/411/sld070.htm
Abstract: Hyperhomocysteinemia In Rheumatoid Arthritis: Influence Of Methotrexat
hyperhomocysteinemia in Rheumatoid Arthritis Influence of MethotrexateTreatment and Folic Acid Supplementation OLE KUDSK JENSEN
http://www.jrheum.com/abstracts/abstracts02/1615.html

Extractions: Home Current Issue Archives Guidelines for Authors ... Contact Info Hyperhomocysteinemia in Rheumatoid Arthritis: Influence of Methotrexate Treatment and Folic Acid Supplementation OLE KUDSK JENSEN, CLAUS RASMUSSEN, FRANK MOLLERUP, PEDER BJERG CHRISTENSEN, HENRIK HANSEN, SUZANNE EKELUND, and ANE MARIE THULSTRUP Objective. To examine the effect of methotrexate (MTX) and folic acid supplementation on the homocysteine level in patients with rheumatoid arthritis (RA). A cross sectional study was performed in 81 patients with RA, comprising a standardized clinical interview, an examination, and a blood specimen test. P-homocysteine in patients with RA receiving MTX and folic acid supplementation did not differ significantly from P-homocysteine in RA patients receiving other types of treatment. (J Rheumatol 2002;29:1615-8)
Treatment Of Hyperhomocysteinemia By Folic Acid In Children On Dialysis
Treatment of hyperhomocysteinemia by Folic Acid in Children on Dialysis. hyperhomocysteinemiais an independent risk factor for cardiovascular diseases.
http://www.multi-med.com/pdi/abstracts/18S-1/pediatrics/34.html

Extractions: Treatment of Hyperhomocysteinemia by Folic Acid in Children on Dialysis Adult patients with renal failure have elevated homocysteine (tHcy) levels in plasma. Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. Vascular damage is the most important cause of death in this patient category. Folic acid is able to lower the tHcy levels in plasma in hyperhomocysteinemia. Whether this results in a reduced risk for cardiovascular disease has still to be proven in intervention studies. The present study relates to two questions: (1) Are tHcy plasma levels elevated in children with end-stage renal failure? and (2) What is the influence of folic acid administration on the tHcy level in plasma? At T=0 the tHcy level in plasma was measured in 21 children (mean age 9.3 years, SD 4.4), 9 treated with hemodialysis (HD) and 12 with peritoneal dialysis (PD). After 4 weeks of treatment (T=4) with 2.5 mg folic acid daily, tHcy levels in plasma were measured again. In HD patients tHcy concentration was also measured after 1 and 2 weeks of treatment. At T=0 the median of the tHcy level in plasma was 20.02 mmol/L [Q1Q3: 13.6525.95 (Q=quartile)]. At T=4 median level was 12.02 mmol/L (Q1Q3: 9.7914.34) (p
Hyperhomocysteinemia And Related Factors In 600 Hospitalized Elderly Subjects.
National Library of Medicine's PubMed directory of MEDLINE citations. hyperhomocysteinemiaand related factors in 600 hospitalized elderly subjects.
http://www.arclab.org/medlineupdates/abstract_11735095.html

Extractions: Aging Research Center Home Page All Previous Aging Related Articles On-line Medical Dictionary National Library of Medicine's PubMed directory of MEDLINE citations. - Ventura P, Panini R, Verlato C, Scarpetta G, Salvioli G Metabolism 2001 Dec;50(12):1466-71. Hyperhomocysteinemia (HHcy) is a metabolic disorder frequently occurring in the elderly population. Recently several reports have suggested abnormalities in homocysteine (tHcy) metabolism implicating HHcy as a metabolic link in the multifactorial processes characterizing many geriatric illnesses-with special emphasis on atherosclerotic vascular diseases and cognitive impairment. The present study was undertaken in a large sample of elderly hospitalized subjects to determine (1) the prevalence of HHcy, (2) the association of HHcy with vascular and cognitive disorders, and (3) the factors independently predicting Hhcy. Six hundred elderly subjects (264 men and 336 women; mean age, 79 +/- 9 years) were randomly chosen from those admitted as inpatients over a period of 3 years. In
Vascular Pathologies Controversies
hyperhomocysteinemia, Severe hyperhomocysteinemia, also reported as homocystinuriais usually associated to abnormal biochemical phenotypes 95 .
http://www.healthandage.com/html/res/controversies/content/chap4/homocysteine_fu

Extractions: In clinical routine, elevated homocysteine levels are found in 1-2% in the general population. Higher prevalence is associated with vascular diseases. Studies on 730 screened vascular patients demonstrated that hyperhomocysteinemia was present in 25-33% of those with peripheral arterial disease, 20-28% of those with cerebrovascular disease and in 15% of those with coronary artery disease Plasma concentrations of homocysteine increase with age, and remain as an independent risk factor for vascular disease in the elderly . The marginal vitamin deficiency, frequent in the elderly, is thought to contribute for the elevation of homocysteine levels . Homocysteine levels increase in post-menopausal women, and are attenuated by hormone replacement therapy
Prevalence Of Factor V Leiden, Hyperhomocysteinemia, Prothrombin G20210A, And Me
Prevalence of factor V Leiden, hyperhomocysteinemia, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations in obstetrical complications.
http://www.john-libbey-eurotext.fr/articles/abc/57/5/539-44/en-resum.htm
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concentrations should be considered in patients with premature atherosclerosis ora strong family history of atherosclerosis, since hyperhomocysteinemia is a
http://www.aafp.org/afp/971015ap/fallest.html

Extractions: A New Risk Factor for Atherosclerosis 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.
Dopamine
Homocysteine hyperhomocysteinemia. Book, Home homocysteine levels; Dose responsecurve lowest Folate, Highest risk. Causes of hyperhomocysteinemia
http://www.fpnotebook.com/CV221.htm

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About Lipid Analysis Inc.
The cause of hyperhomocysteinemia in patients with arterioscleroticcardiovascular disease is complex. hyperhomocysteinemia appears
http://www.lipidanalysis.com/frames/education/hyper.html

Extractions: Prairie Cardiovascular Consultants, Ltd., Springfield, Illinois In summary, we have reviewed the scientific and clinical basis and provided recommendations in the management of patients with hyperhomocysteinemia. As this topic evolves, and as we gain more clinical experience in the management of this disorder, further recommendations will follow. Patients with hyperhomocysteinemia as well as patients with severe hyperlipidemia who have been resistant to therapy are being evaluated at the Prairie Lipid Clinc. Long term prospective randomized placebo controlled trials will answer whether intervention of hyperhomocysteinemia will alter cardiac morbidity and mortality. However, in patients with established atherosclerosis, current pathophysiologic mechanisms and epidemiologic data suggest an aggressive approach in the managment in this subset of important patients. References: New England Journal of Medicine 1991;324:1149-1155.
Dr. Rose's Peripheral Brain--CAD RISK FACTORS
J. Epidemiol. 1411117, 1995abst). hyperhomocysteinemia. Severely increasedlevels in homocystinuria associated with accelerated atherosclerosis;
http://faculty.washington.edu/momus/PB/cadriskf.htm

Extractions: CAD RISK FACTORS n.b. For purposes of guiding management of dyslipidemias, NCEP specifies a small list of risk factors as countingSee under " Dyslipidemias " for details. The NCEP recommends counting CAD risk factors among those in the "major" category below, though sedentary lifestyle and dyslipidemias in general aren't counted; HDL < 35 counts as a risk factor, though; Also, HDL > 59 counts as a "negative" risk factor, i.e. if it's there, you subtract 1 from the count of risk factors MAJOR (per JAMA 269:3015, 1993): Age Family hx Smoking Hypertension Dyslipidemias (high LDL, low HDL, high TC/HDL or LDL/HDL ratio) DM Unknown whether glycemic control affects risk Raises risk more for women than for men (NEJM 332:1758, 1995-rvw) Sedentary lifestyle OTHERS: High HDL (> 60mg/dl) is a "negative" risk factor per NCEP (see under " dyslipidemias ") Obesity Traditionally considered a weak but significant independent factor; may contribute secondarily through effects on glucose metabolism, BP, etc. 115,000 women enrolled in Nurses' Health study 30-55yo and free of CV disease or Ca at enrollment followed for 16y. In multivariate analysis (adjusted for age, tobacco consumption, menopausal status, use of OCP's and postmenopausal HRT, and parental h/o MI before age 60), the following results were obtained

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