41. 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

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.

42. 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-

International Journal of Angiology DOI: 10.1007/s00547-001-0068-2 Mild Hyperhomocysteinemia is Associated with Impaired Renal Function but not with Progression of Small Abdominal Aortic Aneurysms 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

43. Mild Hyperhomocysteinemia Is Associated With Impaired Renal Function But Not Wit http://link.springer-ny.com/link/service/journals/00547/contents/01/0068/

44. 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

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.

45. 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

Welcome guest user home journals A-Z journals by subject advanced search ... Issue 1 Viewing options Abstract Full text PDF Other links: E-mail to a friend Download references Post a comment Search PubMed For Keebler ME De Souza C Fonseca V Report Mary E Keebler BS, Cyrus De Souza MD and Vivian Fonseca MD Section of Endocrinology Department of Medicine, 1430 Tulane Avenue (SL 53), Tulane University School of Medicine, New Orleans, LA, 70112, USA. Current Atherosclerosis Reports Abstract Terms and Conditions Privacy statement Information for advertisers Contact us

46. 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

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.

47. 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

48. 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

49. 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

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50. 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 Direct toxic effects on endothelial tissue promote oxidation of LDL abnormalities in platelet function abnormalities in arachidonic acid metabolism Previous slide Next slide Back to first slide View graphic version

51. Possible Mechanism Of Hyperhomocysteinemia First Previous Next Last Index Text. Slide 70 of 157. http://www.calstatela.edu/faculty/lcalder/411/sld070.htm

52. 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

Search the Journal 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) METHOTREXATE HYPERHOMOCYSTEINEMIA FOLIC ACID SUPPLEMENTATION Supported by The Danish League Against Rheumatism (Gigtforeningen). Address reprint requests to Dr. O.K. Jensen, Department of Internal Medicine, The General Hospital of Randers, DK-8900 Randers, Denmark. Submitted September 18, 2001; revision accepted January 21, 2002.

53. 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

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 [Q1–Q3: 13.65–25.95 (Q=quartile)]. At T=4 median level was 12.02 mmol/L (Q1–Q3: 9.79–14.34) (p

54. 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

Aging Research Center Home Page All Previous Aging Related Articles On-line Medical Dictionary National Library of Medicine's PubMed directory of MEDLINE citations. Hyperhomocysteinemia and related factors in 600 hospitalized elderly subjects. - 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

55. 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

Virginia Berlanga Campos Junqueira, Ph D Ligia Ferreira Gomes, PhD Biochemistry Pages: Hyperhomocysteinemia 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 High homocysteine levels may also occur associated to other risk factors for thrombosis and cardiovascular disease Hyperhomocysteinemia as a clinical finding may result from: pyridoxine, cobalamin or folate deficiency;

56. 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

Annales de Biologie Clinique. Vol. 57, Issue 5, September - October 1999 Prevalence of factor V Leiden, hyperhomocysteinemia, prothrombin G20210A, and methylene tetrahydrofolate reductase C677T mutations in obstetrical complications Annales de Biologie Clinique. Vol. 57, Issue 5, September - October 1999: 539-44, Generals reviews Summary: Author(s): E. Verdy, N. Berkane, A. Magdelaine, F. Soubrier, S. Uzan Keywords: Genetic - Thrombosis - Obstetrical complications. © John Libbey Eurotext

57. Advanced Search 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

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.

58. 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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59. 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

By J. Antonio G. Lopez, M.D., F.A.C.C. and Richard E. Katholi, M.D., F.A.C.C. 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. Atherosclerosis 1988;71:227-233.

60. 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

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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