61. Department Of Pathology And Laboratory Medicine hyperhomocysteinemia. One possible explanation may be the coexistence ofhyperhomocysteinemia and low levels of vitamins B6, B12 and folate. http://www.med.uc.edu/departme/pathdept/web/lablines/vol4iss2.htm

The Department of Pathology and Laboratory Medicine Volume 4, Issue 2 April/March 1998 Hyperhomocysteinemia Authors: Kirby Marsh, M.D., Resident Gregory S. Retzinger, M.D., Ph.D., Associate Professor Introduction and Background Homocysteine is an intermediary metabolic product that derives from the demethylation of the essential amino acid, methionine (Fig. 1). Once formed, homocysteine is either remethylated to methionine in a step involving vitamin B12 and folate, or it is metabolized to cysteine in two vitamin B6-dependent reactions (Fig. 1). Defective homocysteine metabolism results in high plasma levels of both homocysteine and methionine. Several studies have since been published suggesting that hyperhomocysteinemia may play a role in the pathogenesis of both arterial occlusive disease and recurrent venous thrombosis. One study found an odds ratio of 2.0 (95% CI 1.4-2.9) for carotid artery stenosis for subjects with homocysteine levels in the highest quartile as compared to those in the lowest quartile(3). Another study reported an odds ratio of 3.1 (95% CI 1.8-3.5) for recurrent venous thrombosis in subjects with plasma homocysteine levels above the 90th percentile of controls(4). Other studies validate a relationship between hyperhomocysteinemia and cardiovascular disease(5,6). Unfortunately the mechanism by which elevated homocysteine levels lead to cardiovascular disease is unknown. While the extremely high levels of homocysteine found in homocystinuria have been shown to cause damage directly to the endothelium, the slightly elevated levels found in hyperhomocysteinemia do not appear to have the same effect. One possible explanation may be the coexistence of hyperhomocysteinemia and low levels of vitamins B6, B12 and folate. These vitamins are required for homocysteine metabolism(7) (Fig. 1). Indeed, one study demonstrated a relationship between low levels of vitamin B6 and/or folate and carotid artery stenosis(3).

62. Hyperhomocysteinemia In Uremic Patients hyperhomocysteinemia in Uremic Patients. High prevalence (8595%) of hyperhomocysteinemia( 15 mmol/L) was observed in uremic patients. http://www.cgmh.org.tw/intr/intr3/c2150/activity/421/421_paper_4.htm

Hyperhomocysteinemia in Uremic Patients °ª¶¯Âå¾Ç¤j¾Ç¡@µÇŦ¬ì ½²­õ¹ÅÂå®v Homocysteine, a sulfur-containing amino acid, is an intermediate metabolite of methionine. Hyperhomocysteinemia has been identified as an independent risk factor for the development of arteriosclerotic vascular diseases in both general population and in patients with chronic renal failure (CRF). m mol/L) was observed in uremic patients. Hyperhomocysteinemia is also a risk factor for the microalbuminuria in diabetic patients. The major causes of hyperhomocysteinemia in patients with CRF includes: 1) renal failure itself, probably caused by reduced renal clearance or impaired tubular absorption, 2) absolute or relative nutritional deficiencies of folate, vitamin B6 or vitamin B12, 3) genetic defects of m ethylenetetrahydrofolate reductase (MTHFR) at C677T, that leading to impaired remethylation pathway of homocysteine to methionine. The proposed pathogenic mechanisms of accelerated arteriosclerosis by elevated homocysteine include 1) direct endothelial cell injury, 2) enhanced

63. Treatment Of Hyperhomocysteinemia With Folic Acid Does Not Ameliorate Endothelia Treatment of hyperhomocysteinemia with folic acid does not ameliorate endothelialfunction in chronic hemodialysis patients C. VAN GULDENER 1 , MJFM JANSSEN 2 http://www.dialyse-online.de/Content/Bibliothek/medlib/Symp97/p189.htm

Treatment of hyperhomocysteinemia with folic acid does not ameliorate endothelial function in chronic hemodialysis patients C. VAN GULDENER 1 , M.J.F.M. JANSSEN 2 , J. LAMBERT 1 , P.M. TER WEE 2 , A.B.J.M. DONKER 1, 2 and C.D.A. STEHOUWER 1 1 Department of Internal Medicine and 2 Nephrology, University Hospital, Vrije Universiteit, Amsterdam Hyperhomocysteinemia increases the risk of atherosclerosis, an effect possibly mediated by damage to the vascular endothelium. In the hemodialysis population, which is at high risk for atherosclerotic disease, hyperhomocysteinemia and endothelial dysfunction are common features. We, therefore, investigated to what extent folic acid treatment could normalize plasma total homocysteine (tHcy) to m mol/l in these patients and whether this treatment ameliorated endothelial function. 35 chronic hemodialysis patients, not on folic acid supplementation, were randomized to a 12-week treatment with 5 mg folic acid with or without betaine 2 g twice daily. After this, patients were rerandomized to treatment

64. Medical Housestaff Underground Manual The Beth Israel Deaconess Medical Center Medical Housestaff Manual. http://home-dev.caregroup.org/UG_manual/Hyperhomocysteinemia.htm

The Beth Israel Deaconess Medical Center Medical Housestaff Manual Table of Contents Hematology Hyperhomocysteinemia Clinically develop premature arteriosclerosis with PVD, CAD, and strokes. Homozygotes leads to develop very early vascular dz. 60% have thrmoboembolic event before age 40. Heterozygotes leads to develop premature vascular dz. Most commonly from cystathionine beta-synthase deficiency, increasing serum homocysteine levels which in turn down regulates endothelial thrombomodulin function and increases lipoprotein(a) levels. Can also be 5,10-methylene-tetrahydrofolate reductase deficiency or vit B12 deficiency Screen pts with unexplained premature vascular disease particularly of the cerebral or peripheral circulation. Lab tests Check homocysteine level. If increased, check methionine and B12. If increased or nl methionine and nl B12, then c/w cystathionine beta-synthase deficiency and treat with vit B6 which decreased homocysteine levels If normal or decreased methionine and nl B12, then c/w be 5,10-methylene-

65. Methylenetetrahydrofolate Reductase Gene Polymorphism, Hyperhomocysteinemia And Wirta O, Rantalaiho V, Oja SS, Pasternack A, Koivula T, Lehtimäki T. Methylenetetrahydrofolatereductase gene polymorphism, hyperhomocysteinemia and occlusive http://www.hytti.uku.fi/tays/julkaisut/2002/200200674.html

Julkaisu Reference Wirta V, Saransaari P, Wirta O, Rantalaiho V, Oja SS, Pasternack A, Koivula T, Lehtimäki T. Methylenetetrahydrofolate reductase gene polymorphism, hyperhomocysteinemia and occlusive retinal vascular disease in type 2 diabetic and non-diabetic subjects. Clin Nephrol Julkaisutiedot Julkaisutyyppi: Alkuperäisartikkeli. Kansainvälinen. Kieli: Englanti. Teksti/tiivistelmä: Publication data Publication type: Original scientific article. International. In English. Text/summary: Tekijät Contributors Tampereen yliopisto Lääketieteen laitos/sisätautioppi Ole Wirta Amos Pasternack Lääketieteen laitos/fysiologia 1 Sakari Oja Lääketieteen laitos/kliininen kemia Timo Koivula Terho Lehtimäki University of Tampere Medical School/Department of Internal Medicine Ole Wirta Amos Pasternack Medical School/ Department of Physiology 1 Sakari Oja Medical School/Department of Clinical Chemistry Timo Koivula Terho Lehtimäki Tampereen yliopistollinen sairaala Kliininen kemia Valtteri Wirta Timo Koivula Terho Lehtimäki Sisätautien klinikka Ole Wirta Vappu Rantalaiho Amos Pasternack Kliinisen fysiologian yksikkö Sakari Oja Tampere University Hospital Clinical Chemistry Valtteri Wirta Timo Koivula Terho Lehtimäki Department of Internal Medicine Ole Wirta Vappu Rantalaiho Amos Pasternack Clinical Physiology Department Sakari Oja Julkaisutietokanta Publications Data Base

66. Graham/SJBR hyperhomocysteinemia. When dietary intake of folate, vitamin B12, and vitaminB6 are low or absent, there is a higher risk for hyperhomocysteinemia. http://wwwchem.csustan.edu/chem4400/sjbr/Graham01.htm

Hyperhomocysteinemia The metabolism of homocysteine and the effects of elevated levels on cardiovascular, peripheral vascular and cerebrovascular disease. By: James W. Graham Hyperhomocysteinemia (in blood) and Homocysteinuria (in urine) has been known for approximately 30 years.(1,3) Hyperhomocysteinemia, which will be discussed here extensively, is elevated blood plasma level of total homocysteine (tHcy). The tHcy is considered elevated when levels are >15umol/L in blood serum. Patients with hyperhomocysteinemia commonly have tHcy levels of 250umol/L.(2) Normal levels of tHcy has been determined to range from 6.1-15.0umol/L.(6) Patients with elevated blood levels of tHcy, in several studies, has indicated in having an increased risk in cardiovascular, peripheral vascular and cerebrovascular disease.(1,2,4) Hyperhomocysteinemia has been estimated to be in 5% of the general population, and 13-47% of patients with diagnosed symptomatic atherosclerotic vascular disease, also have hyper- homocysteinemia.(1) The causative agents for hyperhomocysteinemia are deficiencies in folate (folic acid), vitamin B12, vitamin B6, a genetic disposition or even kidney problems.(1) This paper will discuss the metabolism of homocysteine and how hyperhomocysteinemia causes an increased risk in cardiovascular, peripheral vascular and cerebrovascular disease. Homocysteine (Hcy) is a sulphydryl-containing amino acid by-product that comes from the demethylation of methionine. The major source of methionine is from animal protein.(1,3) In the plasma, Hcy is available in four forms. Hcy can circulate as a free thiol, is disulphide-bound to plasma proteins such as albumin, combined with itself to form a dimer, or bound with other thiols such as a cysteine. These four forms of homocysteine will be referred to as total homocysteine (tHcy).(1) tHcy is metabolized by remethylation or trans-sulphuration.(5)

67. Hyperhomocysteinemia Jako Czynnik Ryzyka Udaru Mózgu hyperhomocysteinemia jako czynnik ryzyka udaru mózgu. Bozena Adamkiewicz,Andrzej Klimek. Oddzial Neurologiczny WSS im. M. Kopernika Abstract. http://www.neurologiapolska.pl/streszczenia/aaa5.htm

Hyperhomocysteinemia jako czynnik ryzyka udaru mózgu Bo¿ena Adamkiewicz, Andrzej Klimek Oddzia³ Neurologiczny WSS im. M. Kopernika Abstract Hyperhomocysteinemia as a risk factor of stroke Since 1995 hyperhomocysteinemia (hyperHcy) is consider as a new, independent risk factor of vascular diseases. The level of Hcy was performed among 100 patients with ischaemic stroke confirmed by CT scan/MRI to aprove this hypothesis.The rutine lab tests were undertaken. The control group was consist of 20 healthy patients. In the first group the level of Hcy was statistical different and higher than in control. In 17 patients Hcy was elevated, the half of them were over 65 year-old. 30 % of patients had advanced arteriosclerotic process. In the patient with hyperHcy the prevalence of DM was higher, among the elderly with hyperHcy hyperlipidemia or IHD. Authors on the base of this results note that hyperHcy should be treated as the independent risk factor of ischaemic stroke and hyperHcy corelate with intensity of arteriosclerosis. Streszczenie Oddzia³ Neurologiczny WSS im. M. Kopernika

68. Hospital Practice: Capsule & Comment Vol. 23 No. 11 Treatable hyperhomocysteinemia and Atherosclerosis (return to ) Interest in homocysteineas a possible risk factor for arteriosclerosis has stimulated a number http://www.hosppract.com/cc/1999/cc9911.htm

A MONTHLY CRITICAL OVERVIEW OF CURRENT MEDICINE VOL. 23 NO. 11 November 15, 1999 Editor GENE H. STOLLERMAN, M.D. Associate Editor ALAN L. BISNO, M.D. IN THIS ISSUE Treatable Hyperhomocysteinemia and Atherosclerosis Fish Oil Protects Mediterraneans After Myocardial Infarction Paraoxonase Gene Protects Finns Against Myocardial Infarction Omeprazole Test for Cost-Effective GERD Diagnosis ... Botulinum Toxin for Anal Fissure Treatable Hyperhomocysteinemia and Atherosclerosis (return to Interest in homocysteine as a possible risk factor for arteriosclerosis has stimulated a number of studies of the degree of risk and the potential benefit of agents that lower the plasma level of this metabolite. To quantify the risk, investigators at Israel's Hadassah University Hospital studied 1,788 middle-aged and elderly Jerusalem residents. During a decade of observation, 405 deaths were recorded. When the highest and lowest fifths of the cohort's homocysteine distribution were compared (after adjustment for confounding variables), the mortality risk ratio for hyperhomocysteinemia was 2.0, with the association being greater in men than in women. The association applied to both total and cardiovascular mortality and was strongest during the first five years of follow-up. Plasma levels of homocysteine may be determined by both genetic and nutritional factors, the latter including folate, vitamin B

69. Haematologica/journal Of Hematology - Issue #12, 1998 Moderate hyperhomocysteinemia is a highly prevalent defect in Spanish patients withvenous thromboembolic disease Yolanda González, Joan Carles Souto, José http://www.haematologica.org/abstr/fontcuberta8312.html

Medline reference of this article PDF version Moderate hyperhomocysteinemia is a highly prevalent defect in Spanish patients with venous thromboembolic disease jmateo@santpau.es Full text Recent studies suggest that mild hyperhomocysteinemia may be a risk factor for venous thromboembolic disease (VTED). In this work we evaluated the prevalence of moderate hyperhomocysteinemia in patients with VTED in our area. We found hyperhomocysteinemia in 23.4% of 64 patients studied compared with 7.35% of 68 healthy controls (p=0.014). Our results suggest that moderate hyperhomocysteinemia is one of the most prevalent abnormalities associated with VTED. Several studies have concluded that moderate hyperhomocysteinemia is an independent risk factor for atherosclerosis and arterial occlusive diseases in the general population. Recent studies suggest that mild hyperhomocysteinemia may also be a risk factor for venous thromboembolic disease (VTED) and its recurrence. In order to investigate other biological abnormalities causing thrombophilia, we also determined: antithrombin, plasminogen and amidolytic protein C by chromogenic substrates; anticoagulant activity of protein C; total protein S and free protein S by the ELISA method; antiphospholipid antibodies by ELISA; and the factor V Leiden mutation by standardized methods. Hyperhomocysteinemia was defined as fasting plasma homocysteine levels and/or PML absolute increments above the 95 th It would be interesting to perform more studies to clarify the association between hyperhomocysteinemia and VTED in cancer patients.

70. [NMC] Demo : By PROSCOPE Title, hyperhomocysteinemia and unsaturated fatty acids in patients with dialysis. hyperhomocysteinemiais detected in the patients with endstage renal disease. http://www.nmckk.co.jp/english/html/journal/jjcd/vol15/150210000.htm

Nihon Medical Center TOP Magazine The Japanese Journal of Clinical Dialysis Vol.15 No.02 Theme Homocysteinemia in Association with Chronic Renal Failure Title Hyperhomocysteinemia and unsaturated fatty acids in patients with dialysis Author Satoru Hirose Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School [ Summary ] Back

71. [NMC] Demo : By PROSCOPE Chronic Renal Failure. 1, A historical overview on hyperhomocysteinemiaIn respect to chronic renal failure, Kazuo Isoda. 2, Analytical http://www.nmckk.co.jp/english/html/journal/jjcd/vol15/ls_1502.htm

The Japanese Journal of Clinical Dialysis Vol.15 No.02 [ Theme ] Homocysteinemia in Association with Chronic Renal Failure A historical overview on hyperhomocysteinemia In respect to chronic renal failure Kazuo Isoda Analytical methods for measurement of plasma total homocysteine concentrations Hiroaki Ono Age and gender Specific reference intervals for plasma homocysteine in normal subjects Takashi Hasegawa Hyperhomocysteinemia and cerebral infarction Hiromichi Kumagai Progression of arteriosclerosis in patients with renal failure Hyperhomocysteinemia and nitric oxide in renal failure Takeshi Nakanishi Mechanisms of hyperhomocysteinemia Association between a new point mutation in methylenetetrahydrofolate reductase gene and atherosclerosis Katsumi Arai Genetic polymorphism of methylenetetrahydrofolate reductase and atherosclerosis Hiroyuki Morita Homocysteine in maintenance hemodialysis patients Michiya Shinozaki Hyperhomocysteinemia in chronically uremic patients Tai Sakurabayashi Hyperhomocysteinemia and unsaturated fatty acids in patients with dialysis Satoru Hirose Treatment of hyperhomocysteinemia in chronic renal failure Atsushi Araki

72. 5.5 Other Publications Determinants of fasting and postmethionine homocysteine levels in familiespredisposed to hyperhomocysteinemia and premature vascular disease. http://www.med.vu.nl/keb/jaarverslag1998/insu14.html

Other Publications Bioque G, Bouma G, Crusius JBA, Koutroubakis I, Kostense PJ Bioque G, Crusius JBA, Koutroubakis I, Bouma G, Kostense PJ b and IL-1 receptor antagonist genes in inflammatory bowel disease. In: HLA and cytokine gene polymorphisms in inflammatory bowel diseases. Bouma G. Ph.D. Thesis 1998; chap 7: 141-52. Boers M , Verhoeven AC, van der Linden Sj. COBRA: Combinatietherapie bij vroege reumatoide artritis: resultaten van een geneesmiddelenonderzoek. Ned Tijdschr Health Professionals 1998: 1: 13-20. Boers M . The art of cost-effective research. Inaugural speech. Amsterdam, VU Boekhandel/Uitgeverij; 1998. Boers M . De kunst van doelmatig onderzoek. Oratie. Amsterdam, VU Boekhandel/uitgeverij; 1998. Bouma G, Crusius JBA, Oudkerk Pool M, Kolkman JJ, von Blomberg BME, Kostense PJ Bouma G, Crusius JBA, Garcia-Gonzalez M, Meijer BUGA, Hellemans HPR, Schreuder GMT, Bioque G, Kostense PJ Bouter LM Kostense PJ . Review of: Rothman KJ, Greenland S. Modern epidemiology. 2nd ed. Philadelphia: Lippincott-Raven, 1998. [book review]. Ned Tijdschr Geneeskd 1998; 142: 2434-5.

73. Diabetes Forum : Complication_Causes Of  Hyperhomocyst(e)inemia Basics. Info Centre. Case Studies. Myths and Facts. Other Links. SiteMap. Special features. select one. http://www.diabetesforum.net/eng_comp_causehyper .htm

Basics Info Centre Case Studies Myths and Facts ... Site Map Special features select one News Letter Write your own articles Ask questions to doctor Forum Introduction Elevations in homocyst(e)ine are typically caused either by genetic defects in the enzymes involve in homocysteine metabolism or by nutritional deficiencies in vitamin co-factors. Thus, reduction in activity of MS, MTHFR, or CbS, or decreased availability of their co-factors, vitamin B12, folic acid or vitamin B6 respectively, can cause hyperhomocyst(e)inemia. Defects of betaine homocysteine methylene transferase have not been described in literature. Genetic Nutritional Miscellaneous Homocyst(e)ine levels are higher in men than in women, both fasting and post methionine loading, and usually higher in postmenopausal rather than premenopausal women. Homocyst(e)ine also rises with age even when allowance is made for age-related increase in creatinine and decreasing vitamin levels. The rise may be related to age induced reduction in the function of MS or CbS. Other conditions that may be associated with hyperhomocyst(e)inemia are hypothyroidism, impaired kidney function, systemic lupus erythematosus and certain medications, e.g., nicotinic acid, nitrous oxide exposure, theophylline, methotrexate, and L-dopa.

74. BioMed Central | Full Text | Diagnosis And Treatment Of Hyperhomocysteinemia Welcome guest user, http://www.biomedcentral.com/1523-3804/3/54

Welcome guest user home journals A-Z journals by subject advanced search ... my BioMed Central Although all research articles in Current Atherosclerosis Reports are available free, most other articles require a subscription Click here to view an abstract of this article Click here to login if you are already a subscriber to Current Atherosclerosis Reports Subscribe to Current Atherosclerosis Reports Register for a free online trial Ask your librarian to investigate institutional access Athens users please click here to gain access If you believe you are seeing this page in error, or cannot activate your subscription, e-mail us info@biomedcentral.com Terms and Conditions Privacy statement Information for advertisers ... Contact us

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