Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The finding of low plasma pyridoxal-5'-phosphate levels in patients suffering from myocardial infarction has been construed as possible evidence for the pathogenetic role that vitamin B6 deficiency may play in causing premature ischaemic heart disease. However, the presence of normal plasma pyridoxal-5'-phosphate levels in patients with angiographic evidence of coronary artery narrowing but with no previous infarctions prompted the investigation of possible short-term alterations in plasma pyridoxal-5'-phosphate levels during the acute phase of myocardial infarction. In the follow-up of 30 patients with acute myocardial infarction, all of them showed a continuous decrease of approximately 45% in plasma pyridoxal-5'-phosphate levels during the acute phase. These levels subsequently returned back to normal before discharge from hospital. A large number of volunteers from an ethnic group known to have a very low incidence of ischaemic heart disease were found to have both significantly lower total cholesterol and plasma pyridoxal-5'-phosphate levels than a Caucasian group in the same geographic area which is known to have a high incidence of ischaemic heart disease. These findings therefore do not support the contention that vitamin B6 deficiency may be a risk index for ischaemic heart disease.
Atherosclerosis 1987 Feb
PMID:Vitamin B6 and coronary artery disease. Epidemiological observations and case studies. 382 84

This volume details the history of vitamin B6, its chemistry and biochemistry, methods for the assessment of vitamin B6 status, and the clinical chemistry of the vitamin. Since its discovery and synthesis over 40 years ago, vitamin B6 has been implicated in a number of disease states. All approaches to the assessment of vitamin B6 status--direct measurement of blood levels, measurement of the excretion rate of the vitamin, measurement of the metabolites or abnormal metabolic products resulting from a deficient state, or measurement of some other process dependent on the concentration of the vitamin in the body--have significant technical or physiological problems. Dietary allowances vary for different age groups and situations. In the US, the National Academy of Sciences has recommended a daily dietary allowance of 2.2 mg for young adult males and 2.0 mg for young adult females. Additional allowances have been suggested for women during pregnancy and lactation, but not for users of oral contraceptives (OCs). Vitamin B6 deficiency can be either exogenous (when intake falls below the recommended dietary allowance) or conditioned (in cases where the physiologic requirement for the vitamin is higher than the dietary allowance). Conditioned deficiency arises in the following situations: defective intestinal absorption, defective cellular and intercellular transport, and impaired oxidtion or phosphorylation mechanisms in vitamin B6 metabolism. Studies aimed at assessing the abnormal tryptophan metabolism observed in some OC users have produced conflicting results. It appears that severe depression and impairment of glucose tolerance are the only important abnormalities encountered in OC users related to vitamin B6 deficiency. Abnormalities of tryptophan metabolism have been noted in patients with rheumatoid arthritis, some malignant diseases, liver disease, diabetes mellitus, atherosclerosis, and hyperkinetic syndromes.
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PMID:Clinical chemistry of vitamin B6. 639 13

Vitamin B6 is effective in the treatment of carpal tunnel syndrome and related disorders in patients with vitamin B6 deficiency. Hyperhomocysteinemia, a risk factor for atherosclerosis, is associated with deficiencies of vitamin B6, folate, and cobalamin. Patients who were given vitamin B6 for carpal tunnel syndrome and other degenerative diseases were found to have 27% of the risk of developing acute cardiac chest pain or myocardial infarction, compared with patients who had not taken vitamin B6. Among elderly patients of the author (JE) expiring at home, the average age at death from myocardial infarction was 8 years later in those who had taken vitamin B6, compared with those who had not taken vitamin B6. The preventive effect of vitamin B6 on progression of coronary heart disease may be related to increased formation of pyridoxal phosphate, the coenzyme that is required for catabolism of the atherogenic amino acid, homocysteine.
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PMID:Prevention of myocardial infarction by vitamin B6. 855 75

Homocysteine (tHcy) is a risk factor for atherosclerosis in patients with end-stage renal disease and chronic renal insufficiency (CRI). Vitamin B6 deficiency may result in high tHcy levels, especially after a methionine load (PML). Therefore, we evaluated vitamin B6 metabolism and tHcy (fasting and PML) levels in patients with CRI and those on hemodialysis (HD) therapy before and during high-dose sequential vitamin B6 and folic acid supplementation in male patients (27 patients, HD, 17 patients, CRI) and 19 age-matched healthy controls. Vitamin B6 doses were 100 mg/d in patients with CRI and 200 mg/d in HD patients, plus folic acid (5 mg/d), for more than 3 months in each period. We analyzed vitamin B6 metabolites by high-performance liquid chromatography in plasma and red blood cells (RBCs) and fasting tHcy in all cases and PML in subgroups of 11 HD patients and 14 patients with CRI. We found vitamin B6 deficiency and high tHcy (fasting and PML) levels in all patients. Plasma and RBC levels of pyridoxal and pyridoxal phosphate were abnormally low, whereas levels of pyridoxic acid (PA), an end product of vitamin B6 metabolism, were extremely high in both groups. Fasting and PML tHcy levels were partially resistant to vitamin B6 supplements, with different response patterns in HD patients and those with CRI. Thus, the PML defect was more responsive to folic acid in HD patients, whereas vitamin B6 partially reduced PML tHcy levels in patients with CRI. Resistance of tHcy to vitamin B6 treatment in patients with CRI and HD patients is not caused by poor absorption or low tissue stores. Rather, nonvitamin factors or potentially toxic PA levels may be implicated in abnormal vitamin B6 and/or tHcy metabolism during renal insufficiency.
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PMID:Vitamin B6 metabolism and homocysteine in end-stage renal disease and chronic renal insufficiency. 1177 12

Aging is accompanied by a progressive and irreversible non-enzymatic modification of protein by carbohydrates, eventually yielding the advanced glycation end products (AGEs). Age generation (Maillard reaction) is markedly augmented in diabetes with sustained hyperglycemia but also in normoglycemic uremia and atherosclerosis. Recent studies have brought new insights into broad derangements in non-enzymatic biochemistry involving not only carbohydrates but also lipids, present in diabetes, uremia, and atherosclerosis. The latter have in common increased levels of reactive carbonyl compounds (RCOs) with attendant protein modifications ("carbonyl stress"). Carbonyl stress might be derived from 1) hyperglycemia (lipemia), 2) oxidative stress, and/or 3) impaired detoxification of RCOs. Manipulation of carbonyl stress in diabetes, uremia and atherosclerosis opens new therapeutic approaches including redox modulation, RCO detoxification, and carbonyl stress inhibition. The first generation of carbonyl stress inhibitors such as aminoguanidine trap RCOs with its hydrazine group. Unfortunately, aminoguanidine (AG) traps pyridoxal as well as noxious RCOs, so that its long-term administration in animals results in vitamin B6 deficiency and neurotoxicity. Fortunately, newer compounds devoid of such side effects, have opened exciting prospects. Widely used hypotensive agents, such as angiotensin converting enzyme (ACE) inhibitor and angiotensin II receptor antagonist, but not calcium blockers, prove more effective than AG in attenuating the production of AGEs. Unlike AG, they do not act as RCO trapping agents, but impact upon the production of RCO precursors by scavenging a variety of radicals and altering oxidative stress, a mechanism similar to that involved in the inhibitory action of nitric oxide on AGE formation. These results provide a new framework to assess families of compounds according to their mechanisms of action.
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PMID:Alterations of non-enzymatic biochemistry in uremia, diabetes, and atherosclerosis ("carbonyl stress"). 1250 15

The objective of the present review is to highlight the relationship between low vitamin B6 status and CVD through its link with inflammation. While overt vitamin B6 deficiency is uncommon in clinical practice, increasing evidence suggests that marginal vitamin B6 deficiency is rather frequent in a consistent proportion of the population and is related to an increased risk of inflammation-related diseases. Ample evidence substantiates the theory of atherosclerosis as an inflammatory disease, and low plasma vitamin B6 concentrations have been related to increased CVD risk. Several studies have also shown that low vitamin B6 status is associated with rheumatoid arthritis and chronic inflammatory bowel diseases, both of which hold an underlying chronic inflammatory condition. Furthermore, the inverse association observed between inflammation markers and vitamin B6 supports the notion that inflammation may represent the common link between low vitamin B6 status and CVD risk. In addition to the epidemiological evidence, there are a number of cell culture and animal studies that have suggested several possible mechanisms relating impaired vitamin B6 status with chronic inflammation. A mild vitamin B6 deficiency characterises, in most cases, a subclinical at-risk condition in inflammatory-linked diseases which should be addressed by an appropriate individually tailored nutritional preventive or therapeutic strategy.
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PMID:Vitamin B6: a challenging link between nutrition and inflammation in CVD. 2148 13