Low vitamin B6 levels and the risk of recurrent venous thromboembolism

Hron, Gregor; Lombardi, Rossana; Eichinger, Sabine; Lecchi, Anna; Kyrle, Paul A.; Cattaneo, Marco

doi:10.3324/haematol.11318

Cited by 29 publications

(21 citation statements)

References 21 publications

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“…However, in patients with a combination of liver disease and poor nutritional status, such as for alcoholics (1.5 g alcohol/kg/d, >5 years) (43), the risk for pyridoxine deficiency is increased (44). Clinical manifestations of pyridoxine phosphate deficiency are typically unrelated to hyperhomocysteinemia, but observational studies have linked low pyridoxine phosphate levels with an increased risk for first-time and recurrent venous thromboembolism (45). Data from an uncontrolled intervention trial suggested that high dose pyridoxine supplementation decreases the incidence of thromboembolism in patients with homocystinuria (RR=0.09, 95% CI 0.02-0.38) (46); however, the benefit of routine surveillance or treatment of low pyridoxine phosphate levels in the general population remains unknown.…”

Section: Biochemistrymentioning

confidence: 99%

The Treatment of Hyperhomocysteinemia

2009

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The unique biochemical profile of homocysteine is characterized by chemical reactivity supporting a wide range of molecular effects, and a tendency to promote oxidant stress-induced cellular toxicity. Numerous epidemiological reports have established hyperhomocysteinemia as an independent risk factor for cardiovascular disease, cerebrovascular disease, dementia-type disorders, and osteoporosis-associated fractures. Although combined folic acid and B-vitamin therapy substantially reduces homocysteine levels, results from randomized placebo-controlled clinical trials testing the effect of vitamin therapy on outcome in these diseases are mixed, but have generally fallen short of expectations. These results have led some to abandon homocysteine monitoring in the management of patients with cardiovascular or cognitive disorders. These trials, however, have generally included patients with only mildly elevated homocysteine levels, and have not addressed several clinical scenarios in which homocysteine level reduction may be effective, including the primary prevention of atherothrombotic disease in individuals at low-or intermediate-risk, or those with severe hyperhomocysteinemia.

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Section: Biochemistrymentioning

confidence: 99%

The Treatment of Hyperhomocysteinemia

2009

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“…An increased risk of recurrent VTE has been reported in subjects with high levels of thrombin-activable fibrinolysis inhibitor (TAFI) [89], low vitamin B6 levels [90], low levels of free tissue factor pathway inhibitor (TFPI) [91], and elevated albuminuria [92] while high levels of apolipoprotein A1 and HDL have not been reported as being associated with lower risk of recurrence [93]. …”

Section: Risk Factors For Recurrencementioning

confidence: 99%

Recurrent Venous Thromboembolism: What Is the Risk and How to Prevent It

Palareti¹

2012

Scientifica

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Venous thromboembolism (VTE) that includes deep vein thrombosis and/or pulmonary embolism is a frequent, severe, and potentially lethal disease. After a first episode, VTE has a strong tendency to recur. While VTE is an acute disease, it may have variable outcomes in early and late phases after initial presentation. Furthermore, the incidence of late, clinically important consequences (postthrombotic syndrome and/or chronic thromboembolic pulmonary hypertension) increases in case of recurrent events. The aims of the present review are (i) to analyze the incidence and risk factors for recurrence of VTE (either those related to the type of first thrombotic event or to the patients), the risks associated with occurrence of recurrent events, and the problems linked to the diagnosis, not always easy, of recurrent events; (ii) to discuss whether or not it is possible to predict the individual risk of recurrence after a first event, by stratifying patients at high or low risk of recurrence, and how this can influence their treatment; (iii) to comment what the current guidelines and guidance suggest/recommend about anticoagulant treatment after a first VTE event and, finally, to propose practical indications on how to manage individual patients affected by VTE.

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“…The consequences of marginal deficiency are unclear, but chronically low vitamin B6 status is associated with increased risk of cardiovascular disease [12]–[17], deep-vein thrombosis [18]–[20], stroke [21] and certain cancers [22], [23]. The mechanisms responsible for these disease connections are unknown but do not appear to be associated with hyperhomocysteinemia [5].…”

Section: Introductionmentioning

confidence: 99%

Metabolomic Analysis Reveals Extended Metabolic Consequences of Marginal Vitamin B-6 Deficiency in Healthy Human Subjects

et al. 2013

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Marginal deficiency of vitamin B-6 is common among segments of the population worldwide. Because pyridoxal 5′-phosphate (PLP) serves as a coenzyme in the metabolism of amino acids, carbohydrates, organic acids, and neurotransmitters, as well as in aspects of one-carbon metabolism, vitamin B-6 deficiency could have many effects. Healthy men and women (age: 20-40 y; n = 23) were fed a 2-day controlled, nutritionally adequate diet followed by a 28-day low-vitamin B-6 diet (<0.5 mg/d) to induce marginal deficiency, as reflected by a decline of plasma PLP from 52.6±14.1 (mean ± SD) to 21.5±4.6 nmol/L (P<0.0001) and increased cystathionine from 131±65 to 199±56 nmol/L (P<0.001). Fasting plasma samples obtained before and after vitamin B6 restriction were analyzed by 1H-NMR with and without filtration and by targeted quantitative analysis by mass spectrometry (MS). Multilevel partial least squares-discriminant analysis and S-plots of NMR spectra showed that NMR is effective in classifying samples according to vitamin B-6 status and identified discriminating features. NMR spectral features of selected metabolites indicated that vitamin B-6 restriction significantly increased the ratios of glutamine/glutamate and 2-oxoglutarate/glutamate (P<0.001) and tended to increase concentrations of acetate, pyruvate, and trimethylamine-N-oxide (adjusted P<0.05). Tandem MS showed significantly greater plasma proline after vitamin B-6 restriction (adjusted P<0.05), but there were no effects on the profile of 14 other amino acids and 45 acylcarnitines. These findings demonstrate that marginal vitamin B-6 deficiency has widespread metabolic perturbations and illustrate the utility of metabolomics in evaluating complex effects of altered vitamin B-6 intake.

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Low vitamin B6 levels and the risk of recurrent venous thromboembolism

Cited by 29 publications

References 21 publications

The Treatment of Hyperhomocysteinemia

The Treatment of Hyperhomocysteinemia

Recurrent Venous Thromboembolism: What Is the Risk and How to Prevent It

Metabolomic Analysis Reveals Extended Metabolic Consequences of Marginal Vitamin B-6 Deficiency in Healthy Human Subjects

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