Hyperhomocysteinemia In Patients Research Articles

Vitamin B12 status and hyperhomocysteinemia in patients with Rheumatoid arthritis treated with methotrexate and folic acid

BackgroundRheumatoid arthritis (RA) is an inflammatory arthritis in which the immune system targets synovial joints. Methotrexate serves as the mainstay of treatment for RA due to its efficacy. However, patients treated with methotrexate are uniquely at risk for vitamin B12 deficiency and hyperhomocysteinemia due to coincident disease risk factors and the fact that methotrexate use is associated with malabsorption. The objective of this study was to assess for vitamin B12 deficiency among patients with RA treated with methotrexate and folic acid. MethodsThis cross-sectional study included 50 patients with RA treated with methotrexate and folic acid and 49 patients with RA treated with other therapies. Patients were matched by age, sex, race, renal function, and disease activity. We compared plasma vitamin B12, methylmalonic acid, and homocysteine levels between these two groups utilizing quantitative and categorical analyses. ResultsThirty-seven (74%) RA patients on methotrexate and folic acid had elevated plasma homocysteine levels compared with only 27 (55%) RA patients receiving other therapies (P < 0.05). The proportion of patients with low vitamin B12 and high methylmalonic acid levels did not differ between the two groups. ConclusionsOur data show high plasma homocysteine levels among RA patients treated with methotrexate and folic acid. While plasma vitamin B12 levels were similar between the two groups, high plasma homocysteine is also a sensitive marker of vitamin B12 deficiency. Additional studies should evaluate for the presence of clinical features of vitamin B12 deficiency and hyperhomocysteinemia among RA patients treated with methotrexate and folic acid.

Relationship between Neutrophil-to-Lymphocyte Ratio, Platelet-to-Lymphocyte Ratio, and Hyperhomocysteinemia in Patients with Ischemic Stroke: A Proof-of-Concept Randomized Trial

Background. This study is aimed at investigating the relationship between neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and hyperhomocysteinemia (HHCY) in patients with ischemic stroke (IS). Methods. This study retrospectively analyzed the clinical data and laboratory results of 110 IS patients. According to the cut-off value of HCY = 15 μ mol / L , the included patients were divided into the normal HCY (NHCY, n = 69 ) and the high HCY (HHCY, n = 41 ) groups. The relationship between NLR, PLR, and HCY between these groups was then compared. Results. NLR and PLR levels in IS patients with HHCY were significantly higher than those in IS patients without HHCY ( P &lt; 0.05 ). Correlation analysis showed that NLR and PLR were positively correlated with hs-CRP, RDW, N, L, and HCY ( P &lt; 0.05 ). NLR and PLR were the largest predictors of IS-related HHCY, followed by WBC, hs-CRP, RDW, VLDL, and TG. Additionally, NLR and PLR were independent risk factors for IS-related HHCY. Conclusions. NLR and PLR may be fast, cheap, and easy-to-analyze biomarkers for predicting IS-related HHCY.

Hyperhomocysteinemia in patients with riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency.

Riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency (RR-MADD) is an autosomal recessive disease chiefly caused by variants of ETFDH affecting fatty acid metabolism. In our cohort, hyperhomocysteinemia (HHcy) was common. In this study we aimed to identify the association between RR-MADD and HHcy. We performed a retrospective review of 13 patients with RR-MADD. Thirty-three healthy controls were recruited, and logistic regression was used to investigate the association between RR-MADD and HHcy. Muscle tissues from six patients and six controls without myopathies were collected to measure the levels of flavin adenine dinucleotide (FAD), an active form of riboflavin. Whole-exome sequencing was performed to identify the disease-associated variants. The RR-MADD patients had a higher prevalence of HHcy (9 of 12) than controls (6 of 33, P < .001). In the multivariate analysis, RR-MADD was positively related to HHcy (P = .014). Muscular FAD levels were decreased in RR-MADD patients (P = .006). Thirteen variants (8 reported and 5 novel) were identified in ETFDH. Of these, c.250G > A was the most common pathogenic variant with an allelic frequency of 4 of 20. HHcy was associated with RR-MADD and may aid in the diagnosis of the disease. Our findings expand the mutational spectrum of RR-MADD.

Hyperhomocysteinemia in Patients of Essential Hypertension Presenting with Acute Ischemic Stroke

Objective: To determine the frequency of Hyperhomocysteinemia in patients of essential hypertension presenting with acute ischemic stroke. Study Design: Cross-sectional analytical study. Place and Duration of Study: Department of Internal Medicine, Combined Military Hospital, Quetta Pakistan, from Feb 2018 to Jan 2019. Methodology: The patients of essential hypertension presenting with acute ischemic stroke between 20-70 years of age of either gender were evaluated for the serum homocysteine level. Results: A total 195 patients of essential hypertension presenting with acute ischemic stroke for ≥24 hours duration, of age between 20-70 years, of both genders were included in the study by non-probability consecutive sampling. Majority of patients were between 50-59 year of age (34.3%) with majority of them were male (66.4%). Out of 195, 70.3% were smokers, 56.4% were diabetics, 60.5% were obese and 71.7% had hyperhomocysteinemia respectively. The statistical significance was also observed for hyperhomocysteinemia in accordance with age (p=0.04), gender (p=0.02), obesity (p=0.03) smoking (p=0.01) and diabetes mellitus (p=0.03). Conclusion: Hyperhomocysteinemia is more prevalent in patients of essential hypertension with acute ischemic stroke.

Hyperhomocysteinemia in Patients with Newly Diagnosed Primary Hypertension in Can Tho City, Vietnam.

Elevated levels of blood total homocysteine is one of the cardiovascular risk factors in hypertensive patients. Determine the prevalence of hyperhomocysteinemia and its associated factors in newly diagnosed primary hypertension patients. A cross-sectional descriptive study on 105 patients with newly diagnosed primary hypertension at Can Tho University of Medicine and Pharmacy Hospital from May 2017 to May 2018. Total homocysteine levels and related factors were collected at the study time. The mean plasma total homocysteine level was 16.24 ± 4.49 µmol/L. There were 78 patients with elevated plasma total homocysteine levels ≥15 µmol/L, accounting for 74.3% of all patients. Being elderly, gender, hypertension stage, and diabetes were factors associated with hyperhomocysteinemia (p &lt; 0.05). Total homocysteine levels were positively correlated with SBP, DBP, and age with r(SBP) = 0.696, r(DBP) = 0.585, and r(age) = 0.286. Research on the subpopulation of Vietnamese people shows that hyperhomocysteinemia is common in patients with newly diagnosed primary hypertension, and high blood total homocysteine levels are often related to age, sex, hypertension stage, and diabetes.

Relation Between Adropin Levels and Hyperhomocysteinemia in Patients with Coronary Artery Disease

Background and aim: Homocysteine and adropin effects on endothelial function are antagonistic. The current study aimed to evaluate the association between serum levels of adropin and homocysteine and the severity of coronary artery disease (CAD) . Patients and methods: This cross-sectional study included 86 patients submitted to coronary angiography with ≥ 50% stenosis in one or more coronary arteries. Serum Adropin and homocysteine levels were estimated. The anatomical synergy between percutaneous coronary intervention with taxus and cardiac surgery (SYNTAX) score was utilized to assess the severity of CAD. Results: According to serum homocysteine levels, they were classified into patients with normal homocysteine levels (GI; n=54) and patients with hyperhomocysteinemia (GII; n=32). Comparison between the studied groups regarding clinical and laboratory findings revealed that GI patients had significantly shorter duration of diabetes (3.8 ± 5.3 versus 8.2 ± 7.5 years, p=0.009), higher serum triglycerides levels (204.7 ± 99.6 versus 142.9 ± 55.6 mg/dL, p=0.002), lower HbA1c levels (7.2 ± 1.6 versus 8.2 ± 2.0%; p = 0.013) and significantly higher adropin levels (7.4 ± 2.5 versus 1.6 ±1.0, p

Effects of three-months folate supplementation on early vascular abnormalities in hyperhomocysteinemic patients with epilepsy

BackgroundEpilepsy has been associated with an increased risk of cardiovascular events. Anti-seizure medication (ASM) may contribute to vascular risk by several mechanisms, including increased homocysteine levels. This study aims to assess the global vascular burden in hyperhomocysteinemic people with epilepsy (PWE) on long‐term ASM before and after folic acid supplementation and in subgroups of PWE treated with single enzyme-inducing or single non-enzyme inducing ASM. MethodsOne hundred and seventy-four hyperhomocysteinemic (HHcy) PWE who met the inclusion criteria were enrolled. Carotid Doppler ultrasonography, FMD and ultrasound assessment of the brachial artery properties at the baseline and after 90 days of folic acid supplementation were performed. The vascular biomarkers MMP-9 and TIMP-1 were also detected. ResultsAfter folic acid supplementation, in HHcy patients homocysteine levels reduced from 26.8 ± 10.5 to 20.2 ± 5.3 μmol/L, carotid Intima-Media-Thickness reduced from 0.83+0.06 mm to 0.79±0.05 mm, and FMD, distensibility coefficient and β-stiffness improved (p < 0.05). Moreover, MMP-9 and TIMP-1 reduced after supplementation (p < 0.05). PWE treated with a single enzyme-inducing ASM showed an impairment of vascular parameters compared to patients treated with non-enzyme inducing ASM. ConclusionsThe results highlight the importance of assessing homocysteine levels and estimating the cardiovascular risk of PWE, preferring non-enzyme inducing ASM in high cardiovascular-risk patients. An adequate correction of homocysteine levels with folate supplementation should be considered to improve the cardiovascular profile.

Serum uric acid concentration is associated with hyperhomocysteinemia in hypertensive Chinese adults.

This study is to investigate the correlation between serum uric acid levels and hyperhomocysteinemia Chinese adult patients with hypertension. We enrolled 981 hypertensive patients, including unmedicated hypertensives, in our study. There were 453 patients with hyperhomocysteinemia (hyperhomocysteinemia hypertension group) and 528 without it (ordinary hypertension group). We collected histories of coronary heart disease, diabetes, and smoking and tested patients' BMI, blood pressure, fasting serum uric acid, serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, serum creatinine, and homocysteine. Subjects were stratified into four groups according to their serum uric acid quartiles: Q1 group, 249 cases (≤268 μmol/L); Q2 group, 245 cases (269-322 μmol/L); Q3 group, 244 cases (323-378 μmol/L); and Q4 group, 243 cases (≥379 μmol/L). We employ logistic regression analysis to investigate the relationship between serum uric acid levels and the risk of hyperhomocysteinemia in patients with hypertension. We find that there were significant differences in gender distribution, serum uric acid, BMI, serum creatinine, total cholesterol, and diastolic blood pressure between the two groups (P < 0.05). The prevalence of hyperhomocysteinemia in groups Q1 through Q4 was 26.91% (67/249), 45.31% (111/245), 47.01% (117/244), and 65.02% (158/243), respectively, after adjusting for relevant factors, we find that the risk of hyperhomocysteinemia in the Q4 group was significantly higher than that in the Q1 group (odds ratio = 3.00, 95% confidence interval: 1.83-4.93). We find evidence that an elevated serum uric acid level is an independent indicator for hyperhomocysteinemia in patients with hypertension.

Higher gastric parietal cell antibody titer significantly increases the frequencies of macrocytosis, serum vitamin B12 deficiency, and hyperhomocysteinemia in patients with burning mouth syndrome

Background/purposeOur previous study found 109 gastric parietal cell antibody (GPCA)-positive burning mouth syndrome (BMS) patients (so-called GPCA+BMS patients in this study) in a group of 884 BMS patients. This study evaluated whether high-titer (GPCA titer ≥ 160) GPCA+BMS patients had greater frequencies of macrocytosis, anemia, serum iron and vitamin B12 deficiencies, and hyperhomocysteinemia than low-titer (GPCA titer < 160) GPCA+BMS patients or 442 healthy control subjects. Materials and methodsComplete blood count, serum iron, vitamin B12, folic acid, homocysteine, and GPCA levels in 42 high-titer GPCA+BMS patients, 67 low-titer GPCA+BMS patients, and 442 healthy control subjects were measured and compared. ResultsWe found that 33.3%, 38.1%, 19.0%, 33.3%, 2.4%, and 57.1% of 42 high-titer GPCA+BMS patients and 10.4%, 25.4%, 14.9%, 6.0%, 1.5%, and 11.9% of 67 low-titer GPCA+BMS patients were diagnosed as having macrocytosis, blood hemoglobin, iron, vitamin B12, and folic acid deficiencies, and hyperhomocysteinemia, respectively. Moreover, both 42 high-titer and 67 low-titer GPCA+BMS patients had significantly greater frequencies of macrocytosis, blood hemoglobin, serum iron and vitamin B12 deficiencies, and hyperhomocysteinemia than 442 healthy control subjects (all P-values < 0.001). In addition, 42 high-titer GPCA+BMS patients also had greater frequencies of macrocytosis, serum vitamin B12 deficiency, and hyperhomocysteinemia than 67 low-titer GPCA+BMS patients (all P-values < 0.01). ConclusionThe high-titer GPCA+BMS patients have significantly greater frequencies of macrocytosis, anemia, serum iron and vitamin B12 deficiencies, and hyperhomocysteinemia than healthy control subjects and significantly greater frequencies of macrocytosis, serum vitamin B12 deficiency, and hyperhomocysteinemia than low-titer GPCA+BMS patients.

English

BACKGROUND Over the last three decades, prevalence of stroke has been high in India, while the Western countries have witnessed a downward slide. Epidemiological studies suggest that hyperhomocysteinaemia might be a potentially modifiable nonlipid risk factor associated with stroke, in addition to the long-recognized factors like hypertension, diabetes mellitus, hyperlipidaemia and smoking. Hyperhomocysteinaemia occurs due to deviation in the metabolic pathway of methionine, attributed by deficiency of vitamins, enzymes and other factors. The present study was undertaken to assess the proportion of hyperhomocysteinaemia in patients with acute ischemic stroke. We also compared the risk factors associated with stroke and serum levels of homocysteine. METHODS This is a cross sectional observational study conducted in a tertiary care hospital. The sample size was 140. Both male and female consecutive patients of age more than 18 years, with first attack of acute ischaemic stroke admitted in the Department of Neurology were selected. Baseline fasting serum samples were obtained for testing serum homocysteine levels. Statistical tests used were proportion, chi square and logistic regression. RESULTS Among 140 acute ischaemic stroke patients, total homocysteine level was raised in 83.6 % cases. The prevalence of moderate hyperhomocysteinaemia in our study was 65.4 % and intermediate hyperhomocysteinaemia was 17.9 % among stroke patients. The mean (± SD) homocysteine level was 22.75 (± 8.19). CONCLUSIONS A strong association was found between hyperhomocysteinaemia and acute ischaemic stroke. We could not find any significant correlation between total homocysteine level and most risk factors of stroke. KEYWORDS Stroke, Homocysteine, Risk Factors, Endothelial Dysfunction, Atherosclerosis, B Vitamins

Risks of cerebrovascular disorders associated with combined hormonal contraceptives

Introduction. Cerebral circulation disorders (CCD) hold the third place in the structure of complications coupled to combined oral contraceptives (СОСs). Acute disturbance of the cerebral blood supply is the main etiological factor for such complication; and hidden predisposition to thrombotic conditions such as thrombophilia plays a pivotal role in its pathogenesis, which is manifested due to administered hormonal contraceptives.Aim: to assess rate of detected genetic thrombophilic hemostatic defects, congenital and acquired ADAMTS-13 deficiency, antiphospholipid antibodies (APA), antibodies to phospholipid cofactors, hyperhomocysteinemia in patients with CCD administered with СОСs.Materials and Methods. A prospective analysis of 89 COCs use cases in women of reproductive age was carried out, among which 60 cases were selected for this study satisfying to the inclusion and exclusion criteria. Group I consisted of 30 patients manifested with various CCD types due to COCs use, group II – 30 women taking COCs for at least 1 year lacking any thrombotic complications.Results. Women administered with COCs are at the peak CCD risk within the first 2 months after the onset. Somatic diseases differed little in patients from groups I and II. In group I, 5 (41.7 %) patients with venous thrombosis did not have classical thrombophilia, but 4 (33.3 %) women had anti-ADAMTS-13 antibodies combined with elevated von Willebrand factor (vWF) level. Inherited thrombophilia was less prevalent in patients with arterial thrombosis and transient ischemic attack (TIA): 1 (5.5 %) case of Leiden factor V mutation compared to patients with venous blood flow disorders (p &lt; 0.05). Such patients more frequently had criterial APA (61.1 %), so that 5 (27.8 %) patients were found to have more than one type of criterial APA. In 4 (22.2 %) cases these were patients with ischemic stroke, 3 (37.5 %) of which had combination of three criterial APA (triple positivity) and 1 (12.5 %) had two criterial APA (double positivity); among them detection rate of criterial APA was 50.0 %. One patient (double positivity) was with TIA.Conclusion. It was found that: i) genetic and acquired factors were identified at high rate in patients with CCD administered with COCs, contributing to coagulopathy (86.7 %); ii) in case of venous thrombotic CCD coupled to administered COCs, inherited thrombophilia (58.3 %) prevails, in arterial thrombosis – APA circulation (50.0 %); iii) etiopathogenetic role of APA circulation in impaired cerebral blood flow depends on antibody type (criterial APA) and titer; iv) preexisting hypercoagulability leading to CCD coupled to COCs may be linked to several thrombophilic defects unrelated to classical thrombophilia.

Hyperhomocysteinemia in patients with cardiovascular manifestations: to treat or not to treat

Hyperhomocysteinemia in patients with cardiovascular manifestations: to treat or not to treat

Homocysteine and Gliotoxicity.

Homocysteine is a sulfur amino acid that does not occur in the diet, but it is an essential intermediate in normal mammalian metabolism of methionine. Hyperhomocysteinemia results from dietary intakes of Met, folate, and vitamin B12 and lifestyle or from the deficiency of specific enzymes, leading to tissue accumulation of this amino acid and/or its metabolites. Severe hyperhomocysteinemic patients can present neurological symptoms and structural brain abnormalities, of which the pathogenesis is poorly understood. Moreover, a possible link between homocysteine (mild hyperhomocysteinemia) and neurodegenerative/neuropsychiatric disorders has been suggested. In recent years, increasing evidence has emerged suggesting that astrocyte dysfunction is involved in the neurotoxicity of homocysteine and possibly associated with the physiopathology of hyperhomocysteinemia. This review addresses some of the findings obtained from in vivo and in vitro experimental models, indicating high homocysteine levels as an important neurotoxin determinant of the neuropathophysiology of brain damage. Recent data show that this amino acid impairs glutamate uptake, redox/mitochondrial homeostasis, inflammatory response, and cell signaling pathways. Therefore, the discussion of this review focuses on homocysteine-induced gliotoxicity, and its impacts in the brain functions. Through understanding the Hcy-induced gliotoxicity, novel preventive/therapeutic strategies might emerge for these diseases.

Association between vitamin D deficiency and serum Homocysteine levels and its relationship with coronary artery disease.

Homocysteine (Hcy) elevation and vitamin D deficiency have emerged as potential markers of coronary artery disease (CAD). However, even tough hypovitaminosis D has been suggested to interfere with Hcy catabolism, no study has so far addressed the interaction of vitamin D and Hcy and their impact on CAD, that was the aim of present study. A cohort of consecutive patients undergoing coronary angiography in a single center were included and analyzed within the year 2019. Significant CAD was defined as at least 1 vessel stenosis > 50%, while severe CAD as left main and/or three-vessel disease. Hcy and vitamin D levels were assesssed at admission. We included 3150 patients undergoing coronary angiography at our centre, who were divided according to the quartiles values of vitamin D. Patients with lower levels of Vitamin D displayed a higher cardiovascular risk profile and a higher prevalence of CAD. We observed an inverse linear relationship between lower levels of vitamin D and higher Hcy (r = − 0.092, p < 0.001) and a higher prevalence of hyperhomocysteinemia in patients with lower quartiles values of vitamin D (p < 0.001). By forward conditional regression model, low vitamin D appeared as independent predictors of Homocysteine levels above the median (OR[95%CI] = 1.79[1.37–2.33], p < 0.001). In addition, patients with low vitamin D (below the median) and increased Hcy displayed a non-significantly higher rate of CAD (81% vs 77.7%, p = 0.13, adjusted OR[95%CI] = 1.16[0.88–1.54], p = 0.29) but a significant increase in the rate of severe left main/3-vessel CAD (37.4% vs 30.5%, p = 0.005, adjusted OR[95%CI] = 1.29[1.02–1.67], p = 0.04). Among patients with vitamin D levels above the median, Hcy levels did not impact on the prevalence and extent of CAD (77.7 vs 77.2%, p = 0.81, adjusted OR[95%CI] = 0.94[0.73–1.20], p = 0.60 for CAD and 31.8% vs 27.7%, p = 0.08, adjusted OR[95%CI] = 0.97[0.75–1.25], p = 0.81 for severe left main/3-vessel CAD). No significant interaction between Hcy and vitamin D with CAD or severe CAD was observed. The present study shows an independent inverse linear relationship between vitamin D and Hcy values. Moreover, the association of Hcy with the extent of CAD was significant only among patients with hypovitaminosis D, and not in the cohort of subjects with vitamin D levels above the median, suggesting that a normal vitamin D status can prevent the deleterious effects of hyperhomocysteinemia on coronary atherosclerosis, a hypothesis that certainly needs further confirmation in larger randomized trials.Supplementary InformationThe online version of this article (10.1007/s11239-021-02391-w) contains supplementary material, which is available to authorized users.

Plasma Homocysteine and Vascular Disease

Vascular disease is the leading cause of death and disability in the Western World: atherosclerosis is responsible for the majority of deaths in virtually all westernized societies; pulmonary embolism, a complication of deep venous thrombosis, is the leading cause of morbidity and mortality, resulting in approximately 50,000 deaths per year in the United States; approximately 1.5 million acute myocardial infarcts occur each year, each infarction bearing a 30% mortality rate; and strokes represent the third leading cause of death in developed countries (1). While the adverse effects of hypertension, hypercholesterolemia, diabetes, and smoking on the vascular system have received widespread publicity, another important risk factor for vascular disease--less well-known outside the medical community but recently gaining increasing attention in the literature is an elevated plasma level of the amino acid homocysteine. Bolstered by findings of an association between hyperhomocysteinemia and a variety of vascular disorders, theories implicating homocysteine in the pathogenesis of these disorders have inspired researchers to explore novel approaches in the prevention and treatment of vascular disease. With the biochemistry of homocysteine metabolism already well understood, vitamin supplementation has emerged as a promising strategy for reduction of plasma homocysteine levels, with consequent arrest or reversal of the postulated pathogenic mechanisms involved in homocysteine-associated disorders of the vasculature, and, thus, potential prevention and treatment of vascular disease in hyperhomocysteinemic patients.

Prevalence and clinical implications of hyperhomocysteinaemia in patients with hypertrophic cardiomyopathy and MTHFR C6777T polymorphism.

Prevalence and clinical implications of hyperhomocysteinaemia in patients with hypertrophic cardiomyopathy and MTHFR C6777T polymorphism.

The standard deviation of the red blood cells distribution width by volume as an assumed biomarker of chronic alcohol intoxication

Introduction. At present, Russia occupies one of the leading places in the world in ethanol consumption per capita. The actual and unsolved problem remains the diagnosis and prevention of chronic alcoholism. The definition of carbohydrate-deficient transferrin proposed by many authors has many drawbacks, in particular, a rather high cost, as well as a limited sensitivity of the index after two weeks from an episode of ethanol consumption. For this reason, it seems necessary to search for alternative biomarkers of chronic alcoholism. One of the applicants for the role of a marker of chronic alcohol intoxication is the Red blood cell Distribution Width - standard deviation (RDW-SD). The article contains the results of a study of changes in the standard deviation of the RDW-SD in the venous blood of patients with acute ethanol poisoning in cases with chronic alcohol intoxication.The aim of this work was to quantify the change in RDW-SD in patients with alcohol dependence (chronic alcohol intoxication) during periods of exacerbation (acute alcohol poisoning of moderate severity). Material and methods. The research materials were clinical blood tests of 245 patients on the first day after admission to the Department of Toxicology of the I.I. Dzanelidze. Research Institute of Emergency Medicine.Results. From the literature, it is known that the RDW-SD is largely associated with folic acid deficiency. Vitamin B9 deficiency can significantly increase the risk of cardiovascular disease due to the development of hyperhomocysteinemia in patients. Particular attention is required for patients aged 46-65 years, who have the highest level of RDW-SD with an increased risk of developing cardiovascular events. At the same time, the highest mortality rate in this age group from the reasons associated with the use of ethanol is noted, which gives reason to consider RDW-SD as one of the possible indices of the mortality risk. Conclusion. The possibility of using the magnitude of the change in the RDW-SD index as a biomarker of chronic alcohol intoxication in patients with a certain risk of cardiovascular complications is discussed with the rationale for the appointment of folic acid preparations as part of the complex treatment of chronic alcohol intoxication.

Influence of Dietary Supplementation for Hyperhomocysteinemia Treatments.

Hyperhomocysteinemia is recognized as risk factor for cardiovascular and age-associated diseases. Folic acid supplementation efficiently lowers plasma homocysteine (Hcy) levels, but high intake may negatively affect health because of unnatural levels of unmetabolized folic acid in the systemic circulation. Oxoproline (Oxo) provides by glutamic acid production an increase of intracellular folic acid trapping. Aim of this study was to compare the efficacy of three supplementation protocols: (1) traditional therapy (5-methyl-tetrahydrofolate: 15 mg/day); (2) 5 mL/day of Oxo with 300 μg folic acid (oxifolic); (3) 5 mL/day of Oxo alone (magnesio+) in a 90 days randomized trial on thirty-two moderate hyperhomocysteinemic (18.6 ± 2.4 μmol·L−1) patients (age 48 ± 14 years). Thiols: cysteine (Cys), cysteinylglycine (Cys–Gly) and glutathione levels were assessed too. Every supplementation induced significant (p range <0.05–0.0001) reductions of Hcy level and Cys concentration after the three protocols adopted. Otherwise glutathione concentration significantly increased after oxifolic (p < 0.01) and traditional (p < 0.05) supplementation. The integration of Oxo resulted an interesting alternative to traditional therapy because absence or minimal number of folates in the integrator eliminates any chance of excess that can constitute a long-term risk.

A study to evaluate the correlation between increased homocysteine level and hyperlipidaemia: An observational study

: Numerous studies have suggested a possible relation between increased homocysteinemia level and cardiovascular diseases. This relationship is clinically important in the management of cardiac diseases specially in elderly population. However, there is limited data which suggests association between hyperhomocysteinemia and hyperlipidaemia. The aim of this study is to find a relation between hyperlipidaemia and hyperhomocysteinemia in patients who are not on lipid-lowering treatment.A total of 300 hyperlipidemic patients were enrolled who attended medicine OPD. After obtaining informed consent, data were collected by a trained technician according to a standard operating protocol of the laboratory. After an overnight fast of minimum 12 hours, 5 ml of venous blood was taken under aseptic conditions in EDTA tube. The blood was late centrifuged, plasma samples were then separated within half hour of sample collection and were stored at −80 °C in the laboratory. Total cholesterol (TC), Low Density Lipid-Cholesterol (LDL-C), High Density Lipid-Cholesterol (HDL-C) and Triglycerides (TG) were measured on Bene Spheraautoanalyzer. Homocysteine was measured on Robonic ELISA reader.Homocysteine level in blood was directly proportional to increased level of TC, TG, LDL-C and age of the patient. In the same group homocysteine level was inversely proportional to high density lipoproteins. There is strong correlation of increased homocysteine level with hyperlipidaemia.

Hyperhomocysteinemia in patients with acute porphyrias: A potentially dangerous metabolic crossroad?

BackgroundAcute porphyrias (AP) are characterized by heme deficiency and induction of hepatic 5-aminolevulinate synthase (ALAS1). Hyperhomocysteinemia (HHcy) is associated with endothelial damage, neurotoxicity and increased risk for vascular diseases. Interestingly, both heme biosynthesis and sulphur amino acid metabolism require vitamin B6, (Pyridoxal-phosphate, PLP) an important cofactor of ALAS1 and of cystathionine β-synthase (CBS) and cystathionine γ-lyase (CGL) enzymes that catabolize homocysteine (Hcy). Moreover, heme itself is an important cofactor for CBS. Aimto assess plasma Hcy status and HHcy main determinants in patients with AP. Materials and methodsA total of 46 patients with AP (31 with Acute Intermittent Porphyria,15 with Variegate Porphyria) were assessed for clinical status (symptomatic vs. asymptomatic), serum Hcy, Cysteine (Cys), Vit.B6, Vit.B12, red blood cell folates and urinary delta-aminolevulinic acid (ALA) and porphobilinogen(PBG) levels (mean of six measurements). ResultsSymptomatic AP patients had significantly higher urinary ALA and PBG levels, plasma Hcy, HHcy prevalence and Hcy/Cys ratio when compared to asymptomatic carriers of AP. Even though no significant correlation was observed between ALA/PBG urinary levels and serum Hcy levels, patients with higher levels of ALA and PBG had significantly higher levels of Hcy, a higher prevalence of moderate-to severe HHcy and serum PLP levels below the 25th percentile of a reference assessment with 300 healthy Italian subjects(<45nmol/L). ConclusionsMost patients with symptomatic AP present HHcy resulting from alterations in sulphur amino acid metabolism. HHcy may represent an indirect marker of ALAS1 induction and its prevalence may be suggestive of a role of HHcy in the pathogenesis and/or comorbidities of AP.