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Results for “Serum Folate Level”

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PubMed1995

Serum folate and risk for ischemic stroke. First National Health and Nutrition Examination Survey epidemiologic follow-up study.

BACKGROUND AND PURPOSE: A serum folate concentration < or = 9.2 nmol/L has been associated with elevated levels of plasma homocyst(e)ine. Elevated homocyst(e)ine levels have been associated with ischemic stroke in case-control studies; however, the results from prospective studies have been equivocal. We investigated whether a folate concentration < or = 9.2 nmol/L was associated with ischemic stroke in a national cohort. METHODS: We used data from the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study (n = 2006). Cox proportional hazards analyses were used to adjust for differences in follow-up time and covariates. During the 13-year follow-up, 98 ischemic strokes occurred. RESULTS: After adjusting for age, race, sex, education, diabetes, history of heart disease, systolic blood pressure, body mass index, hemoglobin level, cigarette smoking, and alcohol intake, participants with a folate concentration < or = 9.2 nmol/L were at slightly increased risk for ischemic stroke (relative risk [RR], 1.37; 95% confidence interval [CI], 0.82 to 2.29). There was a folate-race interaction (P = .11 for interaction term). Whites with a folate concentration < or = 9.2 nmol/L had a relative risk of 1.18 (95% CI, 0.67 to 2.08), whereas blacks had a relative risk of 3.60 (95% CI, 1.02 to 12.71). CONCLUSIONS: These findings suggest that a folate concentration < or = 9.2 nmol/L may be a risk factor for ischemic stroke, especially in blacks. However, given the small number of stroke events, additional studies are needed to assess the role of folate in the epidemiology of ischemic stroke.

Adult↗

PubMed1975

Remediable defects in Crohn disease: a prospective study of 63 patients.

To identify potentially remediable abnormalities in Crohn disease, 63 patients had evaluations performed for anemia, electrolyte deficiencies, defects of carbohydrate, fat, nitrogen, and vitamin B12 absorption, and jejunal bacterial overgrowth. Ninety percent of the group had two or more potentially correctable defects. More than 50% had anemia associated with iron or folate deficiency of vitamin B12 malabsorption; 33% had low levels of serum sodium, potassium, calcium, or magnesium either singly or in combination; 22% had lactose intolerance, fat malabsorption was persent in 31%; 75% had evidence of disturbed protein metabolism; and bacterial overgrowth of the upper part of the small bowel was identified in 30% of 47 patients.

Adult↗

PubMed2002

Proteinuria as a predictor of total plasma homocysteine levels in type 2 diabetic nephropathy.

OBJECTIVE: Patients with diabetes who manifest proteinuria are at increased risk for cardiovascular events. Some studies suggest that proteinuria exerts its cardiovascular effects at least partly through a positive association with total plasma homocysteine (tHcy). Modestly sized but better designed contrary studies find no such link through a limited range of serum creatinine and proteinuria. We tested the hypothesis that proteinuria independently predicts tHcy levels in a larger cohort of type 2 diabetic patients with nephropathy throughout a much broader range of kidney disease and proteinuria. RESEARCH DESIGN AND METHODS: Baseline data for the cross-sectional study were obtained from 717 patients enrolled in the multicenter Irbesartan Diabetic Nephropathy Trial. All subjects had type 2 diabetes, hypertension, and proteinuria and were between 29 and 78 years of age. Data included age, sex, BMI, serum creatinine and albumin, LDL and HDL cholesterol, triglyceride, proteinuria and albuminuria, plasma folate, B12, and pyridoxal 5'-phosphate (PLP) (the active form of B6), HbA(1c), and tHcy levels. Unadjusted and multivariable models were used in the analysis. RESULTS: Crude analyses revealed significant associations between tHcy and age (r = 0.074; P = 0.008), creatinine (r = 0.414; P < 0.001), PLP (r = -0.105; P = 0.021), B12 (r = -0.216; P < 0.001), folate (r = -0.241; P < 0.001), and HbA(1c) (r = -0.119; P = 0.003), with serum albumin approaching significance (r = 0.055; P = 0.072). Only serum creatinine, plasma folate, B12, serum albumin, sex, HbA(1c), and age were independent predictors of tHcy after controlling for all other variables. CONCLUSIONS: By finding no independent correlation between proteinuria (or albuminuria) and tHcy levels, this study improves the external validity of previous negative findings. Therefore, it is unlikely that the observed positive association between proteinuria and cardiovascular disease is directly related to hyperhomocysteinemia.

Cholesterol, HDL↗

PubMed1999

Hyperhomocysteinemia and hyperlipidemia in coronary heart disease.

OBJECTIVE: To examine the relationship between coronary heart disease (CHD) and serum lipid, plasma homocysteine (HCY) as well as the factors related to HCY metabolisms. METHODS: The mutation of the 677C-->T transition of 5, 10-methylenetetrahydrofolate reductase (MTHFR) was determined by PCR-based assay. Whole-blood and plasma folate and plasma vitamin B12, as cofactors of MTHFR, were determined by radio-immunologic assay. Plasma HCY was determined by HPLC. RESULTS: Patients with CHD had elevated plasma HCY concentrations (17.38 +/- 1.94 mumol/L vs 10.25 +/- 1.57 mumol/L, P < 0.01). In patients with myocardial infarction (MI) and family history (FH) of CHD, plasma HCY were elevated even higher (P < 0.05). Plasma HCY concentrations had significant non-linear inverse correlation with plasma folate and B12 concentrations, i.e. the lower the serum folate or B12 concentrations, the higher the plasma HCY concentrations (P < 0.01). Patients with homozygous mutants had higher plasma HCY concentrations. Patients with CHD had increased serum Chol and LDL-C and Apo-B levels (P < 0.01, P < 0.05 and P < 0.05 respectively). But plasma HCY concentrations had no correlation with serum lipid levels. 24.1% of the patients had high lipid and high HCY level, 25.9% had high lipid level and normal HCY level, 20.4% had normal lipid and high HCY level, and 29.6% had normal lipid and HCY level. CONCLUSIONS: HCY may have strong association with the genesis of CHD. Low plasma folate and B12 concentrations may induce Hyperhomocysteinemia [HH(e)]. Plasma HCY concentrations have no correlation with serum lipid levels, so HCY may be an independent risk factor. CHD may be induced by different mechanisms and can be classified into hyperlipidemia, HH (e) and normolipidemia, and normohomocysteinemia.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗

PubMed2001

Trimethoprim-sulphamethoxazole as primary Pneumocystis carinii prophylaxis does not increase serum homocysteine levels in HIV-positive subjects.

Background: We recently observed that a short course of trimethoprim 300 mg b.i.d. in healthy volunteers can cause a substantial increase in fasting plasma homocysteine levels, up to concentrations reportedly associated with atherothrombotic complications. The purpose of this study was to determine whether primary Pneumocystis carinii prophylaxis (PCP) with trimethoprim-sulphamethoxazole (TMP-SMX) adversely affects serum homocysteine levels in HIV-positive patients. Methods: We studied 34 subjects [29 male, 5 female, mean age 36.8+/-7.9 (S.D.) years] with no prior AIDS-defining disease who required primary PCP prophylaxis (CD4+ T-cell count <200/mm(3)). The common dose of TMP-SMX was 80/400 mg (80 mg trimethoprim and 400 mg sulphamethoxazole) once daily. Serum total homocysteine levels were determined in four samples: two collected prior to the start of TMP-SMX and two collected on average 2.6+/-2.2 and 5.3+/-3.5 months into the first year of prophylactic therapy. Results: Mean serum homocysteine was 13.9+/-3.7 &mgr;mol/l pre-treatment and 14.4+/-5.0 &mgr;mol/l during treatment with TMP-SMX, a non-significant increase of 0.5 &mgr;mol/l (95% CI: -0.5 to +1.4, P=0.34). Folate levels were equally unaffected by TMP-SMX (13.1+/-6.5 nmol/l versus 13.3+/-5.3 nmol/l, before and during therapy, respectively). Baseline folate levels did not predict the response of homocysteine to TMP-SMX, and neither did age, gender, or serum creatinine. Conclusion: Long-term therapy with 80/400 mg TMP-SMX does not adversely affect homocysteine levels.

Journal Article↗

PubMed1978

Folate status during long-term therapy with trimethoprim and sulphadiazine.

It was studied whether treatment with sulphadiazine and trimethoprim for 8 weeks affected the folate status. The therapy did not inhibit the absorption as assessed by the 3H--folic acid absorption (TRIFA) test. Plasma folic acid clearance showed that folate deficiency had not developed. Bone marrow studies revealed that the antifolic action of the drugs did not manifest itself at the cellular level. The Lactobacillus casei method should not be employed in the determinations of the serum folate concentration during the treatment because therapeutic plasma concentrations of the two drugs inhibit the growth of the test bacteria.

Adult↗

PubMed1999

Hyperhomocysteinemia in high-aged subjects: relation of B-vitamins, folic acid, renal function and the methylenetetrahydrofolate reductase mutation.

Moderate hyperhomocysteinemia is an atherogenic risk factor and plays an important role in geriatrics. Here, we have investigated the role of hyperhomocysteinemia in two elderly groups: 104 longeval subjects of 85-102 years, 100 seniors aged 65-75 years, and 75 controls of 19-60 years. Elevated homocysteine levels were found in 58% of longeval subjects in comparison with 32% in seniors. The homocysteine level in serum correlated positively with age as well as serum creatinine, and inversely with serum folate, but there was no correlation with serum B-vitamins. The frequency of vitamin B deficiency in serum of longeval subjects compared to seniors was as follows: vitamin B6 43% vs. 22%, vitamin B12 20% vs. 8%, and folic acid 1% in both groups. Increased serum creatinine levels (> 1.1 mg/dl) were found in 63% of the longeval subjects and in 32% of seniors. The 677-missense mutation in the methylenetetrahydrofolate reductase (MTHFR) gene, responsible for moderate homocysteine elevation, was found in 35, 37 and 27% of alleles in longeval persons, senior subjects and younger controls, respectively, showing no significant difference in frequency distributions of the MTHFR gene mutation. It can be concluded that hyperhomocysteinemia is very common with increased age. Its importance as an atherogenic risk factor with advanced age has to be clarified.

Adult↗

PubMed2004

Mild hyperhomocysteinemia in adult patients with sickle cell disease: a common finding unrelated to folate and cobalamin status.

Homocysteine has associations with both vitamin insufficiency and vascular complications, and its status is therefore of interest in sickle cell disease (SCD). However, information is limited, especially in adults. We studied plasma total homocysteine (tHcy) and three of its major modifiers, cobalamin, folate, and creatinine, in 90 adult patients with SCD and 76 control subjects. The patients had higher tHcy levels than did controls (P = 0.03) and had elevated tHcy more often (20% vs. 3%, P = 0.0005). None of the hyperhomocysteinemic patients had low cobalamin or folate levels; on the contrary, patients with SCD had high folate levels more often than control subjects (32% vs. 7%; P < 0.0001). Although serum creatinine values were lower in SCD patients than in control subjects (P = 0.03), high levels also tended to occur more often (8% vs. 1%; P = 0.054). Most importantly, creatinine levels correlated significantly with tHcy (P < 0.0001) and logistic regression analyses showed creatinine to be the only significant predictor of high tHcy levels in SCD (P = 0.01). Our results show that hyperhomocysteinemia affects 20% of adults with SCD despite routine folate supplementation and is independent of folate and cobalamin status. Creatinine was the major identifiable influence on tHcy, but renal insufficiency explained only 4 of the 18 elevated tHcy levels. Longitudinal studies will be needed to determine whether the frequent hyperhomocysteinemia of SCD influences the vascular complications in SCD. If reducing tHcy becomes advisable, then interventions other than folate therapy will be needed.

Adult↗

PubMed2004

The administration of a multivitamin/mineral fortified dairy product improves folate status and reduces plasma homocysteine concentration in women of reproductive age.

BACKGROUND AND OBJECTIVES: Folate deficiency during the periconceptional period is related to the occurrence and recurrence of neural tube defects. The aim of the study was to assess whether the administration of folic acid and other vitamins and minerals as a fortified dairy product (400 microg per day of folic acid) improves the folate status in women of reproductive age. DESIGN AND METHODS: Plasma and red blood cell folate, plasma vitamin E, B12, total plasma homocysteine, plasma lipid profile, and serum ferritin and transferrin levels were investigated in 31 healthy nonpregnant women receiving 500 mL/day of the fortified dairy product for eight weeks. RESULTS: The women showed a significant increase in plasma levels of folate and vitamin B12 concentrations after four and eight weeks of supplementation. Moreover, we observed an increase in red blood cell folate concentration during the period of the study. Simultaneously, total plasma homocysteine levels decreased significantly during the intervention period. CONCLUSIONS: The regular consumption of a folic acid and other vitamins (mainly vitamins B6 and B12) and minerals in a fortified dairy product improves folate status and reduces total plasma homocysteine concentration in healthy women of childbearing age.

Adult↗

PubMed2004

Association of apolipoprotein E genotypes with serum lipid profiles in a healthy population of Taiwan.

Apolipoprotein E (apoE, protein; APOE, gene) plays a major role in lipoprotein metabolism and lipid transport. Many investigators have described associations between apoE genotypes, coronary artery disease (CAD), and other risk factors. The aim of this study was to investigate the association between apoE genotypes and serum lipid profiles in a healthy population of 220 volunteers at Kaohsiung in Taiwan. Other CAD risk factors such as serum levels of apolipoprotein A-I (apoA-I), apolipoprotein B, (apoB), homocysteine (Hcy), folate, and vitamin B12 were also measured. ApoE genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). In the study population, the frequency of apoE allele epsilon3 was greatest (85.2%); the frequency of epsilon2 was 8.4%; and that of epsilon4 was 6.4%. The serum apoA-1/apoB ratio showed significant difference among the 3 apoE genotype groups (p 0.0001); the apoA-1/apoB ratio was 1.9 +/- 0.1 (mean +/- SD) in the epsilon2 group, vs 1.4 +/- 0.04 and 1.5 +/- 0.12 in the epsilon3 and epsilon4 groups, respectively. No significant associations were found between APOE alleles and the serum levels of the various lipids or other CHD risk factors.

Apolipoproteins E↗

PubMed2003

Erythropoietin mimics the acute phase response in critical illness.

BACKGROUND: In a prospective observational study, we examined the temporal relationships between serum erythropoietin (EPO) levels, haemoglobin concentration and the inflammatory response in critically ill patients with and without acute renal failure (ARF). PATIENTS AND METHOD: Twenty-five critically ill patients, from general and cardiac intensive care units (ICUs) in a university hospital, were studied. Eight had ARF and 17 had normal or mildly impaired renal function. The comparator group included 82 nonhospitalized patients with normal renal function and varying haemoglobin concentrations. In the patients, levels of haemoglobin, serum EPO, C-reactive protein, IL-1beta, IL-6, serum iron, ferritin, vitamin B12 and folate were measured, and Coombs test was performed from ICU admission until discharge or death. Concurrent EPO and haemoglobin levels were measured in the comparator group. RESULTS: EPO levels were initially high in patients with ARF, falling to normal or low levels by day 3. Thereafter, almost all ICU patients demonstrated normal or low EPO levels despite progressive anaemia. IL-6 exhibited a similar initial pattern, but levels remained elevated during the chronic phase of critical illness. IL-1beta was undetectable. Critically ill patients could not be distinguished from nonhospitalized anaemic patients on the basis of EPO levels. CONCLUSION: EPO levels are markedly elevated in the initial phase of critical illness with ARF. In the chronic phase of critical illness, EPO levels are the same for patients with and those without ARF, and cannot be distinguished from noncritically ill patients with varying haemoglobin concentrations. Exogenous EPO therapy is unlikely to be effective in the first few days of critical illness.

Acute Kidney Injury↗

PubMed1989

[Plasma homocysteine, a risk factor for premature vascular disease. Plasma levels in healthy persons; during pathologic conditions and drug therapy].

Homocysteine is a branch-point metabolite, the biological fate of which is linked to vitamin B12, reduced folates and vitamin B6. Various inborn defects in homocysteine metabolism, among which cystathionine beta-synthase deficiency is most common, lead to the clinical condition homocystinuria. A central feature of this clinical state is premature arteriosclerosis. These patients benefit from agents serving as cofactors in homocysteine metabolism which both reduce the homocysteine levels in plasma and the incidence of vascular episodes. Experimental data point to homocysteine as an arteriosclerotic agent. Homocysteine in human plasma exists mainly as mixed disulfides with albumin (70 per cent) and cysteine. New methods determine total plasma homocysteine which includes all these species. Normal values for plasma homocysteine are lower in premenopausal women than in men and postmenopausal women. Impaired homocysteine metabolism seems to exist in 15-30 per cent of patients with premature cardiovascular disease. Moderate homocysteinemia is as a risk factor for cardiovascular disease, independent of conventional risk factors. Apart from homocystinuria, vitamin B12 deficiency causes the most extreme elevations of plasma homocysteine, and it has been established that plasma homocysteine is a more responsive parameter to impaired vitamin B12 function than serum cobalamin. Massive increase in plasma homocysteine level is also observed in folate deficiency, whereas renal failure, some malignant states and psoriasis cause a moderate homocysteinemia. High doses of folic acid reduce plasma homocysteine, and this innocuous mean should be considered as an intervention in patients with increased plasma level. Drugs like methotrexate, some anticonvulsants and 6-azauridine triacetate induce moderate elevation of plasma homocysteine, whereas a reduction is observed after penicillamine administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗

PubMed1999

Modern clinical testing strategies in cobalamin and folate deficiency.

Folate or cobalamin deficiencies are usually detected by hematologic abnormalities, such as a macrocytic megaloblastic anemia, or often milder signs, such as hypersegmented neutrophils. In fact, these vitamin deficiencies may be associated with clinical conditions in which anemia and/or macrocytosis are absent, such as neuropsychiatric disorders and inborn errors of folate or cobalamin metabolism. A battery of sensitive tests, including blood vitamin levels, serum methylmaIonic acid and homocysteine assays, and the deoxyuridine suppression test in the bone marrow, allows for early detection of vitamin deficiency. Additional tests may be included to identify the causes of deficiency, such as the Schilling test using crystalline cyanocobalamin, or a modified Schilling test for showing food cobalamin malabsorption. Strategies for diagnosing a vitamin deficiency differ according to the hematologic and clinical presentations. The deleterious effects (aside from anemia) that arise from cobalamin or folate deficiency and include neurological complications, increased risk of vascular disease due to hyperhomocysteinemia, and increased risk of some types of cancer related to folate deficiency, underscore the importance of making an early diagnosis and instituting treatment with the appropriate vitamin in preventing permanent damage.

Deoxyuridine↗

PubMed2005

Hyper-homocysteinemia is not a main feature of juvenile uncomplicated type 1 diabetes.

Total plasma homocysteine (tHcy) was measured by high pressure liquid chromatography (HPLC) method in 28 patients (12 females and 16 males) at the onset of type 1 diabetes mellitus (T1DM), 4 females during diabetes ketoacidosis (DKA) and 154 (68 females and 86 males) during follow-up. Serum folate, pyridoxal 5' phosphate (PLP) and Vitamin B12 (Vit B12) were also measured. Plasma tHcy levels were not found significantly different in T1DM patients known to have diabetes (males 9.2 +/- 7.7 and females 7.0 +/- 2.8 micromol/l) and in those who were newly diagnosed (males 9.7 +/- 4.8 and females 7.16 +/- 2.8 micromol/l) than in healthy controls (males 8.7 +/- 3.5 and females 7.8 +/- 2.55 micromol/l). Only a significant difference for sex was observed in known diabetes (p = 0.0281). Serum folate, PLP and Vit B12 were normal (12.6 +/- 3.6 ng/ml, 20.11 +/- 0.8 ng/ml and 416.7 +/- 41.9 pg/ml) in all T1DM patients. Age significantly correlated with plasma tHcy. Only in 4 patients, studied during DKA, plasma tHcy was significantly lower (2.76 +/- 1.33 micromol/l, p < 0.001) than the healthy controls.

Adolescent↗

PubMed1987

Is disordered folate metabolism the basis for the genetic predisposition to neural tube defects?

Vitamin levels were measured in twenty women under 35 years of age with a history of two or more neural tube defect pregnancies. Each index case was compared with a female control matched for age, obstetric history and social class. The mean concentration of red cell folate in the subjects was 178 ng/ml, significantly lower than the mean of 268 ng/ml for the control group (P = 0.005). Red cell folate levels showed a linear relationship with the number of neural tube defect pregnancies, the levels being lowest in women who had had three or four affected offspring. There was no significant difference in serum folate; plasma or white cell vitamin C; plasma vitamin A; thiamine, riboflavine or pyridoxine status; serum vitamin B12; plasma vitamin E; total protein, albumin, transferrin, magnesium, copper or zinc. Diet was assessed by a questionnaire. The dietary intakes of total folate and other vitamins except vitamin A were lower in the subjects than the controls but none of the differences were statistically significant. Regression analysis showed a difference between subjects and controls in the relationship of red cell folate to dietary folate. This study demonstrates an association between susceptibility to offspring with neural tube defects and depressed red cell folate levels which cannot be entirely attributed to a lower dietary intake of folate. It is postulated that one factor predisposing to the occurrence of neural tube defects may be an inherited disorder of folate metabolism.

Adult↗

PubMed2001

Folate, vitamin B12, and sulfur amino acid levels in patients with renal failure.

We examined the plasma profile of sulfur amino acids (SAA) in patients with chronic renal failure (CRF) and looked for any correlation with serum folate (FA) and/or vitamin B12. Group 1 comprised 9 patients with CRF and glomerular filtration rate (GFR) >20 ml/min per 1.73 m2, 9 patients with GFR<20 ml/min per 1.73 m2 comprised group 2, and 14 patients on hemodialysis group 3. The control group comprised 16 healthy children. Homocysteine (Hcy), methionine (Met), cysteine (Cys), and serine (Ser) were measured with gas chromatography. FA and vitamin B12 were measured using enzymatic immunoassay. Median SAA concentrations were significantly lower in controls than in the three groups of patients. Hcy concentrations were 0.8 micromol/l in controls versus 5 micromol/(group 1), 9 micromol/l (group 2), and 20 micromol/l (group 3). Met concentrations were 26 micromol/l in controls versus 26 micromol/l (group 1), 66 micromol/l (group 2), and 281 micromol/l (group 3). Cys concentrations were 10 micromol/ in controls versus 98 micromol/l (group 1), 54 micromol/l (group 2), and 122 micromol/l (group 3). Ser concentrations were 88 micromol/ in controls versus 153 micromol/l (group 1), 239 micromol/l (group 2), and 240 micromol/l (group 3). The median concentrations of FA were lower in controls than in groups 2 and 3: 5.5 ng/ml versus 8 ng/ml and 15 ng/ml, respectively. Vitamin B12 concentrations did not differ between groups. Vitamin levels did not correlate with SAA. The only difference between patients with Hcy levels in the lower and upper quartile was in Met concentration (38 vs. 263 micromol/l, P<0.02) and GFR (P<0.01). In conclusion, patients with CRF had higher SAA concentrations than healthy children. FA concentrations are higher in CRF patients than in healthy children but did not correlate with concentrations of SAA.

Adolescent↗

PubMed2006

Serum level of homocysteine is correlated to carotid artery atherosclerosis in Chinese with ischemic stroke.

OBJECTIVES: To investigate the relationship between serum level of homocysteine (Hcy) and carotid artery atheroscleosis (CAA). METHODS: Both sides of the common carotid artery and internal carotid artery in 126 Chinese patients with ischemic stroke were measured by B-mode ultrasound. The patients were divided into groups: normal, A, B, C and D according to the severity of CAAs. With fasting serum, Hcy as well as folate, vitamin B(12) and lipids were detected. The mean +/- SD age was 64 +/- 13 years (range 39-87 years). RESULTS: In a logistic regression model, the Hcy concentrations were associated with an elevated risk of CAAs independent of all traditional risk factors, and when CAAs became severer, the serum Hcy was higher. The levels of the normal group and A, B, C, D groups were 13.22 +/- 6.15 micromol/L, 16.29 +/- 9.81 micromol/l, 19.49 +/- 11.16 micromol/l, 27.21 +/- 17.47 micromol/l, and 24.14 +/- 8.64 micromol/l, respectively. Rank test showed a significant difference between normal and other groups (p<0.05). The levels of folate and vitamin B(12) were negatively correlated with the Hcy concentrations. Spearman correlation coefficient were -0.23 and -0.42 (p<0.05). CONCLUSIONS: Hyperhomocysteinaemia is an independent risk factor of CAAs and the degree of CAAs is highly correlated with the level of Hcy in serum. The causes of hyperhomocysteinemia may be the result from the decrease in folate and vitamin B(12). Clinical trials are now required to evaluate the effect of treatment with these vitamins on the primary and secondary prevention of cerebral vascular diseases.

Adult↗

PubMed1994

Elevated serum homocysteine as a predictor for vitamin B12 or folate deficiency.

Tissue deficiency of vitamin B12 and folate results in an increase in serum homocysteine (sHcy). We have measured sHcy in patients with reduced serum vitamin B12 and/or red cell folate (RCF) to determine its usefulness as a discriminant for the diagnostic interpretation of reduced vitamin levels. Of 3846 patients who had serum vitamin B12 and RCF assayed, 335 (9%) had reduced vitamin levels. Multivariate analysis showed a significant association between sHcy and serum creatinine (p = 0.0001), positive intrinsic factor (IF) antibody or neutrophil hypersegmentation (NHS) (p = 0.001), increased MCV (p = 0.014) and low RCF (p = 0.025) but no relationship with the level of serum vitamin B12 or haemoglobin. After censoring the patients with renal impairment (n = 54), the distribution of the remaining 72 patients with elevated sHcy was 37/151 (25%) with low serum vitamin B12 with or without low RCF and 35/130 (27%) with low RCF alone. sHcy correctly identified response to vitamin therapy in 33/35 (94%) patients who had adequate parameters to assess response. The positive predictive values of IF antibody/NHS, macrocytosis and/or low RCF for elevated sHcy were 100% and 34% respectively. Twenty-four percent of patients with a low serum vitamin B12 and elevated sHcy had no abnormal haematologic parameters as determined by the routine laboratory staff. These data suggest that the usefulness of measuring sHcy in a routine diagnostic setting is limited and a careful review of the peripheral blood for macrocytosis and NHS plus determination of RCF may be a more cost-effective process than sHcy assay in most instances to determine the presence of tissue deficiency.

Adult↗