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PubMed2001

MTHFR gene polymorphism, homocysteine and cardiovascular disease.

Homocysteine is an emerging new risk factor for cardiovascular disease. It is a thiol compound derived from methionine and involved in two main metabolic pathways: the cycle of activated methyl groups, requiring folate and vitamin B12 as cofactors, and the transsulfuration pathway to cystathionine and cysteine requiring vitamin B6 as cofactor. The homocysteine metabolism represents an interesting model of gene-environment interaction. Elevations in homocysteine may be caused by genetic defects in enzymes involved in its metabolism or by deficiencies in cofactor levels. A common polymorphism in the gene coding for the 5,10-methylene tetrahydrofolate reductase (MTHFR) (C677T, Ala --> Val) is associated with a decreased activity of the enzyme due to thermolability. In case of homozygosity for the Val allele, a relative deficiency in the remethylation process of homocysteine into methionine leads to a mild-to-moderate hyperhomocysteinemia, a condition recognized as an independent risk factor for atherosclerosis. The genetic influence of the MTHFR polymorphism on homocysteine levels is attenuated in females in premenopausal age and is not significant in subjects who exhibit serum levels of folate and/or vitamin B12 above the 50th percentile of distribution in the general population. The prevalence of the Val/Val genotype varies among different ethnic groups. It is very low in African populations, whereas in Europe and North America it ranges between 5% and 15%. In Italy an even higher prevalence has been reported in some regions. The question whether the MTHFR polymorphism might be per se an independent contributor to cardiovascular risk is debated. The interaction between this or other genetic factors and environmental/nutritional conditions (i.e. intake of vitamins such as folate) is a key determinant for homocysteine concentrations in healthy conditions as well as in some disease (i.e. in renal disorders). Another example of gene/environment interaction in the field of atherosclerosis is given by the apolipoprotein E polymorphism and its influence in response to diet. The presence of a high prevalence of risk-related allelic variants of such candidate genes within a certain population could serve to locally reinforce the recommendations concerning nutrient intake.

Apolipoproteins E↗
PubMed1975

Effect of oral contraceptive agents on nutrients: II. Vitamins.

Clinical, biochemical and nutritional data were collected from a large population of women using oral contraceptive agents. Higher incidence of abnormal clinical signs related to malnutrition were observed in the lower (B) as compared to the higher (A) socioeconomic groups, and also in the nonsupplemented groups as compared to the supplemented groups in the B subjects. As a rule the intake of oral contraceptive agent subjects of vitamin A, C, B6 and folic acid did not differ from that of the controls As expected, subjects from the supplemented groups had higher intake of vitamin A, C, B6, thiamin, riboflavin and folic acid, and A groups had higher intake of vitamin C, B6, riboflavin and folic acid. Increased plasma vitamin A and decreased carotene levels were observed in oral contraceptive agent users. In general oral contraceptive agents had little or no effect on plasma ascorbic acid. Urinary excretion of both thiamin and riboflavin in subjects using oral contraceptive agents were lower in A groups. Erythrocyte folate and plasma pyridoxal phosphate was decreased in A groups due to oral contraceptive agents. Subjects who took supplements had higher levels of plasma vitamin A, ascorbic acid and folate. But urinary thiamin and riboflavin were higher only in group A subjects who took supplements.

Adolescent↗
PubMed1989

Folic acid deficiency, megaloblastic anemia and peripheral polyneuropathy due to oral contraceptives.

A 34-year-old woman developed megaloblastic anemia and peripheral polyneuropathy following the use of oral contraceptives for 4 years. Low levels of folic acid and vitamin B12 were found. Both the complete recovery after therapy with the vitamins, and the absence of other causes of vitamin B12 and folate deficiency, suggest that the vitamin deficiencies were caused by the oral contraceptives and resulted in the rare combination of megaloblastic anemia and polyneuropathy. The poor response to vitamin B12 alone, and the development of anemia and polyneuropathy 4 months after cessation of vitamin B12 therapy suggest that folate deficiency was the primary problem.

Adult↗
PubMed1983

A prophylactic supplementation of iron and folate in pregnancy.

The supplementation of iron and folic acid were studied in 567 pregnant women with 18 and 26 weeks of gestation. Sixty mg and 180 mg of iron were given daily to pregnant women of group I and group II respectively while 180 mg of iron and 5 mg folic acid were given to group III. The Hb values increased significantly in group II and III after supplementation for 1 1/2 months, however if supplementation was extended for 3 months, highly significant increase in Hb levels were observed in all these groups. These findings indicated that in supplementation for a shorter period, i.e. 1 1/2 months at least 180 mg of iron was needed, and only 60 mg of iron was sufficient to increase Hb levels for a supplementation of 3 months. Vitamin B12 deficiency was not detected in pregnant women both before and after supplementation with iron and iron plus folate for 3 months. It was suggested therefore that perhaps it was not necessary to supplement vitamin B12 to Thai pregnant women. In this study 15% of pregnant women had low serum folate with normal red cell folate level, and a greater number of women with low serum folate concentrations were observed after supplementation with iron alone for 3 months. However, increased serum folate and red cell folate levels after supplementation with 5 mg folic acid indicated that some pregnant women needed folate supplementation in preventing folic acid deficiency during pregnancy.

Adolescent↗
PubMed1989

Clinical experience with leucovorin and 5-fluorouracil.

Two trials of leucovorin (LV) and 5-fluorouracil (5-FU) in patients with metastatic colorectal cancer were done, both using a 3-day loading dose and then weekly doses to minimize toxicity. The first trial used LV administered by intravenous infusion with a constant dose of 5-FU 400 mg/m2, and the second trail used oral LV with increasing doses of 5-FU. In the first trail, 45 eligible patients (20 with and 25 without previous therapy) were treated. Toxicity usually consisted of diarrhea or weakness and was controlled by delaying or decreasing the 5-FU dose. Subjective responses occurred in 75% of patients but did not correlate with antineoplastic effect. Objective responses were seen in 36% and stabilization of disease in 31% of patients; these correlated with prolonged survival. Median survival was 8 months for patients with previous treatment and 10 for those without. Twelve-month survival was 32% and 40%, respectively. There was no correlation between the development of toxicity and response or survival. The second trial was conducted recently in cooperation with Duke University to determine toxicity and efficacy of oral LV with intravenous 5-FU before a randomized trial of this combination versus placebo with intravenous 5-FU. Eighteen patients were treated, and serum levels of folates were obtained on ten. First toxicity occurred at 5-FU doses ranging from 375 to 850 mg/m2, and consisted of diarrhea in nine, lethargy in seven, nausea/vomiting in four, dermatitis in four, conjunctivitis in two, hypersalivation in two, stomatitis in one, and profound granulocytopenia in one. Response rate was 35%, and stabilization was 35% with median survival of 14 months. Twelve-month survival was 56%.

Adenocarcinoma↗
PubMed1988

Clinical experience with CF-FUra.

Two trials of CF-FUra in patients with metastatic colorectal cancer were performed, both using a 3 day loading dose and then weekly maintenance doses to minimize toxicity. The first trial used CF by IV infusion with constant dose of FUra 400 mg/m2, and the second trial used oral CF with escalating doses of FUra. In the first trial, 45 eligible patients (20 with and 25 without prior therapy) were treated. Toxicity usually consisted of diarrhea or weakness and was controlled by delaying or decreasing 5FU dose. Subjective responses occurred in 75% of patients but did not correlate with antineoplastic effect. Objective responses were seen in 36% and stabilization of disease in 31% of patients, and correlated with prolonged survival. Median survival was 8 months for patients with prior treatment and 10 for those without, and 12 month survival was 32% and 40%, respectively. There was no correlation between the development of toxicity and response or survival. The second trial was recently conducted in cooperation with Duke University to determine toxicity and efficacy of oral CP with IV FUra prior to a randomized trial of this combination versus placebo with IV FUra. Eighteen patients were treated and serum levels of folates were obtained on 10. First toxicity occurred at FUra doses ranging from 375 to 850 mg/m2, and consisted of diarrhea in 9, lethargy in 7, nausea/vomiting in 4, dermatitis in 4, conjunctivitis in 2, hypersalivation in 2, stomatitis in 1, and profound granulocytopenia in 1. Response rate was 35% and stabilization was 35% with median survival of 14 months and 12 month survival of 56%.

Adenocarcinoma↗
PubMed1997

Gender differences and other determinants of the rise in plasma homocysteine after L-methionine loading.

The methionine load test is widely used to identify subjects with mild homocysteinemia. We studied factors influencing the rise in plasma homocysteine (tHcy) levels following oral methionine loading, after taking into account determinants of the basal level. The study population comprised 522 persons (mean age 53, range 17 to 95; 63% male; 60% with coronary disease). tHcy was measured fasting and 4 h after administration of L-methionine (dose 4 g/m2). The percentage rise in tHcy was greater in females, at younger ages, and with lower serum creatinine. Basal tHcy was lower in those with high levels of serum folate, red cell folate and serum B12; they also showed a greater percentage rise with loading. After adjustment for age, creatinine and serum vitamins the percent rise was greater in females (mean 230%, S.D. 92) than in males (mean 172%, S.D. 71, P < 0.0001). About 1/4 of this effect was explained by the methionine dose, but important independent gender effects remained. When the results of the loading test were compared with an overall reference range, females were systematically labelled as 'high' but comparison with age and gender-specific reference ranges normalised the sex distribution. Our data show that a single L-methionine loading protocol for both sexes is not appropriate. Gender-specific reference ranges should be used to define post-load homocysteinemia and previous studies which have identified a high proportion of females with this trait probably reflect the need for gender specific reference ranges.

Adolescent↗
PubMed2004

Association study of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with myocardial infarction.

The angiotensin converting enzyme (ACE) is a strong candidate gene for myocardial infarction (MI). Insertion-deletion dimorphism in intron 16 of this gene has been inconclusively found to be associated with it. Several new polymorphisms in the ACE gene have been identified and among these, a dimorphism in exon 17, ACE G2350A, has a significant effect on plasma ACE concentrations. To assess the value of genotyping the ACE G2350A dimorphism in a genetically homogeneous population, we carried out a case-control study of dimorphism G2350A for a putative association with MI among Pakistani nationals. We investigated a sample population of 370 Pakistanis, comprising 163 controls, and 207 patients with clinical diagnosis of acute MI (AMI). ACE G2350A alleles were visualized by assays based on polymerase chain reaction and restriction endonuclease analysis. Frequencies of G alleles were 0.68 among controls and 0.72 among AMI patients. The ACE G2350A dimorphism showed no significant association with MI (chi2 = 0.90, 2 df, P = 0.64), plasma levels of homocysteine (P = 0.52) or with serum levels of folate (P = 0.299). The results indicate that ACE G2350A polymorphism is not associated with risk of myocardial infarction in the Pakistani population investigated here.

Adult↗
PubMed1983

Effect of orange juice, folic acid, and oral contraceptives on serum folate in women taking a folate-restricted diet.

The effect of folate intake from orange juice on serum folate was evaluated in 60 women (age 20-39) during 9 weeks of a folate-restricted diet. Twenty-one were users of oral contraceptives (OCA). Folate intake from the restricted diet was 159 +/- 5 micrograms/day, as assessed by dietary surveys. Serum folate of women taking OCA was lower than in nonusers at the inception of the study (P less than 0.01). During the initial 2 weeks of restricted diet, serum folates decreased significantly (13.8 +/- 1.8 to 8.5 +/- 0.4 ng/ml; P less than 0.002). This decrease was further prevented by supplementation of the diet for 7 weeks with 100 micrograms/day of total folate from reconstituted frozen orange juice or synthetic folic acid (PteGlu). Both folate supplements were effective (P less than 0.05) in increasing serum folate (9.4 +/- 1.0 to 14.5 +/- 1.4 ng/ml, orange juice; 8.4 +/- 0.7 to 20.5 +/- 5.8 ng/ml, folic acid). Serum folates were similar in women taking either orange juice or folic acid. Serum folate of nonsupplemented women decreased from 10.2 +/- 0.8 to 8.3 +/- 0.4 ng/ml (P less than 0.05). No difference between serum folates of OCA users and nonusers was detected during the restricted diet or folate supplementation. These data indicate that folate in reconstituted orange juice was as available as folic acid, and that utilization of both folate forms and folate in a mixed diet was unaffected by oral contraceptives.

Adolescent↗
PubMed1982

Improvement in cervical dysplasia associated with folic acid therapy in users of oral contraceptives.

Forty-seven young women with mild or moderate dysplasia of the uterine cervix (cervical intraepithelial neoplasia) diagnosed by cervical smears, received oral supplements of folic acid, 10 mg, or a placebo (ascorbic acid, 10 mg) daily for 3 months under double-blind conditions. All had used a combination-type oral contraceptive agent for at least 6 months and continued it while returning monthly for follow-up examinations. All smears and a biopsy obtained at the end of the trial period were classified by a single observer without knowledge of treatment status using an arbitrary scoring system (1 normal, 2 mild, 3 moderate, 4 severe, 5 carcinoma in situe). Mean biopsy scores from folate supplemented subjects were significantly better than in folate-unsupplemented subjects (2.28 versus 2.92, respectively; p less than 0.05). Final versus initial cytology scores were also significantly better in supplemented subjects (1.95 versus 2.32, respectively; p less than 0.05), unchanged in patients receiving the placebo (2.27 versus 2.30, respectively). Before treatment the mean red cell folate concentration was lower among oral contraceptive agent users than nonusers (189 versus 269 ng/ml, respectively; p less than 0.01) and even lower among users with dysplasia (161 versus 269 ng/ml, respectively; p less than 0.001). Morphological features of megaloblastosis were associated with dysplasia and also improved in folate supplemented subjects. These studies indicate that either a reversible, localized derangement in folate metabolism may sometimes be misdiagnosed as cervical dysplasia, or else such a derangement is an integral component of the dysplastic process that may be arrested or in some cases reversed by oral folic acid supplementation.

Adolescent↗
PubMed1987

Vitamin and iron status in new vegetarians.

This study assessed the biochemical status of a number of vitamins and iron in a group of new vegetarians. Values were compared with a group of omnivores of similar age. Satisfactory to high levels of serum folate, vitamin E, and riboflavin were found, and all were significantly higher in vegetarians than omnivores. Thiamin status was satisfactory in both groups although a small but statistically significant difference in favor of the omnivores was found. Serum vitamin B-12 was significantly lower in vegetarians, and iron status as measured by serum ferritin was very significantly lower in vegetarians. Pyridoxine status was similar in both groups. A number of sex differences were found in the vegetarian sample. New vegetarian women appear to be at particular risk of developing low iron stores.

Adult↗
PubMed1979

Severe thrombocytopenia probably due to acute folic acid deficiency.

Thirteen patients with significant hemorrhage, severe thrombocytopenia, and megaloblastic bone marrows are described. Unusual features of this problem included its acute onset, frequent absence of the typical peripheral blood changes of megaloblastic anemia, normal serum B12 levels, and serum folates which were often not clearly abnormal. Most patients were critically ill and common clinical features included reduced dietary intake, renal failure, renal dialysis, the postoperative state, and sepsis. These clinical features, the laboratory findings, and a platelet increase in most patients after folate therapy lead to the conclusion that this problem is probably due to acute folic acid deficiency. Possible explanations for the atypical laboratory findings include the acuteness of onset, recent blood transfusion therapy, and impaired folate utilization. This problem may be relatively common. Because of its potential clinical importance, rapid onset, and attendent diagnostic difficulties, prophylactic folic acid is recommended in the clinical setting described.

Acute Disease↗