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Results for “FOLIC ACID DEFICIENCY”

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PubMed2001

Homocysteine-lowering treatment: an overview.

Elevated fasting plasma concentrations of homocysteine have a high prevalence in subjects with cardiovascular disease and have also been associated with an increased risk of atherothrombosis in most, but not all, prospective studies. The most frequent causes of hyperhomocysteinaemia are genetic defects, such as cystathionine-beta-synthase (CBS) deficiency, deficiencies of folic acid and/or vitamin B12, renal failure and interference in homocysteine metabolism by drugs or metabolic alterations. In most cases, no underlying cause can be established. Subjects with CBS deficiency are treated with pyridoxine with additional folic acid and betaine if necessary. Folic acid and vitamin B12 deficiencies should be corrected by supplementation. Increases in folate intake by dietary changes or fortification can also lower plasma homocysteine in vitamin-replete subjects with normal plasma homocysteine levels. In renal failure, folic acid treatment (1-5 mg/day) ameliorates the plasma homocysteine level in most cases but hyperhomocysteinaemia persists in the majority of patients. Primary (fasting) hyperhomocysteinaemia can be treated with folic acid (0.5-5 mg/day). An abnormal methionine-loading test identifies additional patients at risk and postmethionine-loading hyperhomocysteinaemia should be treated with a combination of pyridoxine and folic acid. In the absence of dose-effect studies, a combination of pyridoxine (50 mg) and folic acid (5 mg) is advised. Large clinical trials are currently underway to establish the role of homocysteine-lowering therapy in the secondary prevention of atherothrombotic disease. In view of the effective, cheap and safe character of therapy with folic acid and pyridoxine, a policy can be accepted to screen and treat high-risk patients until these trials have been concluded.

Animals↗
PubMed1975

Diogenes syndrome. A clinical study of gross neglect in old age.

A study of elderly patients (fourteen men, sixteen women) who were admitted to hospital with acute illness and extreme self-neglect revealed common features which might be called Diogenes syndrome. All had dirty, untidy homes and a filthy personal appearance about which they showed no shame. Hoarding of rubbish (syllogomania) was sometimes seen. All except two lived alone, but poverty and poor housing standards were not a serious problem. All were known to the social-services departments and a third had persistently refused offers of help. An acute presentation with falls or collapse was common, and several physical diagnoses could be made. Multiple deficiency states were found--including iron, folate, vitamin B12, vitamin C, calcium and vitamin D, serum proteins and albumin, water, and potassium. The mortality, especially for women, was high (46%); most of the survivors responded well and were discharged. Half showed no evidence of psychiatric disorder and possessed higher than average intelligence. Many had led successful professional and business lives, with good family backgrounds and upbringing. Personality characteristics showed them to tend to be aloff, suspicious, emotionally labile, aggressive, group-dependent, and reality-distorting individuals. It is suggested that this syndrome may be a reaction late in life to stress in a certain type of personality.

Age Factors↗
PubMed1989

The role of vitamins in the etiology of cervical neoplasia: an epidemiological review.

Diet may act as a cofactor in the development of cancer of the cervix. A consistent correlation exists between low tissue concentrations, low serum level, and low intake of vitamin A, beta-carotene, vitamin C, or folic acid and an increased prevalence of cervical neoplasia. A moderate effect is seen in clinical trials with vitamin treatment of cervical intraepithelial neoplasias. The studies reviewed here were not consistent especially in the choice of controls and methods for the assessment of dietary and confounding factors. Proper morphologic identification of cervical intraepithelial neoplasia was not always achieved. Longitudinal and prospective cohort studies using more reliable methods for diet monitoring may be valuable for future research in this field.

Ascorbic Acid Deficiency↗
PubMed1995

Folic acid improves phenytoin pharmacokinetics.

Phenytoin (PHT) therapy to control seizures decreases serum folate levels in half of epileptic patients, thus increasing the risk of folate depletion. Supplementation with folic acid prevents deficiency but also changes PHT pharmacokinetics. Kinetic monitoring of PHT when folic acid is provided as a supplement has not been reported in women of child-bearing age. This study of six fertile women examined the interdependence of PHT and folic acid in a randomized crossover study of two treatments: treatment 1 consisted of 300 mg sodium PHT per day and treatment 2 consisted of 300 mg sodium PHT plus 1 mg folic acid per day. Dietary folic acid intake was calculated daily. During treatment 1, serum folate level decreased 38.0 +/- 18.6% (mean +/- standard deviation) and serum PHT concentration was in the low therapeutic range (43.92 +/- 14.52 mumol/L). During treatment 2, serum folate level increased 26.0 +/- 33.4%, and serum PHT level (39.04 +/- 14.16 mumol/L) was similar to that in treatment 1. Only one subject attained PHT steady state during treatment 1, but four subjects achieved steady state during treatment 2. Dietary folate intakes during treatments 1 and 2 were not significantly different. This study suggests an interdependence between PHT and folic acid and supports the observation that fertile women treated with PHT require folic acid supplementation to maintain a normal serum folate level.

Adult↗
PubMed1987

Elevation of blood levels of zinc protoporphyrin by radiomimetic drugs and Friend leukemia virus.

Sublethal doses of whole-body irradiation induced the elevation of zinc protoporphyrin (ZPP). Experiments were conducted to determine if recovery from radiomimetic drugs also resulted in elevation of ZPP. Daily injections with hydroxyurea and other cytotoxic drugs for 10 days caused ZPP elevation and a dose of radiation too low to cause ZPP elevation by itself caused ZPP elevation when hydroxyurea was administered prior to irradiation. Friend leukemia virus also brought about an elevation of ZPP. However, not all factors that increased erythropoiesis brought about ZPP elevation. The elevated erythropoiesis in response to hypoxia and the enhanced erythropoiesis that followed administration of folic acid to folic acid-deficient mice was not accompanied by ZPP elevation.

Animals↗