scholarly journals Efficacy of Folic Acid Therapy in Primary Prevention of Stroke Among Adults With Hypertension in China

JAMA ◽  
2015 ◽  
Vol 313 (13) ◽  
pp. 1325 ◽  
Author(s):  
Yong Huo ◽  
Jianping Li ◽  
Xianhui Qin ◽  
Yining Huang ◽  
Xiaobin Wang ◽  
...  
2003 ◽  
Vol 73 (3) ◽  
pp. 215-220 ◽  
Author(s):  
de Gómez Dumm ◽  
Giammona ◽  
Touceda

Dyslipidemia and increases in plasma homocysteine usually occur at end-stage renal disease; both are recognized as risk factors for atherosclerosis. Folate administration reduces homocysteine concentration. In this study we determined the effect of a high dose of folic acid (40 mg intravenous injection three times a week) on plasma and red blood cell lipid profiles in twelve chronic renal failure patients on regular hemodialysis. Fasting blood samples were taken at the beginning of the study (baseline) and after 21, 42, and 64 days of treatment. Folic acid supplementation decreased plasma homocysteine. Plasma triglyceride levels decreased whereas polyunsaturated fatty acid values increased after 21 days; then they returned to baseline levels at the end of treatment. Total cholesterol and low-density lipoprotein (LDL) cholesterol were higher than those of the baseline during all the study, whereas high-density lipoprotein (HDL) cholesterol was reduced. In erythrocyte membranes, folic acid therapy enhanced cholesterol/phospholipid ratios and the fluorescence anisotropy of diphenyl-hexatriene. We conclude that large doses of folic acid produce a favorable effect, reducing plasma homocysteine levels and protecting patients from atherosclerosis. However, as this therapy induces significant alterations in both plasma and erythrocyte membrane lipid profiles, plasma lipid values should be controlled throughout the treatment of patients with renal failure.


1977 ◽  
Vol 53 (1) ◽  
pp. 75-80
Author(s):  
H. Taguchi ◽  
Z. Abdul-Cader ◽  
J. Perry ◽  
E. H. Reynolds ◽  
I. Chanarin

1. The isolated choroid plexus of the rabbit takes up 5-methyltetrahydrofolate from the incubation medium. 2. Other folate analogues (pteroylglutamic acid, methotrexate, 5-formyltetrahydrofolate = folinic acid) inhibited the uptake of 5-methyltetrahydrofolate. 3. The uptake of 5-methyltetrahydrofolate was inhibited by low temperature, anaerobic conditions and dinitrophenol. 4. The anticonvulsant drugs, diphenylhydantoin and phenobarbital, had no effect on 5-methyltetrahydrofolate uptake. 5. The inhibitory effect of pteroylglutamic acid on the uptake of 5-methyltetrahydrofolate by the choroid plexus may explain the effect of long-term folic acid therapy in aggravating vitamin B12 neuropathy in pernicious anaemia.


2009 ◽  
Vol 130 (S206) ◽  
pp. 315-320
Author(s):  
Tage Espersen ◽  
Jørgen Jørgensen

PEDIATRICS ◽  
1982 ◽  
Vol 70 (4) ◽  
pp. 648-650
Author(s):  
K. M. Laurence

It is generally agreed that neural tube defects (NTD) have a multifactorial etiology when genetic factors render the developing fetus susceptible to intrauterine environmental factors acting during the fourth week of gestation to interfere with the orderly closure of the neural tube.1 As there is little likelihood that anything can be done about the genetic background, primary prevention would therefore be dependent on eliminating these factors from the environment or avoiding them. My intention here is to enlarge on some aspects of primary prevention of NTD as outlined by Smithells in an earlier issue (Pediatrics 69:498, 1982).2 One environmental factor, poor maternal nutrition and, more particularly, folic acid deficiency seems now to have been identified, but there are almost certainly a number of others.


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