Folate supplementation during the preconception period, pregnancy and puerperium. Polish Society of Gynecologists and Obstetricians Guidelines

Bomba‐Opoń, Dorota; Hirnle, Lidia; Kalinka, Jarosław; Seremak‐Mrozikiewicz, Agnieszka

doi:10.5603/gp.a2017.0113

Cited by 23 publications

(42 citation statements)

References 13 publications

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“…Jest to spowodowane ich labilnością oraz ograniczoną przyswajalnością z żywności. Niewystarczająca podaż i niskie stężenie kwasu foliowego w osoczu związane są z wyższym ryzykiem wystąpienia wad cewy nerwowej, rozszczepem wargi i podniebienia, a także zespołem Downa [4,25]. Innymi konsekwencjami są m.in.…”

Section: Choroby Spowodowane Niedoborem Kwasu Foliowegounclassified

“…poród przedwczesny, niska masa urodzeniowa noworodka, a także spowolnienie wzrostu płodu [28]. Również zaburzenia metabolizmu folianów do aktywnej formy w organizmie mogą wiązać się z powikłaniami ciąży, takimi jak: nawracające poronienia, stany przedrzucawkowe oraz hiperhomocysteinemia [25].…”

Section: Choroby Spowodowane Niedoborem Kwasu Foliowegounclassified

“…W grupie kobiet z otyłością (BMI >30) stwierdzono dwukrotnie większą szansę wystąpienia wad układu nerwowego u płodu w porównaniu do kobiet o właściwej masie ciała (BMI 18,0-24,9). Dodatkowo zauważono, że suplementacja kwasem foliowym zmniejszyła ryzyko wystąpienia wad cewy nerwowej, a szczególnie było to widoczne w grupie osób z BMI >25 niż u kobiet z BMI <25 [25,33]. Sugeruje się, że wady te u płodu częściej występują również u kobiet chorujących na cukrzycę typu 1 oraz typu 2.…”

Section: Choroby Spowodowane Niedoborem Kwasu Foliowegounclassified

“…Szczególną rolę w ich szlaku przemian odgrywa reduktaza MTHFR. Jej zmniejszona aktywność przyczynia się do upośledzenia metabolizmu kwasu foliowego, a gen MTHFR -typu 677CC uważany jest za czynnik ryzyka rozwoju wad cewy nerwowej [25]. W randomizowanym badaniu porównano parametry farmakokinetyczne [6S]-5-MTHF i kwasu foliowego u zdrowych kobiet w wieku rozrodczym, o różnych genotypach MTHFR (677TT n=6, 677CC n=8).…”

Section: Choroby Spowodowane Niedoborem Kwasu Foliowegounclassified

“…Wyniki świadczą o konieczności suplementacji kwasem foliowym, w której warto rozważyć aktywną biologicznie formę, dwanaście tygodni przed zajściem w ciążę. Jest to niezbędne do osiągnięcia właściwego poziomu folianów w krwinkach [25,36]. W II oraz III trymestrze ciąży suplementacja kwasem foliowym stanowi istotny element w zapobieganiu niedokrwistości z powodu niedoboru witaminy B 12 i kwasu foliowego, czyli niedokrwistości megaloblastycznej [27].…”

Section: Choroby Spowodowane Niedoborem Kwasu Foliowegounclassified

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The importance of folic acid for the health of the human body

Banyś¹,

Knopczyk²,

Bobrowska-Korczak³

2020

Farm Pol.

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The importance of folic acid for the health of the human body A well-balanced diet is undoubtedly a key factor to maintain your body's normal state of health. Folic acid is one of the elements of the diet, which is often supplied in insufficient quantities. This vitamin and its derivatives participate in the metabolism of amino acids and nucleic acids. Therefore, it is necessary for the proper functioning of the body's cells and for maintaining homeostasis, especially of the nervous, circulatory and cardiovascular systems. The biological activity of folic acid and its derivatives essentially affects the metabolism of important amino acids, such as methionine, homocysteine, serine, glycine, pyrimidine and purine synthesis and DNA methylation. The synthetic form of folic acid (most oxidized), which can be found in fortified foods, dietary supplements or pharmaceuticals, does not show biological activity. It is transformed in a series of reactions with the participation of many enzymes to form folates, which differ in the number of glutamic acid residues and the degree of oxidation. The actively biological form is reduced folate (L-5-MTHF), which is transported together with the blood to cells where it undergoes biological processes important for our health. The MTHFR gene, coding for the enzyme protein of the same namemethylene tetrahydrofolate reductase, is located on chromosome 1 at the 1p36.3 locus. This protein is responsible for the catalysis of the enzymatic reaction, which is the reduction of 5,10-methylenetetrahydrofolate to L-5-methyltetrahydrofolate, i.e. the active form of folate. This form is necessary in the process of homocysteine degradation, in the aftermath remethylation to methionine. This form is necessary in the process of homocysteine degradation, in the aftermath remethylation to methionine. However, according to available literature, mutation of the MTHFR 677C> T gene occurs in even 53% of the population. Among carriers of the TT genotype, it can cause about 70% reduction of MTHFR reductase activity. It is especially dangerous for people who do not provide adequate amounts of folic acid along with their diet and for those who need a high amount of this vitamin, e.g. due to taking medications that reduce its absorption. Many people metabolize folic acid on insufficient levels. For medical reasons, not the mutation itself is a problem, but too low the folate levels. In recent years, there is more and more discussion about the active form of folic acid and the possibility of effective supplementation with Adres do korespondencji

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Section: Choroby Spowodowane Niedoborem Kwasu Foliowegounclassified

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The importance of folic acid for the health of the human body

Banyś¹,

Knopczyk²,

Bobrowska-Korczak³

2020

Farm Pol.

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Epigenetic Modification in Methylene Tetrahydrofolate Reductase (MTHFR) Gene of Women with Pre-eclampsia

Osunkalu

Taiwo

Makwe

et al. 2020

J Obstet Gynecol India

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Background Genetic and epigenetic factors play significant roles in the aetio-pathogenesis of pre-eclampsia (PE). The effects may vary across racial and geographical boundaries. The role of epigenetic modification in pre-eclampsia was studied among African populations in Lagos, Nigeria. Aim and ObjectivesThis study aimed to determine the pattern of Methylene tetrahydrofolate reductase gene (MTHFR) CpG island methylation in pre-eclampsia, and evaluate associated covariates. Methodology This study was an observational, cross-sectional, study conducted at the Lagos University Teaching Hospital and the Lagos State Island Maternity Hospital. A total of 400 pregnant women consisting of 200 pregnant women diagnosed with pre-eclampsia (study group) and 200 pregnant normotensive and apparently healthy women (control group) were recruited for the study. Demographic and clinical histories were obtained through questionnaires. The DNA Methylation status of the CpG Island in promoter region of the MTHFR gene was assessed using bisulphite conversion and methylation specific PCR method. The biochemical parameters measured in the study were: red cell folate, vitamin B12, plasma homocysteine (Hcy) and methylene tetrahydrofolate reductase enzyme level. Results Homozygous MTHFR CpG island hypomethylation pattern was significantly associated with pre-eclampsia (χ 2 = 22.96; p = 0.000), Mean values of plasma homocysteine in PE women with homozygous hypomethylation (26.1 ± 9.1 umol/L) were significantly higher than (20.1 ± 4.2 umol/L) observed in PE subjects with homozygous hypermethylation (p = 0.008). Homozygous CpG island hypomethylated pattern of the MTHFR promoter region, was associated with the lowest median MTHFR enzyme level (72.8 ± 39.8 pmol/L) compared with heterozygous methylated pattern (91.3 ± 60.9 pmol/L; p = 0.047) and homozygous methylated pattern (82.3 ± 31.0 pmol/L; 0.047). Red cell folate and Vitamin B12 levels were not significantly associated with CpG island methylation status. Conclusion Epigenetic modification plays significant role in the pathogenesis of pre-eclampsia.

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