Dietary supplementation with <scp>l</scp>‐arginine or placebo in women with pre‐eclampsia

Staff, Anne Cathrine; Berge, Lillian Nordbø; Haugen, Guttorm; Lorentzen, Bjørg; Mikkelsen, Bente; Henriksen, Tore

doi:10.1111/j.1600-0412.2004.00321.x

Cited by 38 publications

(37 citation statements)

References 21 publications

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“…It is also suggested that it may play a significant role in fetal growth, by stimulating insulin secretion, and as a precursor for both polyamine synthesis and NO production [10]. L-arginine treatment accelerates fetal weight gain and improves biophysical profile [11].…”

Section: Discussionmentioning

confidence: 99%

Role of l-Arginine in Oligohydramnios

Soni

Seeru

Patel

et al. 2016

J Obstet Gynecol India

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Background Oligohydramnios is a known obstetric complication which is associated with operative interferences and perinatal morbidity and mortality. L-arginine is a precursor of nitric oxide and may play a role in local vasodilatation. Administration of L-arginine has been suggested to improve amniotic fluid index (AFI) in oligohydramnios. Aims and Objectives To study the effect of L-arginine in optimizing fetal outcome in cases of oligohydramnios. Materials and Methods A retrospective study was conducted at Dr L H Hiranandani hospital consisting of 100 antenatal patients diagnosed with oligohydramnios [AFI \ 8 cm] remote from term. Patients were evaluated for all antenatal risk factors and were started on L-arginine

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Section: Discussionmentioning

confidence: 99%

Role of l-Arginine in Oligohydramnios

Soni

Seeru

Patel

et al. 2016

J Obstet Gynecol India

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“…Despite this, L-arginine supplementation to prevent preeclampsia has been tried in several studies. Oral L-arginine supplementation was investigated by our group; the intervention did not alter blood pressure in preeclampsia (32). A recent review found that evidence is still insufficient to draw reliable conclusions as to whether L-arginine can prevent preeclampsia or its complications (33).…”

Section: Discussionmentioning

confidence: 99%

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

et al. 2009

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Preeclampsia is a leading cause of intrauterine growth restriction and preterm birth. Endothelial dysfunction is the common final pathway leading to clinical signs of preeclampsia including hypertension and proteinuria. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from L-arginine. The purpose of this study was to investigate maternal and fetal concentrations of ADMA, L-arginine, and symmetric dimethylarginine (SDMA). Women with preeclampsia (n ϭ 47) and controls (n ϭ 51) who gave birth by cesarean section were included in the study. We analyzed the maternal plasma and umbilical vein and artery plasma. We found that not only maternal concentrations of ADMA and SDMA but also L-arginine were significantly higher in women with preeclampsia than in controls. In fetal samples, only SDMA concentrations were higher in the preeclampsia group than in controls. The median ADMA concentration was three times higher in the fetal circulation than in the maternal circulation, but there was no difference between the preeclampsia group and the control group, and the veno-arterious gradient indicated that the placenta was the source of ADMA. (Pediatr Res 66: 411-415, 2009) P reeclampsia is a common pregnancy complication associated with increased risk of preterm birth and fetal growth restriction (1). The exact etiology of preeclampsia is not known, and hence no definitive preventative measures or treatments are available.Endothelial dysfunction is the common final pathway leading to the clinical signs of preeclampsia including hypertension and proteinuria. It is not known to what extent endothelial dysfunction also affects the infant. Increased concentrations of biomarkers for preeclampsia in the maternal circulation are usually not reflected in the infant. Previously, our group has shown that newborns from preeclamptic pregnancies did not differ from those born after uncomplicated pregnancies with respect to circulating biomarkers of inflammation (CRP and calprotectin) (2), and oxidative stress (3), but newborns from preeclamptic pregnancies had elevated concentrations of homocysteine (4).In women with previous preeclampsia, there is an increased risk for cardiovascular disease later in life (5) and an increased risk of hypertension has also been found for their offspring (6,7).It is not clear whether the increased risk in the offspring is caused by the intrauterine environment, shared genes, or impaired intrauterine growth. In epidemiologic and animal studies, low birth weight by itself is associated with an increased risk of cardiovascular disease and metabolic syndrome (8).NO is essential for vascular tone and endothelial function, and elevated circulating concentrations of asymmetric dimethylarginine (ADMA) are associated with reduced vasodilation and endothelial dysfunction (9). ADMA is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from L-arginine. The ratio...

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“…Staff et al [91] found no significant effect of short-term oral supplementation with L -arginine on blood pressure; however, Germain et al [92] studied 17 women with bilaterally elevated uterine vascular resistance and found that dietary supplementation with 3 g/day of L -arginine starting in the 10th gestational week resulted in significantly reduced blood pressure, improved endothelium-dependent vasodilation, and no abnormal pregnancy outcome. This finding is in accordance with experimental data showing that L -arginine reduced blood pressure in pregnant rats with reduced uterine perfusion [93] .…”

Section: How Can Adma Be Quantified?mentioning

confidence: 99%

The Role of Nitric Oxide Synthase Inhibition by Asymmetric Dimethylarginine in the Pathophysiology of Preeclampsia

Böger

Diemert

Schwedhelm

et al. 2009

Gynecol Obstet Invest

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Preeclampsia is a major cause of maternal and neonatal morbidity and mortality worldwide. Despite recent advances in screening, sensitive and specific biomarkers that help to identify pregnant women at risk of developing preeclampsia are lacking. One of the major mediators from healthy endothelium is nitric oxide; its production is regulated by asymmetric dimethylarginine (ADMA). ADMA has been shown to be elevated in cardiovascular and metabolic diseases; elevated ADMA levels are a prognostic marker for major cardiovascular events and mortality in patients with established cardiovascular disease and in the general population. Several studies have reported elevated ADMA levels in preeclampsia; some studies also suggested that ADMA is elevated in early stages of pregnancy in women who later develop preeclampsia. Moreover, ADMA has been associated with uterine artery flow disturbances. Its plasma concentration is regulated by dimethylarginine dimethylaminohydrolase (DDAH). Single nucleotide polymorphisms in the gene encoding for DDAH have been associated with the incidence of preeclampsia. Recently, diagnostic assays for ADMA, e.g. by ELISA, have become available, which render ADMA a possible biomarker to identify pregnant women at risk of developing preeclampsia.

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Dietary supplementation with l‐arginine or placebo in women with pre‐eclampsia

Cited by 38 publications

References 21 publications

Role of l-Arginine in Oligohydramnios

Role of l-Arginine in Oligohydramnios

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

The Role of Nitric Oxide Synthase Inhibition by Asymmetric Dimethylarginine in the Pathophysiology of Preeclampsia

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