Vitamin C and E supplementation in women at high risk for preeclampsia: A double-blind, placebo-controlled trial

Beazley, Dorothy; Ahokas, Robert A.; Livingston, Jeffrey; Griggs, Mary; Sibai, Baha M.

doi:10.1016/j.ajog.2004.09.005

Cited by 123 publications

(104 citation statements)

References 3 publications

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“…In some pregnant women, perinatal complications were diminished when plasma ascorbate concentrations were increased from approximately 30 to 45 μM, although a vitamin E supplement was coadministered and study subject numbers were relatively low (24). Vitamin E and vitamin C supplements had no effect on perinatal complications in 2 additional studies (26,27), but the relationship between ascorbate intake and plasma concentrations was not determined. Ascorbate concentrations at study entry were estimated to be above 50 μM (28), so that additional supplementation would have minimal effects on plasma concentrations (4,11).…”

Section: Discussionmentioning

confidence: 99%

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Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice

et al. 2010

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Levels of the necessary nutrient vitamin C (ascorbate) are tightly regulated by intestinal absorption, tissue accumulation, and renal reabsorption and excretion. Ascorbate levels are controlled in part by regulation of transport through at least 2 sodium-dependent transporters: Slc23a1 and Slc23a2 (also known as Svct1 and Svct2, respectively). Previous work indicates that Slc23a2 is essential for viability in mice, but the roles of Slc23a1 for viability and in adult physiology have not been determined. To investigate the contributions of Slc23a1 to plasma and tissue ascorbate concentrations in vivo, we generated Slc23a1 -/-mice. Compared with wild-type mice, Slc23a1 -/-mice increased ascorbate fractional excretion up to 18-fold. Hepatic portal ascorbate accumulation was nearly abolished, whereas intestinal absorption was marginally affected. Both heterozygous and knockout pups born to Slc23a1 -/-dams exhibited approximately 45% perinatal mortality, and this was associated with lower plasma ascorbate concentrations in dams and pups. Perinatal mortality of Slc23a1 -/-pups born to Slc23a1 -/-dams was prevented by ascorbate supplementation during pregnancy. Taken together, these data indicate that ascorbate provided by the dam influenced perinatal survival. Although Slc23a1 -/-mice lost as much as 70% of their ascorbate body stores in urine daily, we observed an unanticipated compensatory increase in ascorbate synthesis. These findings indicate a key role for Slc23a1 in renal ascorbate absorption and perinatal survival and reveal regulation of vitamin C biosynthesis in mice.

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Section: Discussionmentioning

confidence: 99%

“…Although controversial, some human studies suggest an association between low intake of vitamins C and E and increased perinatal morbidity and/or mortality (23)(24)(25)(26)(27)(28). To explore this, controls were performed to assess mortality in newborn pups.…”

Section: Figurementioning

confidence: 99%

Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice

et al. 2010

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“…Also, another small study did not demonstrate benefit with 50 treated and control subjects. 85 Larger international multicenter studies testing the efficacy of therapy and definitively establishing proof of safety in pregnancy are now in progress.…”

Section: The Linkage Of Stages 1 Andmentioning

confidence: 99%

Preeclampsia

2005

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Abstract-Preeclampsia is a pregnancy complication with serious consequences for mother and infant. The disorder is diagnosed by gestational hypertension and proteinuria but is far more than pregnancy induced hypertension. Preeclampsia is proposed to occur in 2 stages. Key Words: preeclampsia Ⅲ hypertension, pregnancy Ⅲ oxidative stress Ⅲ endothelium P reeclampsia is a pregnancy complication recognized by new-onset gestational hypertension and proteinuria (see definitions below). The disorder affects both mothers and their infants. Once the disease is evident clinically, it can be cured only by delivery. In developed countries, surveillance for preeclampsia through prenatal care allows for early identification and intervention via delivery. This management has changed little in the last 100 years, and it is very effective at reducing maternal mortality. However, maternal morbidity remains great with preeclampsia, which continues to be one of the leading causes for the admission of pregnant women to intensive care units in the developed world. 1 Furthermore, fetal mortality and morbidity is considerable, related to the effects of the disease on the fetus as well as prematurity. The indicated delivery of women to prevent the progression of preeclampsia is responsible for 15% of all preterm births. 2 In developing countries, where inadequate prenatal care limits preeclampsia surveillance, maternal mortality is common, accounting for 50 000 deaths yearly. 3 The hypertensive disorders of pregnancy include hypertension that antedates pregnancy, chronic hypertension, and gestational hypertension occurring uniquely during pregnancy. When the gestational hypertension is accompanied by new-onset proteinuria, the disorder is termed preeclampsia, and when not associated with proteinuria, transient hypertension of pregnancy. If the woman with chronic hypertension also manifests evidence of preeclampsia, this is classified chronic hypertension with superimposed preeclampsia. Eclampsia is the occurrence of seizures in women with preeclampsia. 4 These criteria have been extraordinarily useful to aid in recognizing pregnant women at risk. Greatest risk for mother and baby is present with preeclampsia, and the risk for chronic hypertensive pregnancy is primarily with superimposed preeclampsia. However, the attention to hypertension has, for many years, limited research attention to primarily mechanisms of hypertension. This has not been helpful. In the last 2 decades, appreciation that preeclampsia is a multisystemic syndrome characterized by vasoconstriction, metabolic changes, endothelial dysfunction, activation of the coagulation cascade, and increased inflammatory response, to mention only some of the organ systems involved, has redirected research. 5 As a result, progress in understanding the disorder has accelerated greatly, with attendant optimism for potentially effective treatments. 5 In this article, we consider this recent progress and its clinical implications.

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“…Vitamins C and E. After contradictory pilot trial findings [287][288][289], vitamins C and E do not decrease preeclampsia risk; rather, they are more frequently associated with birthweight <2.5 kg and adverse perinatal outcomes [290][291][292][293]. There is insufficient evidence to make a recommendation about the usefulness of the following: new severe dietary salt restriction for women with any HDP, ongoing salt restriction among women with pre-existing hypertension, heart-healthy diet, and calorie restriction for obese women (all III-L; all Very low/Weak).…”

Section: Preventing Preeclampsia and Its Complications In Women At Inmentioning

confidence: 99%

RETIRED: Diagnosis, Evaluation, and Management of the Hypertensive Disorders of Pregnancy

Magee

Pels

Helewa

et al. 2008

Journal of Obstetrics and Gynaecology Canada

421

218

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Vitamin C and E supplementation in women at high risk for preeclampsia: A double-blind, placebo-controlled trial

Cited by 123 publications

References 3 publications

Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice

Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice

Preeclampsia

RETIRED: Diagnosis, Evaluation, and Management of the Hypertensive Disorders of Pregnancy

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