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Increase of Prostaglandin E2 in Reversal of Ductal Constriction After Dietary Restriction of Polyphenols

Increase of Prostaglandin E2 in Reversal of Ductal Constriction After Dietary Restriction of Polyphenols

Status
Completed
Phases
NA
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT03111602
Enrollment
75
Registered
2017-04-13
Start date
2011-05-31
Completion date
2017-02-28
Last updated
2017-04-13

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Pregnancy Complications

Keywords

polyphenols, pregnant, fetal ductal constriction, prostaglandin E2

Brief summary

INCREASE OF PROSTAGLANDIN E2 IN REVERSAL OF DUCTAL CONSTRICTION AFTER DIETARY RESTRICTION OF POLYPHENOLS. Clinical trial with a healthy group as comparator. The interventional group was made up of third-trimester mothers whose single fetuses had ductal constriction, excluding those exposed to NSAID, and the control group only by third-trimester normal fetuses. The interventional group was submitted to dietary orientation to restrict polyphenol-rich foods and both groups answered a food frequency questionnaire after fetal Doppler-echocardiographic examination and blood draw for PGE2 levels analysis. After two weeks, the women were again submitted to fetal echocardiogram, dietary assessment and blood draw.

Detailed description

INCREASE OF PROSTAGLANDIN E2 IN REVERSAL OF DUCTAL CONSTRICTION AFTER DIETARY RESTRICTION OF POLYPHENOLS. Fetal ductal constriction is a clinical situation with high morbidity and potential mortality. Patency the fetal ductus arteriosus (DA) depends on circulating prostaglandin (PG), which is produced by the cyclooxygenase (COX) pathway during inflammatory response(1) and from the third trimester of pregnancy on, is physiologically released. COX-inhibiting substances, such as nonsteroidal anti-inflammatory drugs (NSAIDs), can interfere with PG metabolism and induce constriction of the DA. To treat or prevent DA constriction, it is therefore important to reduce fetal exposure to drugs that may interfere with prostaglandin biosynthesis, such as natural anti-inflammatory drugs and polyphenol-rich foods. Polyphenols, the most abundant antioxidants present in the diet, are widely distributed in vegetable foods. One of the possible mechanisms to explain their activity is inhibition of synthesis and release of inflammatory mediators. However, clinical studies investigating the effect of polyphenols on inflammatory responses are inconclusive and, in most cases, only evaluate clinical outcomes. The role of polyphenols on the inflammatory response, and associated modifications of the plasma concentration of PGE2 in pregnant women, has not yet been studied. Despite the potential benefits of a diet rich in polyphenols, a high consumption of these substances in the third trimester of pregnancy may reduce plasma levels of PGE2 and result in DA constriction,so that a restriction in their ingestion during this period is already recommended.This functional problem has high prevalence and may result in severe fetal and neonatal complications. These considerations raised the hypothesis that reversal of fetal ductal constriction after maternal restriction of polyphenol-rich foods is accompanied by increased in prostaglandin E2 levels. Demonstration of this effect would represent an advancement in knowledge and might result in changes in dietary guidance during pregnancy and prevention of perinatal complications, with potential impact in terms of public health. The aim of this study was to test the hypothesis that reversal of fetal ductal constriction in the third trimester of pregnancy, after maternal restriction of polyphenol-rich foods, is accompanied by increased plasma levels of prostaglandin E2.

Interventions

OTHERrestrict polyphenol-rich foods

dietary orientation to restrict polyphenol-rich foods

Sponsors

Instituto de Cardiologia do Rio Grande do Sul
Lead SponsorOTHER

Study design

Allocation
NON_RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
DOUBLE (Caregiver, Investigator)

Masking description

Researchers were blinded to the allocation data of pregnant women in the groups

Intervention model description

Clinical trial with a healthy group as comparator.

Eligibility

Sex/Gender
FEMALE
Age
18 Years to 45 Years
Healthy volunteers
Yes

Inclusion criteria

* Pregnancy with diagnosis of fetal ductal constriction * Single fetus * gestational age from 28 weeks

Exclusion criteria

* cardiac malformations * restricted intrauterine growth * increased nuchal translucency * present or suspected chromosomal disorders * signs of any type of hydrops fetalis * pregnancy * hypertension * diabetes mellitus * structural or functional cardiac disorders * current use of nonsteroidal anti-inflammatory drugs, steroids, antidepressants, illicit drugs, alcohol or smoking * multiple pregnancy * having received previous nutritional guidance in relation to restricted intake of polyphenol-rich foods

Design outcomes

Primary

MeasureTime frameDescription
Plasma levels of prostaglandin E2 (PGE2)baseline and two weeksPGE2 was quantified by capture ELISA. The measurements were obtained through 4-parameter linear regression (Excel, Microsoft), and data were expressed in picograms of protein per milliliter (pg/mL).

Secondary

MeasureTime frameDescription
Consumption of foods rich in Total Polyphenols (TP)baseline and two weeksTP on the maternal diet were quantified using a Food Frequency Questionnaire (FFQ) validated for pregnant women. TP results after analysis of the dietary questionnaires were described in milligrams (mg)

Other

MeasureTime frameDescription
Diagnostic parameters of fetal ductus arteriosus constrictionbaseline and two weeksThe peak systolic, peak diastolic and end diastolic velocities (m/s) were determined. The pulsatility index of the ductus arteriosus was calculated automatically by the echocardiography system after manual tracing of the spectral curve, using the formula: (peak systolic velocity - diastolic peak velocity)/mean velocity.

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026