Evidence map›Paper›PMID 27529241›Full record

ReviewInternational journal of molecular sciences2016

The Risk of Congenital Heart Anomalies Following Prenatal Exposure to Serotonin Reuptake Inhibitors-Is Pharmacogenetics the Key?

Aizati N A Daud, Jorieke E H Bergman, Wilhelmina S Kerstjens-Frederikse, Henk Groen, Bob Wilffert

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Sertraline-induced 5-HT dysregulation in mouse cardiomyocytes and the impact on calcium handling.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  3. Review
  4. Article
  5. Review
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Aizati N A DaudDepartment of Pharmacy, Unit of PharmacoTherapy, -Epidemiology and -Economics, University of Groningen, 9713AV Groningen, The Netherlands. n.a.a.daud@rug.nl.
Jorieke E H BergmanDepartment of Genetics, University Medical Center Groningen, University of Groningen, 9713AV Groningen, The Netherlands. j.e.h.van.kammen@umcg.nl.
Wilhelmina S Kerstjens-FrederikseDepartment of Genetics, University Medical Center Groningen, University of Groningen, 9713AV Groningen, The Netherlands. w.s.kerstjens@umcg.nl.
Henk GroenDepartment of Epidemiology, University Medical Centre Groningen, University of Groningen, 9713AV Groningen, The Netherlands. h.groen01@umcg.nl.
Bob WilffertDepartment of Pharmacy, Unit of PharmacoTherapy, -Epidemiology and -Economics, University of Groningen, 9713AV Groningen, The Netherlands. b.wilffert@rug.nl.
University Medical Center Groningen · NLUniversiti Sains Malaysia · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serotonin reuptake inhibitors (SRIs) are often prescribed during pregnancy. Previous studies that found an increased risk of congenital anomalies, particularly congenital heart anomalies (CHA), with SRI use during pregnancy have created concern among pregnant women and healthcare professionals about the safety of these drugs. However, subsequent studies have reported conflicting results on the association between CHA and SRI use during pregnancy. These discrepancies in the risk estimates can potentially be explained by genetic differences among exposed individuals. In this review, we explore the potential pharmacogenetic predictors involved in the pharmacokinetics and mechanism of action of SRIs, and their relation to the risk of CHA. In general, the risk is dependent on the maternal concentration of SRIs and the foetal serotonin level/effect, which can be modulated by the alteration in the expression and/or function of the metabolic enzymes, transporter proteins and serotonin receptors involved in the serotonin signalling of the foetal heart development. Pharmacogenetics might be the key to understanding why some children exposed to SRIs develop a congenital heart anomaly and others do not.

Indexed as

PharmacogeneticsFemaleHeart Defects, CongenitalHumansPregnancyPregnancy Trimester, FirstPrenatal Exposure Delayed EffectsRisk FactorsSelective Serotonin Reuptake InhibitorsSelective Serotonin Reuptake Inhibitorsantidepressive agentscongenital heart defectsdrug-induced birth defectsheart abnormalitiesserotonin reuptake inhibitorsteratogenesis

Identifiers

PMID27529241
PMCPMC5000730
OpenAlexW2514272885

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.