Evidence map›Paper›PMID 19760168›Full record

ArticleJournal of assisted reproduction and genetics2009

Is gestation in Prader-Willi syndrome affected by the genetic subtype?

Merlin G Butler, Jennifer Sturich, Susan E Myers, June-Anne Gold, Virginia Kimonis, Daniel J Driscoll

Open access · bronzeAbstract read
In one paragraph

Article in Journal of assisted reproduction and genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 52 citations in OpenAlex.

  1. Maternal-fetal conflict and the timing of birth.Evolution, medicine, and public health · 2025
    Review
  2. Long-term effect of growth hormone on sleep-disordered breathing in Malaysian children with Prader-Willi syndrome: a retrospective study.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Birth seasonality studies in a large Prader-Willi syndrome cohort.American journal of medical genetics. Part A · 2019
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Genetics of Prader-Willi syndrome and Prader-Will-Like syndrome.Annals of pediatric endocrinology & metabolism · 2016
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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

6 authors at 5 institutions in 1 country.

Merlin G ButlerDepartments of Psychiatry, Behavioral Sciences and Pediatrics, Kansas University Medical Center, 3901 Rainbow Blvd., MS4015, Kansas City, KS, 66160, USA. mbutler4@kumc.edu
Jennifer Sturich
Susan E Myers
June-Anne Gold
Virginia Kimonis
Daniel J Driscoll
University of California, Irvine · USSaint Louis University · USUniversity Medical Center · USUniversity of Florida · USUniversity of Kansas · US

Funding

RARE DISEASE CRC FOR NEW THERAPIES AND NEW DIAGNOSTICSU54RR019478 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI BEAUDET, ARTHUR L. · 2003 to 2008
$7.3M
NCRR NIH HHS 1U54RR019478NCRR NIH HHS U54 RR019478
6 · The paper itself

Abstract

backgroundPrader-Willi syndrome (PWS) is a complex genetic disorder with errors in genomic imprinting, generally due to a paternal deletion of chromosome 15q11-q13 region. Maternal disomy 15 (both 15s from the mother) is the second most common form of PWS resulting from a trisomic zygote followed by trisomy rescue in early pregnancy and loss of the paternal chromosome 15. However, trisomy 15 or mosaicism for trisomy 15 may be present in the placenta possibly leading to placental abnormalities affecting gestational age and delivery. METHODS AND SUBJECTS: We examined growth and gestational data from 167 PWS infants (93 males and 74 females; 105 infants with 15q11-q13 deletion and 62 infants with maternal disomy 15) to determine if there are differences in gestation between the two genetic subtypes.

resultsNo significant differences in growth data (birth weight, length, head circumference) or average gestational ages were found between the two genetic subgroups. However, post-term deliveries (> 42 weeks gestation) were more common in the maternal disomy group (i.e., 12 of 62 infants) compared with the deletion group (i.e., 7 of 105 infants) (chi-square test = 6.22; p < 0.02). The distribution of gestational ages in the 15q11-q13 deletion group was more bell-shaped or normal while the distribution in the maternal disomy group suggested a bimodal pattern.

conclusionsMaternal disomy 15 in PWS may contribute to disturbances in gestational age and delivery by impacting on placental structure or function secondary to the abnormal chromosomal number in the placental cells or in mechanisms leading to the maternal disomy status in PWS infants.

Indexed as

Gestational AgeBirth WeightBody HeightChromosomes, Human, Pair 15FemaleGene DeletionGenomic ImprintingGenotypeHumansInfantMalePlacentaPrader-Willi SyndromePregnancyUniparental Disomy

Identifiers

PMID19760168
PMCPMC2767487
OpenAlexW2081065383

What OpenQuestion holds

Textmetadata
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.