American Journal of Obstetrics & Gynecology
Volume 201, Issue 6, Supplement , Page S296, December 2009

829: Gonadotropin-releasing hormone and luteinizing hormone receptor polymorphisms and risk of hyperemesis gravidarum

  • Matthew J. Blitz

      Affiliations

    • University of Southern California/Keck School of Medicine, Maternal-Fetal Medicine, Los Angeles, California
  • ,
  • Melissa L. Wilson

      Affiliations

    • University of Southern California/ Keck School of Medicine, OB/GYN & Preventive Medicine, Los Angeles, California
  • ,
  • Sue A. Ingles

      Affiliations

    • University of Southern California/ Keck School of Medicine, OB/GYN & Preventive Medicine, Los Angeles, California
  • ,
  • Daniel H. Desmond

      Affiliations

    • University of Southern California/Keck School of Medicine, Maternal-Fetal Medicine, Los Angeles, California
  • ,
  • Kimber W. Macgibbon

      Affiliations

    • Hyperemesis Education and Research Foundation, Leesburg, Virginia
  • ,
  • Roberto Romero

      Affiliations

    • Wayne State University, Detroit, Michigan
  • ,
  • Thomas Murphy Goodwin

      Affiliations

    • University of Southern California/Keck School of Medicine, Maternal-Fetal Medicine, Los Angeles, California
  • ,
  • Patrick Mullin

      Affiliations

    • University of Southern California/Keck School of Medicine, Maternal-Fetal Medicine, Los Angeles, California
  • ,
  • Marlena Fejzo

      Affiliations

    • University of Southern California/Keck School of Medicine, Maternal-Fetal Medicine, Los Angeles, California

Article Outline

 

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Objective 

Hyperemesis gravidarum (HG), or severe nausea and vomiting of pregnancy, is the most common cause of hospitalization in the first half of pregnancy and is second only to preterm labor for pregnancy overall. HG can be associated with serious maternal morbidity and even maternal and fetal death. There is a strong genetic component to HG and its etiology may be related to defects in pregnancy-related hormones or their receptors. HG has been associated with elevated levels of human chorionic gonadotropin (hCG), whose alpha subunit is identical to that in luteinizing hormone (LH). The release of LH from the pituitary gland is controlled by gonadotropin-releasing hormone (GnRH) from the hypothalamus. No studies to date have examined the possibility of GnRH or LH receptor (LHR) polymorphisms increasing susceptibility to HG.

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Study Design 

Our study population consisted of cases recruited from the Hyperemesis Education and Research Foundation (www.helpher.org) and controls who were friends of the cases and who have had at least two previous unaffected pregnancies. Participants were asked to complete an online survey and submit a saliva sample for DNA analysis. DNA was extracted per ethanol-precipitation protocol provided by the manufacturer (Oragene) and genotyping of single nucleotide polymorphisms was performed by TaqMan assay.

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Results 

See Table 1. The studied GnRH and LHR genotypes do not appear to be associated with HG.

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Conclusion 

Further evaluation of the GnRH/LH axis for potential HG susceptibility is warranted based on the structural similarities between hCG and LH. Future studies should include a larger number of study participants and the study of other GnRH and LHR variants.

PII: S0002-9378(09)01969-3

doi:10.1016/j.ajog.2009.10.846

American Journal of Obstetrics & Gynecology
Volume 201, Issue 6, Supplement , Page S296, December 2009