Inherited mutation of the luteinizing hormone/choriogonadotropin receptor (LHCGR) in empty follicle syndrome

Fertil Steril. 2011 Aug;96(2):e125-30. doi: 10.1016/j.fertnstert.2011.05.057. Epub 2011 Jun 17.

Abstract

Objective: To test by genomic analysis whether empty follicle syndrome (EFS) in a family with two affected sisters has a genetic basis.

Design: Whole-exome sequencing in the context of clinical genetics.

Setting: University hospital.

Patient(s): Two women (36 and 32 years old at the time of the study) with EFS.

Intervention(s): Genetic counseling based on autosomal recessive inheritance.

Main outcome measure(s): Discovery of a mutation in the LH/choriogonadotropin receptor (LHCGR) as the cause of EFS.

Result(s): A novel missense mutation in LHCGR, p.N400S, was homozygous in sisters with EFS and/or infertility, but not in their unaffected siblings or parents. The mutation was not present in 500 ancestry-matched control subjects. Asparagine at residue 400 is highly conserved and its substitution by serine predicted to alter critical interactions that stabilize LHCGR.

Conclusion(s): We describe a genetic basis for EFS and provide strong evidence for the existence of genuine EFS in some patients. A mutation impairing the function of LHCGR explains the lack of response of these patients to repeated administration of β-hCG.

Publication types

  • Case Reports
  • Research Support, American Recovery and Reinvestment Act
  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Chorionic Gonadotropin / metabolism
  • DNA Mutational Analysis
  • Female
  • Fertility / genetics*
  • Genetic Predisposition to Disease
  • Heredity
  • Homozygote
  • Humans
  • Infertility, Female / genetics*
  • Infertility, Female / physiopathology
  • Models, Molecular
  • Mutation, Missense*
  • Ovarian Diseases / complications
  • Ovarian Diseases / genetics*
  • Ovarian Diseases / physiopathology
  • Pedigree
  • Phenotype
  • Protein Conformation
  • Receptors, LH / chemistry
  • Receptors, LH / genetics*
  • Receptors, LH / metabolism
  • Structure-Activity Relationship
  • Syndrome

Substances

  • Chorionic Gonadotropin
  • Receptors, LH