Prioritizing genetic testing in patients with Kallmann syndrome using clinical phenotypes

J Clin Endocrinol Metab. 2013 May;98(5):E943-53. doi: 10.1210/jc.2012-4116. Epub 2013 Mar 26.

Abstract

Context: The complexity of genetic testing in Kallmann syndrome (KS) is growing and costly. Thus, it is important to leverage the clinical evaluations of KS patients to prioritize genetic screening.

Objective: The objective of the study was to determine which reproductive and nonreproductive phenotypes of KS subjects have implications for specific gene mutations.

Subjects: Two hundred nineteen KS patients were studied: 151 with identified rare sequence variants (RSVs) in 8 genes known to cause KS (KAL1, NELF, CHD7, HS6ST1, FGF8/FGFR1, or PROK2/PROKR2) and 68 KS subjects who remain RSV negative for all 8 genes.

Main outcome measures: Reproductive and nonreproductive phenotypes within each genetic group were measured.

Results: Male KS subjects with KAL1 RSVs displayed the most severe reproductive phenotype with testicular volumes (TVs) at presentation of 1.5 ± 0.1 mL vs 3.7 ± 0.3 mL, P < .05 vs all non-KAL1 probands. In both sexes, synkinesia was enriched but not unique to patients with KAL1 RSVs compared with KAL1-negative probands (43% vs 12%; P < .05). Similarly, dental agenesis and digital bone abnormalities were enriched in patients with RSVs in the FGF8/FGFR1 signaling pathway compared with all other gene groups combined (39% vs 4% and 23% vs 0%; P < .05, respectively). Hearing loss marked the probands with CHD7 RSVs (40% vs 13% in non-CHD7 probands; P < .05). Renal agenesis and cleft lip/palate did not emerge as statistically significant phenotypic predictors.

Conclusions: Certain clinical features in men and women are highly associated with genetic causes of KS. Synkinesia (KAL1), dental agenesis (FGF8/FGFR1), digital bony abnormalities (FGF8/FGFR1), and hearing loss (CHD7) can be useful for prioritizing genetic screening.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Anodontia / etiology
  • Cohort Studies
  • DNA Helicases / genetics*
  • DNA Helicases / metabolism
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Extracellular Matrix Proteins / genetics*
  • Extracellular Matrix Proteins / metabolism
  • Female
  • Fibroblast Growth Factor 8 / genetics*
  • Fibroblast Growth Factor 8 / metabolism
  • Finger Phalanges / abnormalities
  • Genetic Association Studies
  • Genetic Testing / economics
  • Health Care Costs
  • Hearing Loss / etiology
  • Humans
  • Kallmann Syndrome / economics
  • Kallmann Syndrome / genetics*
  • Kallmann Syndrome / metabolism
  • Kallmann Syndrome / physiopathology
  • Male
  • Massachusetts
  • Mutation*
  • Nerve Tissue Proteins / genetics*
  • Nerve Tissue Proteins / metabolism
  • Polymorphism, Genetic*
  • Receptor, Fibroblast Growth Factor, Type 1 / genetics*
  • Receptor, Fibroblast Growth Factor, Type 1 / metabolism
  • Severity of Illness Index
  • Signal Transduction
  • Synkinesis / etiology

Substances

  • ANOS1 protein, human
  • DNA-Binding Proteins
  • Extracellular Matrix Proteins
  • FGF8 protein, human
  • Nerve Tissue Proteins
  • Fibroblast Growth Factor 8
  • FGFR1 protein, human
  • Receptor, Fibroblast Growth Factor, Type 1
  • DNA Helicases
  • CHD7 protein, human