Expanding the Phenotype of TRNT1-Related Immunodeficiency to Include Childhood Cataract and Inner Retinal Dysfunction

JAMA Ophthalmol. 2016 Sep 1;134(9):1049-53. doi: 10.1001/jamaophthalmol.2015.5833.

Abstract

Importance: A multiorgan syndromic disorder characterized by sideroblastic anemia, immunodeficiency, periodic fever, and developmental delay with an uncharacterized retinal dystrophy is caused by TRNT1. This report of a family with a homozygous mutation in TRNT1 expands the ocular phenotype to include cataract and inner retinal dysfunction and details a mild systemic phenotype.

Observations: A consanguineous family with 3 affected children was investigated. Key clinical features comprised hypogammaglobulinemia, short stature with microcephaly, cataract, and inner retinal dysfunction without sideroblastic anemia or developmental delay. Two siblings had poor balance and 1 sibling had sensorineural hearing loss. The oldest sibling had primary ovarian failure diagnosed at age 14.5 years. Exome sequencing identified a homozygous missense variant in TRNT1, c.295C>T (p.Arg99Trp) in all 3 patients. The sibling with hearing loss also harbored a homozygous mutation in GJB2, c.71G>A (p.Trp24*), which is an established cause of sensorineural hearing loss.

Conclusions and relevance: This family expands the ocular and systemic phenotypes associated with mutations in TRNT1, demonstrating phenotypic variability and highlighting the need for ophthalmic review of these patients.

Publication types

  • Case Reports

MeSH terms

  • Adolescent
  • Cataract / complications*
  • Cataract / genetics
  • Cataract / metabolism
  • Child
  • Child, Preschool
  • Exome
  • Female
  • Humans
  • Immunologic Deficiency Syndromes / complications*
  • Immunologic Deficiency Syndromes / genetics
  • Immunologic Deficiency Syndromes / metabolism
  • Infant
  • Male
  • Mutation*
  • Nucleotidyltransferases / genetics*
  • Nucleotidyltransferases / metabolism
  • Pedigree
  • Phenotype
  • Retinal Dystrophies / complications*
  • Retinal Dystrophies / genetics
  • Retinal Dystrophies / metabolism
  • Sequence Analysis, DNA

Substances

  • Nucleotidyltransferases
  • TRNT1 protein, human