Neonatal hyperpigmentation: diagnosis of familial glucocorticoid deficiency with a novel mutation in the melanocortin-2 receptor gene

Pediatr Dermatol. 2014 Jan-Feb;31(1):e13-7. doi: 10.1111/pde.12247. Epub 2013 Nov 14.

Abstract

Familial glucocorticoid deficiency (FGD), a rare autosomal recessive disorder of insensitivity to adrenocorticotropic hormone (ACTH), is characterized by isolated glucocorticoid deficiency and preserved mineralocorticoid production. The clinical features include generalized hyperpigmentation, hypoglycemia, failure to thrive, and recurrent infections. Here we describe the case of an infant who exhibited generalized hyperpigmentation and hypoglycemia. A high morning blood ACTH level and low blood cortisol level confirmed the diagnosis of FGD. The patient was found to be homozygous for a novel mutation in the melanocortin-2 receptor gene (635insC, I154H). Early initiation of corticosteroid treatment led to normalization of morning blood ACTH levels and the patient thrived, with subsequent fading of the hyperpigmentation.

Publication types

  • Case Reports

MeSH terms

  • Adrenal Insufficiency / diagnosis
  • Adrenal Insufficiency / genetics*
  • Family
  • Humans
  • Hyperpigmentation / diagnosis
  • Hyperpigmentation / genetics*
  • Infant
  • Male
  • Pedigree
  • Point Mutation
  • Receptor, Melanocortin, Type 2 / genetics*
  • Steroid Metabolism, Inborn Errors / diagnosis
  • Steroid Metabolism, Inborn Errors / genetics*

Substances

  • Receptor, Melanocortin, Type 2

Supplementary concepts

  • Familial Glucocorticoid Deficiency 1