Hypercortisolism due to a Pituitary Adenoma Associated with Beckwith-Wiedemann Syndrome

Horm Res Paediatr. 2016;86(3):206-211. doi: 10.1159/000446435. Epub 2016 Jun 3.

Abstract

Background: Beckwith-Wiedemann syndrome (BWS) is an overgrowth syndrome with an increased risk of cancer. Most BWS patients show a molecular defect in the 11p15 region that contains imprinted genes. BWS has been associated with malignant neoplasms during infancy. Descriptions of benign tumors, especially in adult patients, are rarer.

Methods/results: We report the case of a BWS patient with pituitary adenoma caused by loss of methylation (LOM) at ICR2 (locus CDKN1C/KCNQ1OT1). The patient was referred to an endocrinology unit for suspicion of Cushing's disease due to a history of macroglossia and hemihyperplasia. Biological tests led to the diagnosis of ACTH-dependent hypercortisolism. MRI showed a microadenoma of the pituitary gland, confirming the diagnosis of Cushing's disease. DNA methylation analysis revealed LOM at ICR2 that was in a mosaic state in the patient's leukocytes, but was present in nearly all cells of the pituitary adenoma. The epigenetic defect was associated with a somatic USP8 mutation in the adenoma.

Conclusion: Pituitary adenoma rarely occurs in patients with BWS. However, BWS should be considered in cases of pituitary adenoma with minor and/or major signs of BWS. The association between ICR2 LOM and USP8 mutation in the adenoma is questionable. © 2016 S. Karger AG, Basel.

Publication types

  • Case Reports

MeSH terms

  • Adenoma* / genetics
  • Adenoma* / metabolism
  • Adolescent
  • Adult
  • Beckwith-Wiedemann Syndrome* / complications
  • Beckwith-Wiedemann Syndrome* / genetics
  • Beckwith-Wiedemann Syndrome* / metabolism
  • Cushing Syndrome* / etiology
  • Cushing Syndrome* / genetics
  • Cushing Syndrome* / metabolism
  • Cyclin-Dependent Kinase Inhibitor p57 / genetics
  • Cyclin-Dependent Kinase Inhibitor p57 / metabolism
  • DNA Methylation*
  • Endopeptidases* / genetics
  • Endopeptidases* / metabolism
  • Endosomal Sorting Complexes Required for Transport* / genetics
  • Endosomal Sorting Complexes Required for Transport* / metabolism
  • Epigenesis, Genetic*
  • Female
  • Genetic Loci*
  • Humans
  • Pituitary Neoplasms* / genetics
  • Pituitary Neoplasms* / metabolism
  • Potassium Channels, Voltage-Gated / genetics
  • Potassium Channels, Voltage-Gated / metabolism
  • Ubiquitin Thiolesterase* / genetics
  • Ubiquitin Thiolesterase* / metabolism

Substances

  • CDKN1C protein, human
  • Cyclin-Dependent Kinase Inhibitor p57
  • Endosomal Sorting Complexes Required for Transport
  • KCNQ1OT1 long non-coding RNA, human
  • Potassium Channels, Voltage-Gated
  • Endopeptidases
  • USP8 protein, human
  • Ubiquitin Thiolesterase