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Disrupted glutamate-gaba balance in children with adenoid hypertrophy:a targeted metabolomic and clinical correlation

Tuğba Yemiş1, Medeni Arpa2, Mehmet Birinci3

  • 1Medical Faculty, Department of Otorhinolaryngology, Recep Tayyip Erdogan University, Rize, Turkey. tugba.yemis@erdogan.edu.tr.

European Archives of Oto-Rhino-Laryngology : Official Journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : Affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
|November 12, 2025
PubMed

Insights

Pediatric adenoid hypertrophy (AH) is linked to altered plasma amino acids, with some elevated and others decreased. These metabolic changes may contribute to AH complications and suggest new therapeutic targets.

Area of Science:

  • Metabolomics
  • Pediatric Medicine
  • Biochemistry

Background:

  • Adenoid hypertrophy (AH) is a common condition in children, but its underlying molecular mechanisms and systemic effects remain unclear.
  • Understanding the metabolic profile of AH is crucial for developing effective diagnostic and therapeutic strategies.

Purpose of the Study:

  • To investigate plasma amino acid alterations in children with adenoid hypertrophy.
  • To explore associations between these amino acid changes and systemic inflammatory markers.
  • To identify potential metabolic biomarkers for AH-related airway obstruction and its complications.

Main Methods:

  • Prospective study comparing pediatric patients with AH and healthy controls.
  • Targeted metabolomic analysis of plasma amino acids using liquid chromatography-mass spectrometry (LC-MS/MS).
  • Statistical analyses, correlation studies, and pathway enrichment mapping to assess metabolic alterations and clinical relevance.

Main Results:

  • Eight out of 36 analyzed amino acids showed significant differences between groups.
  • Elevated levels of glutamic acid, phenylalanine, and leucine were observed in AH patients.
  • Decreased levels of GABA, tryptophan, alanine, citrulline, and anserine were found in AH patients, with pathway analysis indicating dysregulation in alanine, aspartate, and glutamate metabolism.

Conclusions:

  • This study provides the first metabolomic characterization of systemic responses in adenoid hypertrophy.
  • Amino acid dysregulation in AH may contribute to local tissue proliferation and multisystem complications.
  • Findings suggest potential early biochemical markers for AH and support the development of targeted metabolic therapies.
Abstract

Keywords:
Adenoid hypertrophyAmino acidLC–MS/MSTargeted metabolomics

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