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Arginine:glycine amidinotransferase deficiency
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Condition

Arginine:glycine amidinotransferase deficiency

Arginine:glycine amidinotransferase deficiency is an inherited metabolic disorder that impairs the body's ability to produce creatine, primarily affecting brain function and development.

Overview

Arginine:glycine amidinotransferase deficiency is an inherited disorder that primarily affects the brain. Individuals with this condition often experience mild to moderate intellectual disability and delayed speech development. Some may exhibit autistic behaviors that impact communication and social interaction. Seizures, particularly triggered by fever, are also a common feature.

Symptoms

  • Mild to moderate intellectual disability
  • Delayed speech development
  • Autistic behaviors affecting communication and social interaction
  • Seizures (especially during fevers)
  • Failure to thrive (inability to gain weight or grow at the expected rate)
  • Delayed development of motor skills, such as sitting and walking
  • Weak muscle tone
  • Tendency to tire easily

Causes

The disorder is caused by mutations in the GATM gene, which provides instructions for making the enzyme arginine:glycine amidinotransferase. This enzyme is responsible for the first step in the synthesis of creatine, a compound essential for the body to store and use energy properly.

Mutations in the GATM gene impair the enzyme's ability to participate in creatine synthesis, leading to a shortage of creatine. The impact of this deficiency is most severe in organs and tissues with high energy demands, particularly the brain.

Inheritance

This condition is inherited in an autosomal recessive pattern, meaning both copies of the gene in each cell must have mutations. Parents of an affected individual typically each carry one copy of the mutated gene but do not show signs or symptoms of the condition.

Frequently Asked Questions

Carriers (heterozygous for a GATM mutation) are usually asymptomatic and do not require treatment. However, because the disorder is autosomal recessive, siblings of an affected child have a 25 % chance of being affected and a 50 % chance of being carriers. Offering carrier testing and, if appropriate, biochemical screening to at‑risk siblings is recommended to enable early diagnosis and treatment.
Oral creatine monohydrate supplementation (400 mg/kg/day divided into 2–3 doses) is the standard therapy and can improve speech, cognition, and seizure control, especially when started early. Monitoring includes periodic plasma creatine levels and neurodevelopmental assessments. Adjunctive therapies such as physical, occupational, and speech therapy are essential for maximizing functional gains.
Diagnosis begins with clinical suspicion based on intellectual disability, speech delay, seizures, and low muscle tone. Confirmatory testing includes plasma and urine creatine and guanidinoacetate measurements (low creatine, high guanidinoacetate) followed by molecular genetic testing of the GATM gene to identify pathogenic variants.
Early treatment (before age 2) combined with intensive rehabilitation often leads to significant gains; many children achieve independent walking and develop functional speech, though some residual mild intellectual disability may persist. Long‑term outcomes vary, but early intervention markedly improves quality of life compared with untreated cases.
Source: MedlinePlus, National Library of Medicine

MedlinePlus brings together authoritative health information from the National Library of Medicine (NLM), the National Institutes of Health (NIH), and other government agencies and health-related organizations.

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