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Phosphoglycerate dehydrogenase deficiency
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Condition

Phosphoglycerate dehydrogenase deficiency

Phosphoglycerate dehydrogenase deficiency is a rare metabolic condition characterized by microcephaly, psychomotor retardation, and recurrent seizures.

Overview

Phosphoglycerate dehydrogenase deficiency is characterized by an unusually small head size (microcephaly), impaired development of physical reactions, movements, and speech (psychomotor retardation), and recurrent seizures (epilepsy). The condition involves a progressive loss of brain tissue, specifically affecting the fatty tissue known as myelin that surrounds nerve cells.

Symptoms

Symptoms vary by the age of onset:

  • Infantile form: The most severe and common form, characterized by infantile spasms, difficulty feeding, and failure to achieve developmental milestones.
  • Juvenile form: Typically involves epilepsy, mild developmental delay, and intellectual disability.
  • Adult form: Very rare; symptoms include mild intellectual disability, difficulty coordinating movements (ataxia), and numbness, tingling, and pain in the limbs (sensory neuropathy).

Causes

The condition is caused by mutations in the PHGDH gene, which provides instructions for making the phosphoglycerate dehydrogenase enzyme. This enzyme is essential for the production of the amino acid serine. Because brain cells must produce their own serine—as dietary serine cannot cross the blood-brain barrier—a deficiency leads to impaired production of neurotransmitters and myelin, disrupting brain development.

Inheritance

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

Frequently Asked Questions

Infants with the classic infantile form often have delayed or absent motor milestones, persistent seizures, and feeding difficulties; with aggressive serine therapy and seizure control, some achieve limited sitting or rolling by 12–18 months, but most require ongoing physical, occupational, and speech therapy.
Broad‑spectrum agents such as levetiracetam, valproic acid, or topiramate are commonly used; however, drugs that exacerbate metabolic stress (e.g., phenobarbital) should be avoided when possible, and dosing should be individualized to minimize sedation while achieving seizure freedom.
Diagnosis combines clinical presentation with biochemical testing (low serine levels in plasma/CSF) and confirmation by molecular genetic testing that identifies pathogenic variants in the PHGDH gene.
Yes, high‑dose L‑serine (often 0.5–1 g/kg/day divided into multiple doses) can increase brain serine availability, improve myelination, and reduce seizure frequency; treatment should be started under metabolic specialist supervision with regular monitoring of plasma serine and neurologic status.
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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