What it is
Pompe disease (glycogen storage disease type II) is an inherited condition caused by deficiency of the enzyme acid alpha-glucosidase (GAA), so glycogen builds up in muscle and other tissues.
Signs and symptoms
Cardiomegaly
In the severe infantile form, the heart muscle thickens and the heart becomes enlarged early in life.
Autosomal recessive inheritance
Pompe disease is inherited in an autosomal recessive pattern, needing a changed copy of the GAA gene from each parent.
Proximal muscle weakness
Weakness of the muscles closest to the trunk (proximal muscle weakness) is a core feature, alongside weakening of the muscles used for breathing.
Muscle weakness
Muscle weakness is a defining feature and, in infants, can come with feeding difficulties.
Treatment and management
What the research describes, not a recommendation. Treatment decisions belong with your clinician.
This covers treatments that appear in the published research mapped here. Investigational and experimental therapies are not included, so their absence is a boundary of this map, not a sign they do not exist.
Alglucosidase alfa
Alglucosidase alfa is an enzyme replacement therapy that supplies the missing GAA enzyme and is the main treatment for Pompe disease.
Used to help with: Glycogen storage disease II.
“- Source: Short-Term Intensive Avalglucosidase Alfa Regimen in Late-Diagnosed Infantile Pompe Disease: A Case Report. - Source ID / type: PMID:41718282 / peer_reviewed_study - Publication date: 2026 - Study design: Case Reports, Journal Article Sample size: ## Finding Background and Clinical Significance: Classic infantile-onset Pompe disease (IOPD) is the most severe form of Pompe disease, manifesting within the first months of life with hypertrophic cardiomyopathy and severe hypotonia.”
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How to read the evidence labels
Where this comes from
This guide is built from 2 published source(s). Every claim above links back to one of them. Click any source ID to read the original on PubMed.