Glycogen storage diseases

Glycogen Storage Diseases (GSD Types I – VI)

Type & Name Deficient Enzyme Key Clinical Presentation & Diagnostics
Type I
Von Gierke
Glucose-6-Phosphatase Severe fasting hypoglycemia, massive hepatomegaly, lactic acidosis, hyperuricemia (gout), and hyperlipidemia. Doll-like facies. Does NOT respond to glucagon.
Type II
Pompe
Lysosomal α(1→4)-Glucosidase (Acid Maltase) Infantile hypertrophic cardiomegaly, profound hypotonia (“floppy baby”), and early death. Glycogen accumulation inside membrane-bound lysosomes. Blood glucose is normal.
Type III
Cori
Debranching Enzyme (α-1,6-glucosidase) Milder fasting hypoglycemia, hepatomegaly. Accumulation of abnormal limit dextrins (short outer branches). Blood lactate levels are NORMAL; gluconeogenesis remains intact.
Type IV
Andersen
Branching Enzyme (α-1,4 → α-1,6 transglucosidase) Infantile cirrhosis, massive hepatosplenomegaly, progressive hepatic failure. Accumulation of abnormal, unbranched long chains (polyglucosan bodies) that provoke an immune response.
Type V
McArdle
Skeletal Muscle Glycogen Phosphorylase Muscle cramps and weakness during initial exercise, “second-wind” phenomenon (due to fatty acid utilization). Severe exertion triggers rhabdomyolysis and myoglobinuria (burgundy urine). Normal blood glucose.
Type VI
Hers
Hepatic Glycogen Phosphorylase Mild fasting hypoglycemia, hepatomegaly. Often benign and discovered incidentally during childhood workup, it improves with age.
High-Yield Diagnostic Yields:

  • The Lactate Differential Trap: Type I (Von Gierke) and Type III (Cori) present with identical fasting hypoglycemia and hepatomegaly. Differentiate them solely by blood lactate: Type I has massive lactic acidosis, while Type III has normal lactate.
  • Ischemic Forearm Exercise Test: Used to diagnose Type V (McArdle). Squeezing a dynamometer with a blood pressure cuff inflated leads to a normal rise in ammonia but zero rise in post-exercise blood lactate due to blocked glycogenolytic flux.
  • “Pompe Trashes the Pump”: Type II (Pompe) is fundamentally a lysosomal storage disease affecting muscular structures, heavily destroying cardiac muscle walls, whereas standard hepatic variants primarily disrupt systemic glycemic stability.