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Free Radic Biol Med 102:203216

Firoozrai, H

Clinically, many late-onset MADD patients respond dramatically to high-dose riboflavin (100400 mg/day), confirming residual enzyme function amenable to cofactor restorationclassifying MADD as a prototype FAD-responsive metabolic myopathy (70)

Mice lacking the intestinal and renal neutral amino acid transporter SLC6A19 demonstrate the relationship between dietary protein intake and amino acid malabsorption

Most GHI cases have autosomal recessive inheritance and in the vast majority a molecular defect has been identified involving homozygous or compound heterozygous mutations (Lupu et al., 2001)