glycogen storage disease type iii/епилептични припадъци

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The effect of tailoring of cornstarch intake on stature in children with glycogen storage disease type III.

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OBJECTIVE To determine the individual fasting tolerance for patients with glycogen storage disease type III (GSD III) and to assess their linear growth velocity after tailoring of dose intervals of oral uncooked cornstarch. METHODS A prospective cohort study included 32 patients with GSD III aged 6

[Mutation analysis of glycogen debrancher enzyme gene in five Chinese patients with glycogen storage disease type III].

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OBJECTIVE Type III glycogen storage disease (GSD-III, McKusick 232400), is a rare autosomal recessive disorder, also known as Cori's or Forbe's disease. The affected enzyme is amylo-1,6-glucosidase, 4-alpha-glucanotransferase (glycogen debrancher enzyme, GDE or amylogluco-sidase, AGL), which is

Glycogen storage disease type III in Egyptian children: a single centre clinico-laboratory study.

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OBJECTIVE Glycogen storage disease type III (GSD III) is an autosomal recessive disorder caused by deficiency of glycogen debrancher enzyme and is characterised by clinical variability. METHODS We herein describe the clinical and laboratory findings in 31 Egyptian patients with GSD III presenting to

Spectrum of amyloglucosidase mutations in Asian Indian patients with Glycogen storage disease type III.

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Glycogen storage disease type III (GSD III) is a rare autosomal recessive inborn error of glycogen degradation pathway due to deficiency or reduced activity of glycogen debranching enzyme (GDE) that results in accumulation of abnormal glycogen in the liver, muscle, and heart. The cardinal hallmarks

Glycogen storage disease type III presenting with secondary diabetes and managed with insulin: a case report.

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BACKGROUND Reports of secondary diabetes in glycogen storage disease type III have been very limited, where the pathogenesis and management have not been clear. Here we report on a rare case of secondary diabetes in glycogen storage disease type III that has been successfully managed with

Diet therapy in severe clinical expression of debrancher deficiency.

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An eleven year old boy was referred because of sudden loss of consciousness, muscular weakness, poor general health, severe hypoglycemia with seizures and hepatomegaly. Response to oral glucose and galactose increased blood lactic acid and glucose at different times. Fasting values of blood lactic

A nonsense mutation due to a single base insertion in the 3'-coding region of glycogen debranching enzyme gene associated with a severe phenotype in a patient with glycogen storage disease type IIIa.

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Glycogen storage disease type III (GSD-III) is an autosomal recessive disease resulting from deficient glycogen debranching enzyme (GDE) activity. A child with GDE deficient in both liver and muscle (GSD-IIIa) had recurrent hypoglycemia, seizures, severe cardiomegaly, and hepatomegaly and died at 4

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