glycogen storage disease type iii/triglyceride

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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

Biochemical and molecular investigation of two Korean patients with glycogen storage disease type III.

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BACKGROUND Glycogen storage disease type III (GSD-III) is an inborn error of glycogen metabolism caused by a deficiency of the glycogen debranching enzyme, amylo-1,6-glucosidase,4-alpha-glucanotransferase (AGL). Here, we describe two unrelated Korean patients with GSD-III and review their clinical

Glycogen storage disease type III with hypoketosis.

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A rare case of glycogen storage disease type III with unusually absent ketone body production during hypoglycemia is presented. A 10-month-old boy presented with asymptomatic hepatomegaly. GOT/GPT 2555/1160 IU/L, CK 302 IU/L, triglycerides 1223 mg/dL, cholesterol 702 mg/dL and uric acid 7.9 mg/dL.

Blood lipids and endothelial function in glycogen storage disease type III.

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We have assessed early indicators of arterial disease in patients with glycogen storage disease type III (GSD III; McKusick 232400), investigating the plasma lipid and lipoprotein profile and endothelial function. Eleven patients, aged 10-39 years, were recruited together with age-, sex- and smoking

Liver fibrosis during clinical ascertainment of glycogen storage disease type III: a need for improved and systematic monitoring.

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In glycogen storage disease type III (GSD III), liver aminotransferases tend to normalize with age giving an impression that hepatic manifestations improve with age. However, despite dietary treatment, long-term liver complications emerge. We present a GSD III liver natural history

Reduced bone mineral density in glycogen storage disease type III: evidence for a possible connection between metabolic imbalance and bone homeostasis.

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BACKGROUND Glycogen storage disease type III (GSDIII) is an inborn error of carbohydrate metabolism caused by deficient activity of glycogen debranching enzyme (GDE). It is characterized by liver, cardiac muscle and skeletal muscle involvement. The presence of systemic complications such as growth

Modified Atkins ketogenic diet improves heart and skeletal muscle function in glycogen storage disease type III.

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Glycogen storage disease type III (GSDIII) management in adult patients includes a high-protein diet with cornstarch supplementation to maintain a normal level of glucose in the blood. This regimen can prevent hypoglycaemia but does not seem to improve skeletal muscle and heart function. A 34

Dietary management in glycogen storage disease type III: what is the evidence?

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In childhood, GSD type III causes relatively severe fasting intolerance, classically associated with ketotic hypoglycaemia. During follow up, history of (documented) hypoglycaemia, clinical parameters (growth, liver size, motor development, neuromuscular parameters), laboratory parameters (glucose,

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