acanthocheilonemiasis/carbohydrate

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Complex carbohydrates in the dietary management of patients with glycogenosis caused by glucose-6-phosphatase deficiency.

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Carbohydrates with digestion characteristics between those of lente uncooked starches and rapidly digestible oligosaccharides were administered in a dose of 1.5 g/kg body weight to five patients with glycogenosis from glucose-6-phosphatase deficiency. Postprandial duration of normoglycemia and

Glucose-6-phosphatase deficiency glycogen storage disease. Studies on the interrelationships of carbohydrate, lipid, and purine abnormalities.

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Urinary lactate excretion in normal children and in children with enzyme defects of carbohydrate metabolism.

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Urinary lactate was analyzed in 53 normal children, 7 children with glucose-6-phosphatase-deficient glycogenosis, 1 child with fructose-1,6-diphosphatase deficiency and 1 child with pyruvate dehydrogenase deficiency. Lactate in 24-h urine was expressed as concentration, total excretion, excretion

[Hypoglycemias in childhood. Pathophysiologic reflections and examples of hypoglycemias in hereditary disorders of carbohydrate metabolism].

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For the understanding and interpretation of hypoglycemia it is important to know the many complex endocrine and metabolic regulations in the homoeostasis of blood glucose. Glucose-absorption, distribution and availability, glycolysis, production and utilization of glycogen as well as gluconeogenesis

[Glycogenosis type I]

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OBJECTIVE: To o present up-to-date knowledge about Glycogen storage disease type I (GSD-type I) - a disease caused by the deposit of glycogen resulting from the deficiency of the enzyme glucose-6- phosphatase - and to provide the pediatricians with the necessary information for a precocious

[Diagnostic procedures in pediatric hypoglycemias].

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Depending on its etiology hypoglycemia appears after short or prolonged periods of fasting and shows different metabolite and hormonal patterns. In children it is caused by a disturbed homoeostasis of blood glucose (hormonal disorders, decreased activity of glycogenolysis or gluconeogenesis), by a

Physiological aspects of the regulation of ketogenesis.

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The importance of ketone bodies (acetoacetate and 3-hydroxybutyrate) as substrates for peripheral tissues, especially nervous tissue, of man is now firmly established. This has renewed interest in the factors that control the production of ketone bodies by the liver in various physiological

[Glycogen storage disease type I with normal in vitro activity of glucose-6-phosphatase (author's transl)].

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A 4.5 months old girl was suspected to have Glycogenosis type I because of hepatomegalie and recurrent hypoglycemia. Liverbiopsy revealed a normal glycogen content and a normal in vitro activity of glucose-6-phosphatase. We then examined the carbohydrate metabolism and could demonstrate that in

Perioperative management of benign hepatic tumors in patients with glycogen storage disease type Ia.

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Glycogen storage disease type Ia (GSD-Ia; von Gierke disease) is an inherited disorder caused by glucose-6-phosphatase deficiency, and there have been some reports of hepatic tumors in patients with this disease. We report two patients with benign hepatic tumors with GSD-Ia. One is a 19-year-old man

Nutrition therapy for hepatic glycogen storage diseases.

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Hepatic glycogen storage diseases (GSD) are a group of rare genetic disorders in which glycogen cannot be metabolized to glucose in the liver because of one of a number of possible enzyme deficiencies along the glycogenolytic pathway. Patients with GSD are usually diagnosed in infancy or early

Hepatocellular carcinoma and focal nodular hyperplasia of the liver in a glycogen storage disease patient.

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Glycogen storage disease type Ia (GSD-Ia; also called von Gierke disease) is an autosomal recessive disorder of carbohydrate metabolism caused by glucose-6-phosphatase deficiency. There have been many reports describing hepatic tumors in GSD patients; however, most of these reports were of

Intragastric feeding in type I glycogen storage disease: factors affecting the control of lactic acidemia.

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Continuous nocturnal intragastric feeding, combined with frequent daytime feedings, has been reported to improve both linear growth and the metabolic abnormalities in patients with glucose-6-phosphatase deficiency (Type I Glycogen Storage Disease). However, elevated blood levels of lactate have

Glucose-6-phosphate: a key compound in glycogenosis I and favism leading to hyper- or hypolipidaemia.

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The glycogen storage disorders (GSD)-I, -III, -VI and -VIII are associated with hypertriglyceridaemia or mixed hyperlipidaemia which poses the question whether these patients have an increased risk for atherosclerosis. The atherogenicity of triglycerides has remained controversial, while increased

Clinical and biochemical heterogeneity between patients with glycogen storage disease type IA: the added value of CUSUM for metabolic control.

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To study heterogeneity between patients with glycogen storage disease type Ia (GSD Ia), a rare inherited disorder of carbohydrate metabolism caused by the deficiency of glucose-6-phosphatase (G6Pase). Descriptive retrospective study of longitudinal clinical and biochemical data and long-term

Recoverable, Record-High Lactic Acidosis in a Patient with Glycogen Storage Disease Type 1: A Mixed Type A and Type B Lactate Disorder.

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A 17-year-old patient with GSD type 1a (von Gierke disease) was hospitalized with an extremely elevated serum lactate following an intercurrent infection and interruption of his frequent intake of carbohydrates. The patient developed shock, oliguric renal failure, and cardiorespiratory failure

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