acanthocheilonemiasis/triglyceride

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Urate production in heterozygotes for glucose-6-phosphatase deficiency.

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Identifikohuni Regjistrohu

Urate production and excretion were studied in heterozygous parents of a child with glucose-6-phosphatase deficiency. Both parents demonstrated glucose-6-phosphatase concentrations in platelets intermediate between those in the homozygote and the normal. The miscible urate pool and turnover rate,

Continuous ambulatory peritoneal dialysis (CAPD) in a patient with glucose-6-phosphatase deficiency.

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Identifikohuni Regjistrohu

The metabolic disturbances in glucose-6-phosphatase deficiency (von Gierke's disease) are the consequence of hypoglycemia, occurring mostly during the night. Continuous provision of glucose is the aim of every recently introduced treatment procedure. We studied the influence of continuous ambulatory

[Continuous nocturnal intragastric feeding in glycogenosis type I and III].

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Identifikohuni Regjistrohu

Three patients with type I glycogen storage disease (GT I) and four patients with type III glycogen storage disease (GT III) have been treated with nocturnal intragastric feeding and frequent daytime meals for 2 to 8.5 years. In all of them, hypoglycemia was well controlled. Patients with GT. I

Induction of autophagy improves hepatic lipid metabolism in glucose-6-phosphatase deficiency.

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Identifikohuni Regjistrohu

OBJECTIVE Glucose-6-phosphatase (G6Pase α, G6PC) deficiency, also known as von Gierke's disease or GSDIa, is the most common glycogen storage disorder. It is characterized by a decreased ability of the liver to convert glucose-6-phosphate (G6P) to glucose leading to glycogen and lipid

ATP depletion, a possible role in the pathogenesis of hyperuricemia in glycogen storage disease type I.

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Identifikohuni Regjistrohu

Other investigators have shown that fructose infusion in normal man and rats acutely depletes hepatic ATP and P(i) and increases the rate of uric acid formation by the degradation of preformed nucleotides. We postulated that a similar mechanism of ATP depletion might be present in patients with

Disturbed lipid metabolism in glycogen storage disease type 1.

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Identifikohuni Regjistrohu

Glycogen storage disease type 1 (GSD1) is an inborn error of metabolism caused by deficiency of glucose-6-phosphatase, the enzyme catalysing the conversion of glucose-6-phosphate (G6P) to glucose. GSD1 is associated with severe hyperlipidaemia and hepatic steatosis. The underlying mechanisms

Lactate as a cerebral metabolic fuel for glucose-6-phosphatase deficient children.

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Identifikohuni Regjistrohu

The main substrates for brain energy metabolism were measured in blood samples taken from the carotid artery and the internal jugular bulb of four children with glycogen storage disease caused by deficiency of glucose-6-phosphatase. Multiple paired arterial and venous blood samples were analyzed for

Effects of cornstarch treatment in very young children with type I glycogen storage disease.

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Identifikohuni Regjistrohu

Three children aged 1-2 years with glycogenosis type I were treated with 2 g/kg bodyweight oral cornstarch per meal (4-5 times a day) for a period up to 16 months. In comparison to the previous dietary regimen (day and nocturnal feedings every 3 h) the cornstarch diet stabilised serum glucose

Gastric drip feeding in patients with glycogen storage disease type I: its effects on growth and plasma lipids and apolipoproteins.

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Identifikohuni Regjistrohu

In 19 patients with a deficiency of glucose-6-phosphatase and 1 patient with a deficiency of glucose-6-phosphate translocase, the effect of nocturnal gastric drip feeding (GDF) on growth and plasma lipids and apolipoproteins was studied. The effect on growth was estimated by determining the height

Variability of clinical and biochemical phenotype in liver phosphorylase kinase deficiency with variants in the phosphorylase kinase (PHKG2) gene

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Identifikohuni Regjistrohu

Background PHKG2-related liver phosphorylase kinase deficiency is inherited in autosomal recessive pattern and is a rare type of liver glycogenosis. We demonstrated the clinical presentation and genetic determinants involved in children with PHKG2- related liver phosphorylase kinase deficiency.

Apolipoprotein E polymorphism and serum concentrations in patients with glycogen storage disease type Ia.

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Identifikohuni Regjistrohu

In patients with glycogen storage disease type Ia (glucose-6-phosphatase deficiency), serum triglyceride concentrations are markedly raised, whereas phospholipids and cholesterol levels are only moderately elevated. In addition, both VLDL and LDL lipoprotein fractions are raised. Despite these

Nocturnal gastric drip feeding in glucose-6-phosphatase deficient children.

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Identifikohuni Regjistrohu

Six patients with glucose-6-phosphatase deficiency were treated for 12 hr at night with gastric drip feeding (GDF), containing soy milk plus glucose, dextrimaltose, and starch. An alarm system (thermistor), connected to the gastric tube, was devised in case of displacement of the tube by the child.

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

Glycogen storage disease type III with hypoketosis.

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Identifikohuni Regjistrohu

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.

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

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Identifikohuni Regjistrohu

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

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