citrullinemia/kunona

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Steatogenesis in adult-onset type II citrullinemia is associated with down-regulation of PPARα.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

SLC25A13 (citrin or aspartate-glutamate carrier 2) is located in the mitochondrial membrane in the liver and its genetic deficiency causes adult-onset type II citrullinemia (CTLN2). CTLN2 is one of the urea cycle disorders characterized by sudden-onset hyperammonemia due to reduced argininosuccinate

Citrullinemia stimulation test in the evaluation of the intestinal function.

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Ingia / Ingia

BACKGROUND Citrullinemia is been reported as a quantitative parameter of the enterocyte mass and function. OBJECTIVE The objective of this research is to analyse the value of fasting and stimulated citrullinemias in the intestinal function evaluation. METHODS A case-control study was undertaken,

Chronic hepatitis without hepatic steatosis caused by citrin deficiency in a child.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Citrin deficiency manifests as both neonatal intrahepatic cholestasis (NICCD) during early infancy and adult-onset type II citrullinemia during adulthood. Hepatic steatosis is most frequently observed in patients with citrin deficiency. Thus, non-alcoholic fatty liver disease that is unrelated to

Citrin deficiency as a cause of chronic liver disorder mimicking non-alcoholic fatty liver disease.

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Ingia / Ingia

OBJECTIVE Citrin deficiency caused by SLC25A13 gene mutations develops into adult-onset type II citrullinemia (CTLN2) and may be accompanied with hepatic steatosis and steatohepatitis. As its clinical features remain unclear, we aimed to explore the characteristics of fatty liver disease associated

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