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• W2113233886 abstract "Abstract Significant progress has been made in recent years in the elucidation of the molecular genetic basis for several rare forms of hypertension that are often first diagnosed in childhood. This review summarizes these findings. Glucocorticoid remediable aldosteronism has been shown to be caused by unequal crossing over between the genes for 11β-hydroxylase and aldosterone synthase so that corticotropin (ACTH) becomes the major controller of the latter enzyme activity, meaning greatly elevated aldosterone synthesis and thus sodium retention, volume expansion and high blood pressure. Mutations in the 11β-hydroxylase gene are the cause of 11β-hydroxylase deficiency, another form of childhood hypertension. Apparent mineralocorticoid excess has been found to involve mutation of the gene encoding 11β-hydroxysteroid dehydrogenase type 2, which means instead of being destroyed in aldosterone target cells in the kidney, cortisol is able to bind to the mineralocorticoid receptor, leading to greatly enhanced sodium reabsorption by the kidney. Liddle's syndrome is another condition seen early in life and can involve mutations in the carboxyl terminal region of the β- or γ-subunits of the amiloride-sensitive epithelial sodium channel gene. This prevents binding of a protein that tags the channel for endocytosis and degradation so that channel activity is increased. Other forms of hypertension of early onset such as Gordon's syndrome, pheochromocytoma and brachydactyly are also discussed. The review thus highlights the major advances that have occurred in understanding the molecular basis for various forms of hypertension seen in children." @default.
• W2113233886 created "2016-06-24" @default.
• W2113233886 creator A5022264359 @default.
• W2113233886 date "1998-12-01" @default.
• W2113233886 modified "2023-09-27" @default.
• W2113233886 title "Molecular genetics in childhood hypertension" @default.
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• W2113233886 doi "https://doi.org/10.1016/s1058-9813(99)00007-7" @default.
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