Primary aldosteronism(PA) is the most frequent cause of secondary hypertension in adults, accounting for 5% to 15% of hypertensive patients, depending on the severity of blood pressure levels. Patients with PA undergo a higher rate of cardiovascular complications compared with essential hypertensives, and, thus, the screening of hypertensive subgroups of patients with higher prevalence of PA is recommended. Three genetic forms of PA have been described so far: familial hyperaldosteronism type I, II and III (FH-I to FH-III). In this issue of Hypertension, Aglony et al report a high prevalence of FH-I among hypertensive children in Chile. Detection of familial forms of hyperaldosteronism is of paramount importance to prevent the detrimental effects of aldosterone on the cardiovascular system. Patients with FH-I display higher morbidity and mortality from cerebrovascular events at a young age. The results of the studies of Fardella’s group, together with the demonstration of the genetic alterations responsible for FH-III and the relatively high prevalence ofFH-II, which may be widely unrecognized in children, highlight the necessity for an increased awareness of these forms in hypertensive children. Future research should be addressed toward understanding the genetic causes of FH-II, the prevalence of mutations in KCNJ5 in “sporadic” PA, and the necessity of beginning pharmacological therapy in normotensive children with genetic alterations responsible for familial hyperaldosteronism.
Is familial hyperaldosteronism underdiagnosed in hypertensive children?
MULATERO, Paolo;WILLIAMS, Tracy Ann;MONTICONE, Silvia;VEGLIO, Franco
2011-01-01
Abstract
Primary aldosteronism(PA) is the most frequent cause of secondary hypertension in adults, accounting for 5% to 15% of hypertensive patients, depending on the severity of blood pressure levels. Patients with PA undergo a higher rate of cardiovascular complications compared with essential hypertensives, and, thus, the screening of hypertensive subgroups of patients with higher prevalence of PA is recommended. Three genetic forms of PA have been described so far: familial hyperaldosteronism type I, II and III (FH-I to FH-III). In this issue of Hypertension, Aglony et al report a high prevalence of FH-I among hypertensive children in Chile. Detection of familial forms of hyperaldosteronism is of paramount importance to prevent the detrimental effects of aldosterone on the cardiovascular system. Patients with FH-I display higher morbidity and mortality from cerebrovascular events at a young age. The results of the studies of Fardella’s group, together with the demonstration of the genetic alterations responsible for FH-III and the relatively high prevalence ofFH-II, which may be widely unrecognized in children, highlight the necessity for an increased awareness of these forms in hypertensive children. Future research should be addressed toward understanding the genetic causes of FH-II, the prevalence of mutations in KCNJ5 in “sporadic” PA, and the necessity of beginning pharmacological therapy in normotensive children with genetic alterations responsible for familial hyperaldosteronism.File | Dimensione | Formato | |
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