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Familial hyperaldosteronism type III.
Monticone, S; Tetti, M; Burrello, J; Buffolo, F; De Giovanni, R; Veglio, F; Williams, T A; Mulatero, P.
Affiliation
  • Monticone S; Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy.
  • Tetti M; Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy.
  • Burrello J; Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy.
  • Buffolo F; Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy.
  • De Giovanni R; Unit of Internal Medicine and Angiology, Department of Internal Medicine, Riccione Hospital, AUSL, Romagna, Italy.
  • Veglio F; Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy.
  • Williams TA; Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy.
  • Mulatero P; Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, München, Germany.
J Hum Hypertens ; 31(12): 776-781, 2017 12.
Article de En | MEDLINE | ID: mdl-28447626
Primary aldosteronism is the most common form of endocrine hypertension. This disorder comprises both sporadic and familial forms. Four familial forms of primary aldosteronism (FH-I to FH-IV) have been described. FH-III is caused by germline mutations in KCNJ5, encoding the potassium channel Kir3.4 (also called GIRK4). These mutations alter the selectivity filter of the channel and lead to abnormal ion currents with loss of potassium selectivity, sodium influx and consequent increased intracellular calcium that causes excessive aldosterone biosynthesis. To date, eleven families have been reported, carrying six different mutations. Although the clinical features are variable, FH-III patients often display severe hyperaldosteronism with an early onset, associated with hypokalemia and diabetes insipidus-like symptoms. In most cases FH-III patients are resistant to pharmacological therapy and require bilateral adrenalectomy to control symptoms. In the present manuscript, we review the genetics and pathological basis of FH-III, the diagnostic work-up, clinical features and therapeutic management. Finally, we will describe a new case of FH-III of an Italian patient carrying a Gly151Arg mutation.
Sujet(s)

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Canaux potassiques rectifiants entrants couplés aux protéines G / Hyperaldostéronisme Limites: Humans / Male / Middle aged Langue: En Journal: J Hum Hypertens Sujet du journal: ANGIOLOGIA Année: 2017 Type de document: Article Pays d'affiliation: Italie Pays de publication: Royaume-Uni

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Canaux potassiques rectifiants entrants couplés aux protéines G / Hyperaldostéronisme Limites: Humans / Male / Middle aged Langue: En Journal: J Hum Hypertens Sujet du journal: ANGIOLOGIA Année: 2017 Type de document: Article Pays d'affiliation: Italie Pays de publication: Royaume-Uni