Elevated Serum Interleukin 6 Levels in Normotensive Individuals With Familial Hyperaldosteronism Type 1

Abstract

To the Editor: Experimental and clinical evidence suggests that aldosterone excess is associated with adverse cardiovascular sequelae, including remodeling, fibrosis, left ventricular (LV) dysfunction, stroke, myocardial infarction, and arrhythmias, independent of its effects on blood pressure (BP).1 Although the underlying mechanisms have yet to be fully elucidated, results from animal studies suggest the involvement of inflammatory pathways.1 Familial hyperaldosteronism type 1 (glucocorticoid remediable aldosteronism [FH-1]) is a rare form of primary aldosteronism in which inheritance of a “hybrid” 11β-hydroxylase/aldosterone synthase gene leads to excessive aldosterone production regulated by corticotropin rather than renin-angiotensin.2 Genetic testing has permitted the identification of individuals with FH-1 with biochemical evidence of aldosterone excess but normal BP, providing a unique opportunity to investigate adverse effects of aldosterone excess without the confounding influences of BP elevation. We have reported previously that these individuals have increased echocardiographically measured LV wall thicknesses and reduced LV diastolic function when compared with normotensive controls matched for age, sex, and BP.3 In the current study, we sought evidence in these same individuals of aldosterone-mediated cardiovascular inflammation by comparing their blood levels of 3 markers of inflammation (interleukin 6 [IL-6], osteopontin …