Exp Clin Endocrinol Diabetes 2015; 123 - LB_18
DOI: 10.1055/s-0035-1549084

Paradoxical worsening of lipid metabolism after successful treatment of primary aldosteronism

C Adolf 1, A Dietz 1, E Fischer 1, M Bidlingmaier 1, F Beuschlein 1, M Treitl 1, K Hallfeldt 1, J Seissler 1, M Reincke 1
  • 1Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, München, Germany


Primary aldosteronism (PA) represents the most frequent cause of secondary arterial hypertension. Aldosterone is known to influence glucose metabolism. Conflicting data have been published regarding the effect of aldosterone on lipid metabolism.


Our aim was to analyze changes in lipid metabolism in a cohort of PA patients. Prospective follow-up investigations were performed in patients before and one year after successful treatment (adrenalectomy/MR-antagonists) to assess the metabolic outcome.


Triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were measured after a 12-hour fasting period.


129 consecutive patients with both unilateral aldosterone-producing adenoma (APA, n = 84) and bilateral idiopathic adrenal hyperplasia (IHA, n = 45) were recruited through the Munich center of the German Conn's Registry.


One year after treatment HDL-C and triglycerides changed inversely. HDL-C was significantly lower in patients with APA (56.75 ± 16.33 vs. 54.07 ± 16.49 [mg/dl], p = 0.03) and IHA (54.42 ± 15.78 vs. 50.44 ± 15.21 [mg/dl], p = 0.02) after treatment. Triglycerides were significantly higher in both subgroups (IHA 111.40 ± 46.18 vs. 146.76 ± 83.31 [mg/dl], p = 0.00, APA 110.17 ± 47.69 vs. 127.48 ± 64.10 [mg/dl], p = 0.01) at follow-up.

For LDL-C there was also a trend towards higher values after treatment without reaching statistical significance, whereas BMI remained unchanged and fasting plasma glucose even improved in follow-up patients with APA (105.06 ± 20.40 vs. 99.70 ± 16.37 [mg/dl], p = 0.00).


Our results show that treatment of PA causes a worsening of lipid metabolism. This effect may be mediated via direct or indirect changes on plasma cholesteryl ester transfer (CET) and/or the plasma cholesteryl ester transfer protein (CETP). Further investigations are required to better understand the effect of hyperaldosteronism on lipid metabolism.