Context:
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.
Objective:
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.
Methods:
Triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C) and
high-density lipoprotein cholesterol (HDL-C) were measured after a 12-hour fasting
period.
Patients:
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.
Results:
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).
Conclusion:
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.
