Primary aldosteronism (PA) is characterized by development of cardiovascular and metabolic complications. We retrospectively analyzed 78 patients with PA: 29 had aldosterone-producing adenoma (APA), and 49 had idiopathic hyperaldosteronism (IHA). The study of complications was performed by examining the lipid and glucose profiles (OGTT, HOMA and Quicki indexes) and the echocardiographic parameters. Single-nucleotide polymorphisms (SNPs) of the aldosterone synthase (minus 344C/T, minus 470C/T) and nitric oxide synthase (4VNTR, G894T) genes were evaluated. The duration of disease was longer in IHA than in APA group (p minor 0.05). BMI and WHR were comparable in the two groups. HOMA-IR index was higher in IHA than in APA group. Linear multiple regression analysis between the HOMA index IR, beta cell and Quicki index and some clinical parameters showed a significant correlation in these patients for waist circumference, and for glycaemia and insulin levels at 120 minutes after OGTT. Values for echocardiografic parameters (LVMi, IVST and PWT) didn't differ between APA and IHA patients, although IHA group showed slightly higher values compared to APA. Aldosterone synthase SNPs, were found in linkage and associated to increased plasma aldosterone levels (344TT/470CC 42 plus/minus 4 nanograms per deciliter, 344CT/470CT 51 plus/minus 5 nanograms per deciliter, 344CC/470TT 69 plus/minus 8 nanograms per decilitre, p minor 0.05) as well as to plasma glucose levels at 120 minutes after OGTT (344TT/470CC 177 plus/minus 15 milligrams per deciliter, 344CT/470CT 123 plus/minus 12 milligrams per deciliter, 344CC/470TT 129 plus/minus 9 milligram per decilitre, p minor 0.05). A similar trend was observed for glucose levels at 120 minutes after OGTT and nitric oxide SNPs(p minor 0.05). Our data show that dysmetabolic and cardiac alterations already known to be present in PA are more evident in IHA than in APA patients. The aldosterone synthase and nitric oxide genes seem to have a substantial impact on glucose levels in PA.
04 - 06 Apr 2005
British Endocrine Societies