Aldosterone-producing
adenoma was detected in more than two thirds of patients (n = 135), whereas idiopathic
hyperaldosteronism was found in 46 patients. Other subtypes of
primary hyperaldosteronism occurred less frequently (unilateral primary adrenocortical
hyperplasia in 5 patients and
adrenocortical carcinoma in one patient). For the diagnosis of
familial hyperaldosteronism type I, molecular
biological studies of the
aldosterone-synthase/11beta-
hydroxylase gene chimera were carried out in 30 patients but none of them showed the presence of the chimeric gene. When comparing the clinical parameters of patients with
aldosterone-producing
adenoma and idiopathic
hyperaldosteronism, no significant differences were found in the time period between the diagnosis of
hypertension and the diagnosis of primary
aldosteronism, or in the systolic and diastolic blood pressure values. The mean of the lowest documented serum
potassium concentration was slightly lower in patients with
aldosterone-producing
adenoma (2.8 +/- 0.1 mmol/l) compared to those with idiopathic
hyperaldosteronism (3.1 +/- 0.2 mmol/l), but the difference was not significant. Normokalemic
primary hyperaldosteronism was found in 7 cases. The ratio of plasma
aldosterone concentration (ng/dl) to plasma
renin activity (ng/ml/h) was above 20 in all patients with
aldosterone-producing
adenoma and in all but 5 cases with idiopathic
hyperaldosteronism. To confirm the diagnosis and to differentiate the subtypes of primary
aldosteronism, the postural test combined with
furosemide administration was performed in the majority of patients. When cases showing an elevation of plasma
cortisol level during the test were excluded, this test differentiated patients with
aldosterone-producing
adenoma from those with idiopathic
hyperaldosteronism with a sensitivity of 69% and a specificity of 92%. In cases of
adrenocortical adenomas not or not clearly detectable by radiological imaging techniques, as well as in cases with bilateral
adrenocortical adenomas, selective adrenal vein sampling was performed (n = 55). All but 4 patients with
aldosterone-producing
adenoma underwent
adrenalectomy. Histology and postoperative
hormone results confirmed the preoperative diagnosis in all operated patients. After surgery serum
potassium concentration returned to normal in all patients showing low serum
potassium levels before surgery. Also, the moderate to severe preoperative
hypertension disappeared or improved after surgery.
CONCLUSIONS: These observations are in contrast with the results of international studies which showed a high frequency of normokalemic primary
aldosteronism and a more frequent occurrence of idiopathic
hyperaldosteronism well treatable with
aldosterone-antagonists. Therefore, it can be presumed that a significant number of primary
aldosteronism cases that are not accompanied with severe
hypokalemia remain undetected in Hungary.