Context Recent studies support a bidirectional interaction between aldosterone and parathyroid hormone (PTH), possibly increasing the individual cardiovascular risk. Primary aldosteronism (PA) and primary hyperparathyroidism can occur simultaneously. Objective Our aim was to investigate the prevalence of hyperparathyroidism in PA. Patients We performed a case finding of primary hyperparathyroidism in a retrospective series of 503 patients with PA (cohort 1). We analysed primary and secondary hyperparathyroidism in 141 prospective PA patients who underwent PTH, serum calcium and phosphate measurements at time of diagnosis of PA (cohort 2). Results The prevalence for primary hyperparathyroidism was 1.2% in cohort 1, and 2.1% in cohort 2. Secondary hyperparathyroidism was found in 54.6% of the patients. Patients with secondary hyperparathyroidism had significantly higher aldosterone and lower potassium levels and took more antihypertensive medications compared to those with normal PTH levels. In multivariate analysis, aldosterone and 25-hydroxyvitamin D levels were significantly correlated with serum PTH levels. There was a nonsignificant trend to a higher cardiovascular morbidity in patients with secondary hyperparathyroidism. Patients with aldosterone producing adenoma had significantly higher PTH levels compared to patients with bilateral adrenal hyperplasia. After treatment, there was a significant decrease of PTH levels in both groups. Conclusion Patients with PA frequently have primary or secondary hyperparathyroidism, which is alleviated by correction of PA by surgical or medical means. Patients affected by secondary hyperparathyroidism seem to have a more severe phenotype of PA and have a trend towards more cardiovascular co-morbidities.

Primary aldosteronism (PA) is the most frequent cause of secondary arterial hypertension. Beyond its effects on intravascular volume and blood pressure, PA causes metabolic alterations and a higher cardiovascular morbidity, which is reduced by PA-directed therapy. Experimental studies demonstrated that mineralocorticoid excess may also influence mineral homeostasis. A role in cardiovascular disease has also been attributed to parathyroid hormone (PTH). Increasing evidence supports a bidirectional interaction between aldosterone and PTH.Primary hyperparathyroidism is associated with arterial hypertension and an increased cardiovascular morbidity and mortality, which might be associated to higher aldosterone values; parathyreoidectomy results in lowered aldosterone and blood pressure levels. PA leads to secondary hyperparathyroidism, which is reversible by PA-directed therapy. A lower bone mineral density and a higher fracture rate were also shown to be reversible by PA-directed therapy. There is a suspicion of a bidirectional interaction between aldosterone and PTH, which might lead to a higher cardiovascular risk. There are more and more reports about coincident PA and primary hyperparathyroidism. From a pathophysiologic point of view this constellation is best characterized as tertiary hyperparathyroidism. Future aspects should further clarify the extent of these endocrine interactions and analyze the influence of this interplay on cardiovascular morbidity and mortality and bone health.

Context: Primary aldosteronism (PA) represents the most frequent cause of an endocrine arterial hypertension. PA is also common in patients with mild forms of hypertension and normokalemia. Objective: Our aim was to identify the prevalence of PA in newly diagnosed hypertensive patients in primary care in Southern Germany. Patients and methods: Newly diagnosed hypertensive patients in 27 primary care centers in Munich agreed to participate to the study. Patients had screening for PA with aldosterone to renin ratio (ARR). In case of elevated ARR, confirmation testing was performed. After diagnosis of PA, subtype differentiation and subsequent therapy of PA was initiated. Results: A total of 235 patients with newly discovered arterial hypertension were initially screened for PA. Of these patients, 35 were excluded because the medication indicated pre-existing treated arterial hypertension or they were on interfering antihypertensive medication. 2.0 % of the patients had hypokalemia at first screening. Of the 200 patients with newly discovered arterial hypertension, 42 had an elevated ARR. The incidence of the presence of a hypokalemia did not differ according to normal or pathological ARR. Nine patients (21 %) did not show up for further testing and were lost to follow-up, 33 patients underwent a saline infusion test. Of these, 11 patients were diagnosed with PA, leading to a prevalence of at least 5.5 % of PA in the collective. None of the diagnosed PA patients was hypokalemic at screening. Conclusion: Our data of untreated newly diagnosed patients with hypertension demonstrates a prevalence of 5.5 % of PA.