Deficiency of vitamin D and elevated aldosterone in prostate hyperplasia

Epidemiological studies have confirmed the association between vitamin D deficiency and benign prostate hyperplasia (BPH). Lately, serum calcium and parathyroid hormones were shown to stimulate prostate growth, assuming an interplay between elements of the calcium metabolism rather than a sole role of any. Finally, aldosterone actions were found to be affected by vitamin D.

We have sufficient reason to believe that human disease, BPH in this case, is a dysfunction of a fine network rather than a failure of a particular substance. Unfortunately, previous studies include results of studies that fall short in combining the overall structure. This study aimed to investigate these four parameters in BPH patients.

Twenty five patients with BPH (median age 62 years) and 30 volunteer healthy controls (median age 63.5 years) were enrolled. Serum total prostate specific antigen (PSA), intact parathormone (PTH), calcium, 25-hydroxy vitamin D (25-(OH) 2D), aldosterone and lipids were measured.

We found serum aldosterone levels significantly higher in BPH patients (p = 0.04). BPH patients had significantly higher serum PSA levels (p < 0.0001). 25-(OH) 2D levels were lower in the BPH group (p = 0.05). Median serum 25-(OH) 2D levels in both groups were lower than the threshold reference limit (20 ng/mL).

The co-existence of vitamin D deficiency and elevated levels of aldosterone in BPH, presented for the first time in literature, strongly favors a link between the renin-angiotensin system (RAS), vitamin D and BPH pathogenesis. Our findings may influence studies with larger groups of subjects.