An investigation on the relevance of prolactin, insulin-like growth factor-1 and 25-hydroxyvitamin D(25-OHD) in canine benign prostatic hyperplasia in a predisposed breed model.

Abstract

Serum concentrations of prolactin (PRL), insulin-like growth factor-1 (IGF-1) and 25 hydroxyvitamin D(25-OHD) were analysed to investigate their possible involvement in the pathogenesis of benign prostatic hyperplasia (BPH). For this, dogs of the Rhodesian Ridgeback (RR) breed were used because of a verified breed disposition for the development of BPH. Labrador Retrievers (LR) served as controls. The prostate gland status was characterised by the prostate gland volume, clinical signs of BPH (haemospermia and sonographic findings) and the plasma concentration of canine prostate-specific arginine esterase (CPSE). Breed specificity in the RR was expressed by a correlation of PRL with breed (p&#xa0;<&#xa0;0.05). Similar relationships existed in the dogs with normal CPSE (CPSEn) with respect to the IGF-1 concentrations (LR: p&#xa0;<&#xa0;0.05). The latter were negatively correlated with prostatic volume and age (both p&#xa0;<&#xa0;0.05). Concentrations of 25-OHDwere tendentially (p&#xa0;=&#xa0;0.18) lower in the RR with increased CPSE (CPSEi) compared with the CPSEn LR and RR showing clinical signs of BPH. A negative correlation between serum 25-OHDand age (p&#xa0;<&#xa0;0.05) existed in the CPSEi RR. Proof of 25-OHDin prostatic secretion proved to be a breed specific feature in the RR (p&#xa0;<&#xa0;0.0001). For all RR dogs showing clinical signs of BPH, a close to significant (p&#xa0;=&#xa0;0.06) positive correlation with prostate gland volume was found. The results of the present study reveal no clear hints towards the significance of PRL and IGF-1 in the pathogenesis of canine BPH. In the RR breed there were indications of a causal relationship with age-dependent changes in the vitamin D metabolism. The data suggest the possibility of preventing or treating canine BPH by administering vitamin D or substances involved in the intraprostatic vitamin D metabolism.