The role of insulin-like growth factor I (IGF-I) in prostate development is currently under thorough investigation because it has been claimed that IGF-I is a positive predictor of prostate cancer. To assess the effect of GH and IGF-I levels on prostate pathophysiology, 46 acromegalic (30 in active disease, 10 cured from acromegaly, and 6 affected from GH deficiency) and 30 age-matched male controls, free from previous or concomitant prostate disorders, underwent pituitary, androgen, and prostate hormonal assessments and transrectal ultrasonography. Compared to control values, GH (P <0.0001), IGF-I (P <0.0001), and IGFBP-3 (P <0.001) levels were increased, whereas testosterone (P <0.0001) and dihydrotestosterone levels (P <0.0001) were reduced in active acromegalic patients. Hypogonadism was present in 28 of the 46 acromegalic patients (60.8%). The antero-posterior (P <0.05), and transverse (P <0.0001) prostate diameters and the transitional zone volume (P <0.05) were increased in acromegalic patients compared to those in controls. Prostate volume (PV) was significantly higher in untreated acromegalic patients than in controls (41.7 ± 3.2 vs. 21.9 ± 1.4 mL; P <0.0001), cured patients (23.6 ± 1.6 mL; P <0.0001), and GH-deficient patients (17.5 ± 1.1 mL; P <0.0001). In the patients, PV was correlated with disease duration (r = 0.606; P <0.0001) and age (r = 0.496; P <0.0001), whereas in controls it was correlated with age (r = 0.476; P <0.01) and IGF-I levels (r = -0.448; P <0.05). Benign prostate hyperplasia (PV ≥30 mL) was found in 58% of the acromegalics and 26.6% of the controls. When grouped by age (60 yr), PV was increased in elderly patients compared to younger patients (P <0.05) and to controls (P <0.01). The prevalence of structural abnormalities, including calcifications, nodules, cysts, and vesicle inflammation, was significantly increased in patients compared to controls (78.2% vs. 23.3%; X 2 = 5.856; P <0.05). No clinical, transrectal ultrasonography, or cytological evidence of prostate cancer was detected in acromegalic or control subjects. In conclusion, chronic excess of GH and IGF-I cause prostate overgrowth and further phenomena of rearrangement, but not prostate cancer.
|Number of pages||6|
|Journal||Journal of Clinical Endocrinology and Metabolism|
|Publication status||Published - 1999|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism