Effect of GH and/or testosterone deficiency on the prostate: an ultrasonographic and endocrine study in GH-deficient adult patients

Citation
A. Colao et al., Effect of GH and/or testosterone deficiency on the prostate: an ultrasonographic and endocrine study in GH-deficient adult patients, EUR J ENDOC, 143(1), 2000, pp. 61-69
Citations number
31
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
EUROPEAN JOURNAL OF ENDOCRINOLOGY
ISSN journal
08044643 → ACNP
Volume
143
Issue
1
Year of publication
2000
Pages
61 - 69
Database
ISI
SICI code
0804-4643(200007)143:1<61:EOGATD>2.0.ZU;2-R
Abstract
Background: The role of IGF-I in prostate development is currently under th orough investigation since it has been claimed that IGF-I is a positive pre dictor of prostate cancer. Objective: To investigate the effect of chronic GH and IGF-I deficiency alo ne or associated with testosterone deficiency on prostate pathophysiology i n a series of patients with hypopituitarism. Design: Pituitary, androgen and prostate hormonal assessments and transrect al prostate ultrasonography (TRUS) were performed in 30 men with adulthood onset GH deficiency (GHD) and 30 age-matched healthy controls, free from pr evious or concomitant prostate disorders. Results: Plasma IGF-I levels were significantly lower in GHD patients than in controls (Pearson's coefficient P < 0.0001). At study entry, 6 of the 13 hypogonadal patients and 7 of the 17 eugonadal patients had plasma IGF-I b elow the age-adjusted normal range. At study entry, testosterone levels wer e low in 13 patients (mean +/- S.E.M., 3.8 +/- 1.0 nmol/l) while they were normal in the remaining 17 (19.4 +/- 1.4 nmol/l). No difference in prostate -specific antigen (PSA), and PSA density was found between GHD patients (ei ther hypo- or eugonadal) and controls, while free PSA levels were significa ntly higher in eugonadal GHD than in controls (0.4 +/- 0.04 vs 0.2 +/- 0.03 mu g/l; P < 0.01). No difference in antero-posterior prostate diameter and transitional zone v olume (TZV) was observed among groups, while both transverse and cranio-cau dal diameters were significantly lower in hypogonadal (P < 0.01) and eugona dal GHD patients (P < 0.05) than in controls. Prostate volume (PV) was sign ificantly lower in hypogonadal GHD patients (18.2 +/- 3.0 ml) and eugonadal GHD patients (22.3 +/- 1.6 ml), than in controls (25.7 +/- 1.4, P < 0.05). The prevalence of prostate hyperplasia (PV > 30 ml) was significantly lowe r in hypogonadal and eugonadal GHD patients, without any difference between them (15.3% and 5.8%), than in controls (43.3%) (chi(2) = 6.90, P = 0.005) . No difference was found in PV between patients with normal or deficient I GF-I levels both in the hypogonadal group (19.9 +/- 4.7 vs 17.3 +/- 4.0 ml) and in the eugonadal group (22.6 +/- 2.3 vs 21.8 +/- 2.5 ml). When control s and patients were divided according to age (<60 years and >60 years), PV was significantly lower in hypogonadal GHD patients aged below 60 years tha n in age-matched controls (P < 0.01) or eugonadal GHD patients (P < 0.01), without any difference between controls and eugonadal GHD patients. Control s aged above 60 years had significantly higher PV than both hypogonadal and eugonadal GHD patients (P < 0.01), Calcifications. cysts or nodules were f ound in 56.7% of patients and in 50% of controls (chi(2) = 0.067, P = 0.79) . In controls, but not in GHD patients, PV and TZV were correlated with age (r = 0.82, r = 0.46, P < 0.0001 and P < 0.01 respectively). PV was also co rrelated with GH (r = -0.52, P = 0.0026), IGF-I (r = -0.62, P = 0.0002) and IGF-binding protein 3 (IGFBP-3) levels (r = -0.39, P = 0.032) but neither with testosterone or dihydrotestosterone (DHT) levels. In GHD patients TZV but not PV was correlated with age (r = 0.58, P = 0.0007) and neither TZV n or PV were correlated with GH, IGF-I or IGFBP-3 levels. Conclusions: Chronic GH deficiency in adulthood causes a decrease in prosta te size, mostly in patients with concomitant androgen deficiency and age be low 60 years, without significant changes in the prevalence of structural p rostate abnormalities.