Endocrine Abstracts

Men with spinal cord injury (SCI) exhibit a prostate volume significantly smaller compared to age-matched able-bodied men^1–3. As men with chronic SCI (lasting more than 1 year) also display a very high prevalence of androgen deficiency^4,5, a protective role of low testosterone against prostate enlargement could be hypothesized in this population. This study aimed to identify independent determinants of prostate volume in men with chronic SCI. As assessed by trans-rectal ultrasonography, the median value of prostate volume in 138 men with chronic SCI (mean age: 53 ± 18 years) was 23.43 ml. Men with prostate volume smaller than 23.4 ml exhibited significantly lower levels of total testosterone (TT) and calculated free testosterone (cFT), as well as a higher prevalence of biochemical androgen deficiency (TT lower than 264 ng/dl), that in the entire population was observed in 29.7% (41/138) of subjects. At the univariate analysis, a larger prostate volume was associated to higher TT (P = 0.00001) and cFT (P = 0.001), SCI level below T12 (P = 0.007), more advanced age (P = 0.04), lower body mass index (P = 0.04), higher functional independence score (P = 0.06), higher values of prostate-specific antigen (P = 0.12) and shorter duration of the injury (P = 0.21). However, at the multiple regression analyses, an independent and positive association only persisted between prostate volume with either TT or cFT levels, and, to a lesser extent, with age and a level of spinal lesion below T12. A prostate volume below the median value (23.4 ml) was observed in 91.4% (32/35) of patients with both biochemical androgen deficiency and spinal lesion level at or above T12, but in only 16.5% (2/12) of patients with both normal androgen levels and spinal lesion level below T12 (P = 0.001). In conclusion, lower testosterone levels and, to a lesser extent, a younger age and a spinal lesion level at or above T12 represent the only variables exhibiting an independent association with a smaller prostate volume in men with SCI. It could be hypothesized that the combination of these factors could be protective against the development of proliferative prostatic diseases, including benign prostatic hyperplasia. Prospective studies might assess the validity of this hypothesis.

References

1. Hvarness et al., Scand J Urol Nephrol. 2007 41(2) 120–123.

2. Bartoletti et al., Eur Urol. 2009 Jul 56(1) 142–148.

3. Pannek et al., BJU Int. 2013 Aug 112(4) 495–500.

4. Barbonetti et al., Andrology. 2014 Sep 2(5) 721–728.

5. Barbonetti et al., J Endocrinol Invest. 2019 Feb 42(2) 167–173.