Impact of pharmacologic therapy for benign prostatic hyperplasia on prostate volume and free testosterone and consequently on urinary parameters and sexual desire in men
Abstract
Background/Aim. Pharmacologic therapy for benign prostatic hyperplasia (BPH) relieves disease progression and affects the androgen hormone status. A decrease in the level of free testosterone (freeT) within total testosterone (totalT) leads to symptoms of sexual dysfunction. The aim of this study was to show the impact of pharmacological treatment for BPH on prostate volume (PV) and levels of freeT and, consequently, on urinary parameters and sexual desire in men during 6 months of administration. Methods. This clinical prospective study included 156 BPH patients with moderate urinary symptoms – International Prostate Symptom Score (IPSS) < 19, PV > 30 mL and prostate specific antigen (PSA) value < 4 ng/mL. The average age of patients was 61.16 ± 2.97 years. The performed tests included determination of tumor markers (PSA, free PSA), hormones (totalT, freeT, freeT/totalT ratio), trans abdominal ultrasonography and uroflowmetry. Urinary symptoms were measured by IPSS and the Quality of Life (QoL) questionnaire while the changes in sexual desire were measured using the International Index of Erectile Function (IIEF) questionnaire. Four groups were formed, 39 patients each. The group 1 received alpha1-blocker (AB) tamsulosin, the group 2, 5 alpha-reductase inhibitor (5-ARI) finasteride, the group 3, combined therapy of both drugs (tamsulosin and finasteride), while the group 4 (control group) had no therapy. Follow-ups were performed every three and six months during therapy administration. Results. Prostate volume significantly decreased in the patients on combined therapy (-6.95 ± 2.00; p < 0.001) and finasteride (-6.67 ± 3.35). In the finasteride group, the levels of freeT (-4.23 ± 5.2; p < 0.001) and freeT/totalT ratio (-0.12 0.08; p < 0.001) significantly decreased as did the freeT (-2.64 ± 7.81) and freeT/totalT ratio (-0.09 ± 0.13) in the combined therapy group. Uroflowmetry showed a significant improvement in all parameters and all the therapy groups. Combined therapy provided the greatest improvement in the maximum flow rate (Qmax) (+4.06 ± 1.75; p < 0.001) and urinary symptoms (-10.95 ± 3.19). A significant improvement of sexual desire occurred in the patients on tamsulosin (+0.78 ± 1.00; p < 0.001), with a slight deterioration in the finasteride group, but without statistical significance. Conclusion. Hormonal component of pharmacologic therapy for BPH most effectively reduces PV and freeT levels, improves urinary symptoms with a slight decline of sexual desire in men on finasteride monotherapy.
References
Patel ND, Parsons JK. Epidemiology and etiology of benign prostatic hyperplasia and bladder outlet obstruction. Indian J Urol 2014; 30(2): 170−6.
Kirby R. Improving lower urinary tract symptoms in BPH. Practitioner 2011; 255(1739): 15−9, 2.
Cooper LA, Page ST. Androgens and prostate disease. Asian J Androl 2014; 16(2): 248−55.
Buvat J, Maggi M, Guay A, Torres LO. Testosterone deficiency in men: systematic Review and standard operating procedures for diagnosis and treatment. J Sex Med 2013; 10: 245−84.
Maggi M, Buvat J, Corona G, Guay A, Torres LO. Hormonal causes of male sexual dysfunctions and their management (hy-perprolactinemia, thyroid disorders, GH disorders, and DHEA). J Sex Med 2013; 10: 661−77.
Seisen T, Rouprêt M, Gallais JL, Costa P. Relevant clinical and bi-ological criteria for the diagnosis of androgen deficiency in the aging male (ADAM). Prog Urol 2012; 22(Suppl 1): S21−6. (French)
Russo A1, La Croce G, Capogrosso P, Ventimiglia E, Colicchia M, Serino A, et al. Latest pharmacotherapy options for benign prostatic hyperplasia. Expert Opin Pharmacother 2014; 15(16): 2319−28.
Osman NI, Mangera A, Chapple CR. Non-Hormonal treatment of BPH/BOO. Indian J Urol 2014; 30(2): 194−201.
Azzouni F, Mohler J. Role of 5α-reductase inhibitors in benign prostatic diseases. Prostate Cancer Prostatic Dis 2012; 15(3): 222−30.
Rick FG, Saadat SH, Szalontay L, Block NL, Kazzazi A, Djavan B, et al. Hormonal manipulation of benign prostatic hyperplas-ia. Curr Opin Urol 2013; 23(1): 17−24.
Giuliano F. Questionnaires in sexual medicine. Prog Urol 2013; 23(9): 811−21.
Paick S, Meehan A, Lee M, Penson D, Wessells H. The relationship among lower urinary tract symptoms, prostate specific antigen and erectile dysfunction in men with benign prostatic hyperplasia: results from the proscar long-term efficacy and safety study. J Urol 2005; 173(3): 903−7.
Kaplan SA, Lee JY, Meehan AG, Kusek JW, MTOPS Research Group. Long-term treatment with finasteride improves clinical progression of benign prostatic hyperplasia in men with an enlarged versus a smaller prostate: Data from the MTOPS trial. J Urol 2011; 185(4): 1369−73.
Zabkowski T. Evaluation of the clinical indications, adverse drug reactions, and finasteride use in patients with benign prostatic hyperplasia in Poland. Pharmacol Rep 2014; 66(4): 565−9.
Kaplan SA, Chung DE, Lee RK, Scofield S, Te AE. A 5-year ret-rospective analysis of 5alpha-reductase inhibitors in men with benign prostatic hyperplasia: Finasteride has comparable uri-nary symptom efficacy and prostate volume reduction, but less sexual side effects and breast complications than dut. Int J Clin Pract 2012; 66(11): 1052−55.
Favilla V, Cimino S, Castelli T, Madonia M, Barbagallo I, Morgia G. Relationship between lower urinary tract symptoms and serum levels of sex hormones in men with symptomatic benign prostatic hyperplasia. BJU Int 2010; 106(11): 1700−3.
Park DS, Hong JY, Hong YK, Lee SR, Hwang JH, Kang MH, et al. Correlation between serum prostate specific antigen level and prostate volume in a community-based cohort: large-scale screening of 35, 223 Korean men. Urology 2013; 82(6): 1394−9.
Welliver C, Butcher M, Potini Y, McVary KT. Impact of alpha blockers, 5-alpha reductase inhibitors and combination therapy on sexual function. Curr Urol Rep 2014; 15(10): 441.
Gur S, Kadowitz PJ, Hellstrom WJ. Effects of 5-alpha reductase inhibitors on erectile function, sexual desire and ejaculation. Expert Opin Drug Saf 2013; 12(1): 81−90.
Gacci M, Eardley I, Giuliano F, Hatzichristou D, Kaplan SA, Maggi M, et al. Critical Analysis of the Relationship Between Sexual Dysfunctions and Lower Urinary Tract Symptoms Due to Be-nign Prostatic Hyperplasia. Eur Urol 2011; 60(4): 809−25.
Irwig MS. Persistent sexual side effects of finasteride: Could they be permanent. J Sex Med 2012; 9(11): 2927−32.
Trost L, Saitz TR, Hellstrom WJ. Side effects of 5-alpha reduc-tase inhibitors A comprehensive review. Sex Med Rev 2013; 1: 24−41.
Lee JH, Kim Y, Park YW, Lee DG. Relationship between be-nign prostatic hyperplasia/lower urinary tract symptoms and total serum testosterone level in healthy middle-aged eugonad-al men. J Sex Med 2014; 11(5): 1309−15.
Kim MK, Zhao C, Kim SD, Kim DG, Park JK. Relationship of sex hormones and nocturia in lower urinary tract symptoms induced by benign prostatic hyperplasia. Aging Male 2012; 15(2): 90−5.
Joo KJ, Sung WS, Park SH, Yang WJ, Kim TH. Comparison of α-blocker monotherapy and α-blocker plus 5α-reductase inhibitor combination therapy based on prostate volume for treatment of benign prostatic hyperplasia. J Int Med Res 2012; 40(3): 899−908.
Son H, Cho SY, Park S, Kang JY, Kim CS, Kim HG. A retrospec-tive study of clinical outcomes of α-blocker or finasteride monotherapy followed by combination therapy: determination of the period of combination therapy of α-blocker and finas-teride. Int J Clin Pract 2013; 67(4): 351−5.
Bechis SK, Otsetov AG, Ge R, Olumi AF. Personalized Medicine for the Management of Benign Prostatic Hyperplasia. J Urol 2014; 192(1): 16−23.