PERBEDAAN IPSS, Q MAX, DAN VOLUME PROSTAT PADA PEMBERIAN KOMBINASI INHIBITOR 5α-REDUKTASE (DUTASTERIDE) DAN ANTI ESTROGEN (TAMOXIFEN) PADA PASIEN BPH YANG MENGALAMI LUTS TANPA KOMPLIKASI

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Kurnia Penta Seputra Soetojo Soetojo Doddy M Soebadi

Abstract

Objective: To compare the IPSS, Q max, and volume of the prostate pre and post treatment of 5α-reductase inhibitor and tamoxyfen in patients with BPH. Material and Methods: We collected 40 patients who had been diagnosed as BPH without urine retention. They were classified in to 4 groups, each group contained of 10 patients who were given tamoxifen, dutasteride, combination tamoxyfen with dutasteride, or placebo. We recorded IPSS, uroflow, and volume of the prostate before and after 3 months of medication. Data were analyzed by the SPSS 12 program. Results: Q max (7,75 + 3,5538 to 9,15 + 2,9448) and IPSS (z score –1,633) after treatment with tamoxyfen (p > 0,05) was not improved. We found significant decrease of the prostate volume (40,124 + 7,9129 to 36,323 + 8,2573) after treatment with tamoxifen (p < 0,05). There is significant improvement of Q max (9,55 + 3,2793 to 15,12 + 4,3522), IPSS (z score –2,887), and significant decrease of the prostate volume (30,93 + 9,0031 to 24,506 + 7,3267) after treatment with dutasteride (p < 0,05). There was also significant improvement of Q max (6,55 + 2,5435 to 8,86 + 4,4475), IPSS (z score –2,449), and decrease of prostate volume (31,403 + 9,0031 to 26,78 + 7,3267) after treatment with the combination dutasteride and tamoxifen (p < 0,05). None of those parameters were improved in placebo group. Conclusion: Q max and IPSS improve significantly in the dutasteride and the combination group. There was a significant decrease of the prostate volume in all groups except the placebo group.


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Keywords

BPH, LUTS, dutasteride, tamoxifen

References

Boyle P, Liu GF. Epidemiology and natural history. In: Chatelain C, Denis L. Benign prostate hyperplasia, 5th Eds. United Kingdom: Plymbrige; 2001. p. 19 – 61.

Jones D A. Benign prostatic hypertrophy and lower urinary tract dysfunction. In: Weis MR, George N Jr., O’Reilly P H, eds. Comprehensive Urology. London: Mosby; 2001. p. 451 – 63.

Presti JC Jr. Neoplasma of the prostate gland. In: Tanagho EA, Mc Anich JW, eds. Smith’s General Urology, 15th Ed. International edition. Mcgraw Hill; 2000. p. 399 – 417.

Prasetyo RB, Soetojo. Profile BPH di RSU Dr. Soetomo Surabaya periode Januari 2005 – Desember 2005. Surabaya 2006. p. 1 – 29.

Rahardjo D. Prostat. Edisi 1. Asian Medical. Jakarta 1999. p. 10 – 11.

Lee C, Cockett A. Regulation of prostate growth. In: Chatelain C, Denis L. dkk. Benign prostate hyperplasia, 5th Eds. United Kingdom: Plymbrige; 2001. p. 81 – 99.

Hardjowijoto S, Taher A. Pedoman penatalaksanaan BPH di Indonesia. Surabaya 2003. p. 1 – 10.

Soetojo. Pengaruh pemberian kombinasi 5α reduktase inhibitor dan estrogen pada proliferasi jaringan Pprostat. Surabaya 2004. p. 1 – 169.

Nugroho E, Soetojo. Perbandingan kadar estrogen dalam serum dan TGF-1 dalam plasma pada penderita BPH – non BPH di atas 50 tahun, dan usia muda. Surabaya 2006. p. 1 – 72.

Tewari A, Shinohara K, Narayan P. Transition zone volume and transition zone ratio: predictor of uroflow response to finasteride therapy in benign prostatic hyperplasia patients, discussion 265. Urology. 1995; 45: 258 – 64.

Seppelt U. Correlation among prostat stroma, plasma estrogen levels, and urinary estrogen excretion in patients with benign prostatic hypertrophy. Journal of Clinical Endocrinology & Metabolism. 1978; 47: 1230 – 5 (Abstract).

Marberger M, Roehborn CG. Relationship among serum testosterone, sexual function and response to treatment in men receiving dutasteride for benign prostatic hyperplasia. The journal of clinical endocrinology & metabolism. January 2006; 91 (4): 1323 – 8.

Group FS. Finasteride (MK-906) in the treatment of benign prostatic hyperplasia. The Finasteride study group, prostat. 1993; 22: 291 – 9.

Goldfien A. Hormon dan penghambat gonad. Dalam: Katzung BG. Farmakologi dasar dan klinik, edisi 6. EGC: Jakarta; 1997. p. 633 – 60.

Brosman SA. Prostate spesific antigen. June 17, 2002. http://www.emedicine.com

Partin AW, Rodriguez R. The molecular biology, endocrinology, and physiology of the prostat and seminal vesicles. Dalam: Walsh PC, Retik AB, Vaughan ED Jr, Wein A, eds. Campbell’s urology, 8th ed. WB Saunders: Philadelphia; 2002. p. 1237 – 84.

Matsuda T, Yamamoto T, Muraguchi A, Saatcioglu F: Cross-talk between transformating growth factor-beta and estrogen reseptor signaling Through Smad3. J. Biol Chem. 2001; 276 (46): 42908 – 14.

Dolder CR. Dutasteride: A dual 5α reductase inhibitor for the treatment of symptomatic benign prostatic hyperplasia. The Annals of pharmacotherapy. 2006; 40 (4): 658 – 65.

Gittelman M. Dutasteride improves objective and subjective disease measures in men with benign prostatic hyperplasia and modest or severe prostat enlargement. Journal of Urology. 2006; 176 (3): 1045 – 50.

Liu J. Effect of tamoxifen on stromal protein syntesis in human prostate. Journal of clinical endocrinology and metabolism. 1984; 59: 710 – 3.

Di Silverio F. D'Eramo G: Pharmacological combinations in the treatment of benign prostatic hypertrophy. J. Urol. France. 1993; 99 (6): 316 – 20.

Habib FK. Effects of tamoxifen on the binding and metabolism of testosteron by human prostatic tissue and plasma in vitro. Journal of Endocrinology. 1979; 83 (3): 369 – 78.

Clark RV, Hermann DJ. Marked suppression of dihydrotestosteron in men with benign prostatic hyperplasi by dutasteride a dual 5α-reductase inhibitor. The journal clinical endokrinology and metabolism. 2004; 89 (5): 2179 – 84.

Nickel JC. Placebo therapy of benign prostatic hyperplasia: A 25-Month Study, Brit. J. Urol. 1998; 81: 383 – 7.

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Department of Urology, Faculty of Medicine/Airlangga University