Reversal of benign prostate hyperplasia by selective occlusion of impaired venous drainage in the male reproductive system: novel mechanism, new treatment.
The prostate is an androgen-regulated exocrine gland producing over 30% of the noncellular components of the semen and promoting optimal conditions for survival and motility of sperm in the vagina. Benign prostate hyperplasia (BPH) is the most common benign neoplasm in men. Its aetiology is not clear, and therefore, current medical treatments are directed towards the symptoms. Though testosterone is known to be the promoter of prostate cell proliferation, no causal relation between serum testosterone levels and BPH has been found. In this study, we propose a novel and tested pathophysiological mechanism for the evolution of BPH and suggest a tested and effective treatment. We found that in all BPH patients, the one-way valves in the vertically oriented internal spermatic veins are destroyed (clinically manifested as varicocele), causing elevated hydrostatic pressure, some 6-fold greater than normal, in the venous drainage of the male reproductive system. The elevated pressure propagates to all interconnected vessels leading to a unique biological phenomenon: venous blood flows retrograde from the higher pressure in the testicular venous drainage system to the low pressure in the prostatic drainage system directly to the prostate (law of communicating vessels). We have found that free testosterone levels in this blood are markedly elevated, with a concentration of some 130-fold above serum level. Consequently, the prostate is exposed to: (i) increased venous pressure that causes hypertrophy; (ii) elevated concentration of free testosterone causing hyperplasia. We have treated 28 BPH patients using a technique that restores normal pressure in the venous drainage in the male reproductive system. The back-pressure and the back-flow of blood from the testicular to the prostate drainage system were eliminated and, consequently, a rapid reduction in prostate volume and a regression of prostate symptoms took place.
Gat
Y
Y
Andrology-Interventional Radiology Maynei Hayeshua Medical Center and Sub-Micron Research Department ofCondensed Matter Physics, Weizmann Institute of Science, Rehovot, Israel.yigalgat@weizmann.ac.il
Gornish
M
M
Heiblum
M
M
Joshua
S
S
D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D005500:Follow-Up Studies; D006801:Humans; D006874:Hydrostatic Pressure / Q000009:adverse effects; D008297:Male; D008866:Microsurgery / Q000379:methods*; D008875:Middle Aged; D010690:Phlebography / Q000379:methods*; D011187:Posture / Q000502:physiology; D011467:Prostate / Q000098:blood supply / Q000503:physiopathology / Q000601:surgery; D011470:Prostatic Hyperplasia / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*; D012189:Retrospective Studies; D015911:Sclerotherapy / Q000379:methods*; D013737:Testis / Q000098:blood supply; D013739:Testosterone / Q000097:blood; D014646:Varicocele / Q000150:complications* / Q000503:physiopathology / Q000628:therapy*
D013739:Testosterone