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Benign Prostatic Hyperplasia
Reversal of Benign Prostate Hyperplasia by
Super-selective Intraprostatic Androgen Deprivation Therapy
Yigal Gat
1,2
and Michael Gornish
2
1. Sub-micron Research, Condensed Matter Physics, Weizmann Institute of Science, Rehovot;
2. Andrology and Interventional Radiology, Maynei Hayeshua Medical Centre, Bnei Brak
Abstract
The prostate – an exocrine gland regulated by testosterone that is produced by the testes – is an essential and integral part of the male
reproductive system. By producing approximately 30% of the non-cellular components of semen, it has a crucial and essential function in
the creation of an optimal environment for the survival and motility of sperm in the long, hostile route to meet and fertilise the egg in the
fallopian tube. Benign prostate hyperplasia (BPH) is the most common benign neoplasm in men. Although testosterone has been known to
be the promoter of prostate cell proliferation since 1941, when Huggins and Hodges published their landmark work on prostate cancer, in
the 60 years that have passed no causal relationship between serum testosterone and BPH has yet been established. The aetiology of BPH
is unknown, and researchers have been puzzled by the following paradox: relatively low levels of serum testosterone are found in patients
with BPH. Thus, it has remained unclear whether BPH is related to serum testosterone or attributable to other factors. Recent studies have
proposed a novel and tested explanation of a pathophysiological mechanism for the evolution of BPH and suggest a tested and effective
treatment. It was found that in all BPH patients the one-way valves (OWVs) in the vertically orientated internal spermatic veins (ISVs) are
destroyed (clinically manifested as varicocele, a phenomenon that increases rapidly with age). It causes elevated hydrostatic pressure –
some six-fold greater than normal in the venous drainage of the male reproductive system – which leads to a unique biological phenomenon:
venous blood flows retrograde from the higher pressures in the testicular venous drainage system to the lower pressures in the prostatic
drainage system. Free testosterone (FT) levels in this blood are markedly elevated, with a concentration of some 130 times serum level.
Consequently, the prostate is exposed to increased venous pressure, which causes hypertrophy, and elevated concentrations of FT, causing
hyperplasia. BPH patients were treated using the Gat–Goren technique, which restores normal pressure in the venous drainage of the male
reproductive system, eliminating back-pressure and the back-flow of blood from the testicular to the prostate drainage system.
Consequently, stable reduction in prostate volume and regression of prostate symptoms were observed in the treated patients.
Keywords
Benign prostate hyperplasia (BPH), testicular drainage systems, super-selective intraprostatic androgen deprivation therapy
Disclosure: The authors have no conflicts of interest to declare.
Received: 30 May 2009 Accepted: 10 July 2009
Correspondence: Yigal Gat, Sub-micron Research, Condensed Matter Physics, Weizmann Institute of Science, Rehovot, 76100 Israel. E: yigal.gat@weizmann.ac.il
The prostate is an integral and essential part of the male reproductive sex-hormone-binding globulin (SHBG), in which form it is not able to
system. It is a testosterone-regulated exocrine gland producing >30% diffuse into the prostatic cells. Upon entering the prostatic cell
of the non-cellular components of the semen, promoting optimal cytoplasm, 90% of FT is converted irreversibly by the 5α-reductase
conditions for survival and motility of sperm in the hostile environment enzymes to dihydrotestosterone (DHT) – a more potent androgenic
in the vagina and retaining its reproductive potential for fertilisation in hormone that has an obligatory role in the development of BPH.
the fallopian tube. DHT has a five- to 10-fold higher affinity for the androgen receptor
(AR) than FT.
2–4
FT and DHT control and regulate a diverse range of
The testes are the production site of two products: sperm and free target genes to produce various proteins that are involved in
testosterone (FT). The testes drain their waste products and FT via prostate cell proliferation, survival, maintenance, homeostasis,
the internal spermatic veins (ISVs) to the systemic circulation. angiogenesis, differentiation and apoptosis.
2,3
Epidemiological studies in castrated males strongly support the
important role of the testes in the pathogenesis of benign prostate The one-way valves (OWVs) in the ISVs facilitate venous blood flow
hyperplasia (BPH).
1,2
FT diffuses into prostate cells and is known to upwards against gravity since there is no ‘active pump’ in the
be a promoter of prostate cell proliferation.
3
It is mainly produced vertically orientated testicular venous drainage system found in
by the testes and, under normal conditions, reaches the systemic the erect male. Recent studies have demonstrated that the
blood through the testicular venous drainage system (ISV; see destruction of OWVs, recognised clinically as varicocele, is a bilateral
Figure 1). It eventually reaches the prostate via the prostate artery vascular disease.
5,6
Its incidence is high in the ageing male,
7
with a
after it has passed through the venous and arterial circulation, prevalence that increases rapidly with age, reaching >75% at 70 years
where it undergoes marked dilution and >98% binds to albumin and of age
7
and >86% above 80 years of age.
8
10 © TOUCH BRIEFINGS 2009
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