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ipertrofia prostatica benigna.PPT [Sola lettura] - E-learning

ipertrofia prostatica benigna.PPT [Sola lettura] - E-learning

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ALPHA-BLOCKER<br />

Rationale<br />

• The rationale for a-adrenergic blockers in the treatment of<br />

BPH is based on the hypothesis that the pathophysiology<br />

of clinical BPH is in part caused by BOO, which is<br />

mediated by a1 adrenoceptors (a1 AR) associated with<br />

prostatic smooth muscle (Caine, 1986).<br />

• Several investigators subsequently demonstrated that the<br />

tension of prostate smooth muscle is mediated by the a1<br />

AR (Hieble et al, 1985; Lepor et al, 1988; Gup et al, 1989).<br />

• The most definitive evidence that blockade of prostate a1<br />

AR relieves BOO was the observed direct relationship<br />

between the area density of prostate smooth muscle and<br />

the change in the PFR in 26 subjects undergoing prostatic<br />

biopsy before initiating a-blocker therapy with terazosin<br />

(Shapiro et al, 1992).<br />

Finasteride<br />

FINASTERIDE<br />

Rationale<br />

• The rationale for androgen suppression is based<br />

on the observation that the embryonic<br />

development of the prostate is dependent on the<br />

androgen dihydrotestosterone (DHT) (Shapiro,<br />

1990).<br />

• Testosterone is converted to DHT by the enzyme<br />

5a-reductase. The genetic deficiency of 5areductase<br />

in males results in a rudimentary<br />

prostate and in feminized external genitalia<br />

(Walsh et al, 1974).<br />

• The development of BPH is also an androgendependent<br />

process (Coffey and Walsh, 1990).<br />

Laser<br />

Termoterapia<br />

< 40-60 grammi > 40-60 grammi<br />

Microonde<br />

Radiofrequenza<br />

8

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