Finasteride-Its Impact on Sexual Function and Prostate Cancer

Abstract

Finasteride, a specific and competitive inhibitor of 5alpha-reductase enzyme Type 2, inhibits the conversion of testosterone to dihydrotestosterone (DHT). In adults, DHT acts as primary androgen in prostate and hair follicles. The only FDA-approved dermatological indication of finasteride is androgenetic alopecia. But, apprehension regarding sexual dysfunction associated with finasteride deters dermatologists from prescribing the drug and patients from taking the drug for androgenetic alopecia. Testosterone, through its humoral endocrine and local paracrine effects is relevant in central and peripheral modulation of sexual function than locally acting DHT. Several large population-based long-term placebo-controlled studies, using International Index of Erectile Function-5 questionnaire and objective method (Nocturnal Penile Tumescence) to assess the erectile function have demonstrated no clear evidence of the negative effect of finasteride on erectile function. Reduction in ejaculatory volume is the only established causal relationship between finasteride and sexual dysfunction. Though finasteride causes significant reduction in all the semen parameters except sperm morphology, they did not fall below the threshold levels to interfere with fertility. Therefore, the sexual adverse effects associated with finasteride should be viewed in relation to normal prevalence and natural history of erectile dysfunction in the population, age of the patient, other confounding factors and also nocebo effect. The impact of finasteride on the prevention of prostate cancer has been discussed extensively. Finasteride is found to be effective in significantly reducing the incidence of low-grade prostate cancer. But the paradoxical increase in high-grade cancer in the finasteride group has been attributed to increased sensitivity and improved performance of prostate specific antigen levels to detect all grades of prostate cancer.

Full text

Journal of Cutaneous and Aesthetic Surgery - Jan-Jun 2009, Volume 2, Issue 1
12
Anitha B, Arun C Inamadar, Ragunatha S
Department of Dermatology, Venereology and Leprosy, Shri B.M. Patil Medical College Hospital and Research Centre, Bijapur, Karnataka, India
DOI: 10.4103/0974-2077.53093
Address for correspondence:
Dr. Arun C. Inamadar, Department of Dermatology, Venereology and Leprosy, Shri B.M. Patil Medical College Hospital and Research Centre, Bijapur - 586 103,
Karnataka, India. E-mail: aruninamadar@gmail.com
PHARMACOLOGY OF FINASTERIDE
Finasteride is a specic and competitive inhibitor of
Type 2 5α-reductase. The enzyme, 5α-reductase is
required for conversion of testosterone to DHT. It exists
in two isoenzyme forms. Type 1 is predominant in the
sebaceous glands and liver, and Type 2 is predominant in
the prostate, seminal vesicles, epididymes, hair follicles
and liver.[3] Finasteride has no afnity for androgen
receptor and hence has no androgen-related actions like
androgenic, antiandrogenic, estrogenic, antiestrogenic or
progestational effects.[4]
The administration of finasteride 5 mg/day for the
treatment of BPH results in 60-93% reduction in
circulating DHT levels from the baseline[1] with a 15 - 25%
rise in testosterone levels.[2,5]. The effects of nasteride
5 mg and 1 mg/day result in almost similar changes in
DHT and testosterone levels in serum, prostate and scalp
skin. However, a signicantly greater fall of prostate
INTRODUCTION
Androgens, otherwise known as sex hormones, are
essential for the development of external genitalia, testes,
and maintenance of spermatogenesis and secondary
sexual characters. Testosterone and dihydrotestosterone
(DHT) are the main biologically active forms of
androgens. Testosterone is synthesized by both
gonads and adrenal glands. In the testes, testosterone
is synthesized by the Leydig cells in response to
stimulation by lutenizing hormone.[1] In men, 4-8% of
testosterone is converted to the more potent androgen,
DHT by the action of 5α-reductase enzyme.[2] During
embryogenesis, testosterone plays a role in Wolfan
ductal differentiation whereas DHT mediates male
external genitalia and prostate differentiation.[3] In
adults, DHT acts as primary androgen in prostate and
hair follicles which tend to accelerate benign prostatic
hypertrophy (BPH) and androgenetic alopecia.[2]
Finasteride, a specific and competitive inhibitor of 5α-reductase enzyme Type 2, inhibits the conversion of testosterone
to dihydrotestosterone (DHT). In adults, DHT acts as primary androgen in prostate and hair follicles. The only
FDA-approved dermatological indication of finasteride is androgenetic alopecia. But, apprehension regarding sexual
dysfunction associated with finasteride deters dermatologists from prescribing the drug and patients from taking the
drug for androgenetic alopecia. Testosterone, through its humoral endocrine and local paracrine effects is relevant
in central and peripheral modulation of sexual function than locally acting DHT. Several large population-based
long-term placebo-controlled studies, using International Index of Erectile Function-5 questionnaire and objective
method (Nocturnal Penile Tumescence) to assess the erectile function have demonstrated no clear evidence of the
negative effect of finasteride on erectile function. Reduction in ejaculatory volume is the only established causal
relationship between finasteride and sexual dysfunction. Though finasteride causes significant reduction in all the
semen parameters except sperm morphology, they did not fall below the threshold levels to interfere with fertility.
Therefore, the sexual adverse effects associated with finasteride should be viewed in relation to normal prevalence
and natural history of erectile dysfunction in the population, age of the patient, other confounding factors and
also nocebo effect. The impact of finasteride on the prevention of prostate cancer has been discussed extensively.
Finasteride is found to be effective in significantly reducing the incidence of low-grade prostate cancer. But the
paradoxical increase in high-grade cancer in the finasteride group has been attributed to increased sensitivity and
improved performance of prostate specific antigen levels to detect all grades of prostate cancer.
KEYWORDS: Finasteride, prostate cancer, sexual function
Finasteride-Its Impact on Sexual Function and Prostate Cancer
rEViEW articlE
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Anitha, et al.: Finasteride
DHT levels after six to eight weeks of therapy has
been reported in patients taking nasteride 5 mg/ day
compared to those taking nasteride 1 mg/day.[6]
The bioavailability of nasteride 1 mg following oral
intake ranges from 26-170% with a mean of 65%.
The average peak plasma concentration has been
found to be 9.2 ng/mL measured 1-2 h post dose.
The bioavailability of nasteride is not related to food
intake. Finasteride is extensively metabolized in the
liver by Cytochrome P450 3A4 enzyme subfamily and
excreted both in urine and feces. The terminal half-life is
approximately 5-6 h in men between 18-60 years of age
and 8 h in men more than 70 years of age.[4]
The FDA-approved dermatologic indication is male
pattern androgenetic alopecia. Other dermatologic
uses include hirsutism, acne vulgaris, and hidradenitis
suppurativa. Various adverse effects of finasteride
include sexual dysfunctions; hypersensitivity reactions
such as rash, pruritus, urticaria, and swelling of the lips
and face; breast tenderness and enlargement; severe
myopathy and testicular pain. It is also known to have
teratogenic effects in animals.[7]
FINASTERIDE AND SEXUAL FUNCTION
To understand the impact of finasteride on sexual
function, it is important to know the normal physiology
of male sexual function and the role of testosterone and
DHT in erectile function.
Normal male sexual function
Male sexual function normally requires intact libido;
the ability to achieve and maintain penile erection;
ejaculation; and detumescence. Androgens, especially
testosterone increases the libido. A variety of visual,
olfactory, tactile, auditory and imaginative stimuli can
also inuence the libido. The penile erection is mainly
under the control of the parasympathetic nervous system.
The nitric oxide released from the non-adrenergic, non-
cholinergic autonomic bers causes relaxation of smooth
muscles in the penis, leading to increased ow and
accumulation of blood in the lacunar network of corpora
which are converted into non-compressible cylinders
resulting in erection. The nitric oxide is synthesized in
the cavernosal tissue of penis by nitric oxide synthetase.
Ejaculation and detumescence require intact sympathetic
system.[8]
Role of androgens in erectile function
The integrity of structural and cellular components of
the penis, and veno-occlusive mechanism is essential
for normal erectile function. It has been demonstrated
that deprivation of testosterone results in apoptosis
of cells from the cavernosal and spongiosal tissue. In
animal experiments on castrated rats, the importance of
testosterone in normalizing erectile function and nitric
oxide synthetase activity has been demonstrated.[1] Even
an individual with low testosterone levels can achieve
erection. However, in elderly males, normal testosterone
levels appear to be important for erection.[8] Unlike
testosterone, DHT does not seem to affect the erectile
function. DHT is a paracrine hormone exerting its action
in the tissue of origin. The intact erectile function in the
presence of low DHT levels in men with 5α- reductase
enzyme deciency and in men receiving nasteride,
and restoration of erectile function in hypogonadal
men in response to 7-alpha- methyl- 9-nortestosterone,
a 5α-reductase-resistant androgen, suggests that
conversion of testosterone to DHT is not necessary for
penile erection.[1]
Thus, the testosterone, through its humoral endocrine
and local paracrine effects is relevant in central and
peripheral modulation of sexual function than locally
acting DHT.[1]
Finasteride and sexual dysfunction
A comprehensive literature review of all the publications
concerning 5α-reductase inhibitors and sexual adverse
effects has revealed that sexual adverse effects occur at
the rates of 2.1-38%, erectile dysfunction (ED) being the
commonest followed by ejaculatory dysfunction and
loss of libido.[9]
Erectile dysfunction
Review of the literature on ED in men taking nasteride
revealed the incidence of ED to be between 0.8-33%.
However, randomized controlled studies reported ED
to be between 0.8-15.8%.[1]
The clinical studies which reported increased incidence
of ED in patients taking nasteride (5 mg or 1 mg/ day)
did not either assess the baseline sexual function or
use a validated questionnaire.[10-12] The ED occurred
predominantly during the first year of therapy and
subsequently by the end of three to seven years of therapy
it resolved completely in half of the patients.[13-15] Thus
the prevalence of ED declined with increased duration
of therapy. Therefore, large population-based long-term
placebo-controlled clinical studies using a validated
questionnaire and objective method of assessment of
sexual function are required to establish the causal
relationship between nasteride and ED.
The Proscar (Finasteride 5 mg/day) Long-term Efcacy
and Safety Study (PLESS) where more than 3000 men
with benign prostatic hyperplasia (BPH) were assessed
over a period of four years concluded that mild to
moderate ED which resolved in about half of the patients
after discontinuation of either nasteride or placebo, is
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Anitha, et al.: Finasteride
consistent with the natural history of ED in the patient
population (>50 years) and concurrent substantial
placebo effect.[15] In a double-blind placebo-controlled
study using nocturnal penile tumescence (NPT) as
an objective method of assessing erectile function,
nasteride (5 mg/day for 12 weeks) failed to suppress
consistent sleep- related penile erections.[16]
The clinical trials using International Index of Erectile
Function-5 (IIEF-5) questionnaire to assess the sexual
adverse effects of finasteride 1 mg/day used in the
treatment of male pattern hair loss have reported no
statistically signicant difference between the IIEF-5 scores
obtained in patients receiving nasteride and placebo.
[17,18]
The ED due to nasteride has also been related to the
nocebo effect i.e., an adverse effect that is not a direct
result of the specic pharmacological action of the drug.
In a study, the group informed about the sexual adverse
effects of nasteride reported increased incidence of ED
when compared to the group without such information.[19]
Dutasteride, a dual 5α-reductase enzyme inhibitor,
reduces the DHT levels to a greater extent than
nasteride. Several placebo-controlled studies have
evaluated the efcacy and side-effects of dutasteride
0.5 mg/day in the treatment of BPH and prostate cancer.
The ED has been reported to be signicantly higher
in the dutasteride group than in the placebo group
(6.1% vs. 3.0%[20] and 4.7% vs. 1.7%[21]) during the rst
year of treatment. However, by the end of two years,
the prevalence of ED was similar in both the groups
(1.3% vs. 1.3%[20] and 0.8% vs. 0.9%[21]).
The analysis of results of the above mentioned clinical
studies shows no clear evidence of negative effect of
finasteride (5 mg or 1 mg/day) on erectile function.
Therefore, ED occurring during finasteride therapy
should be viewed in terms of normal prevalence and
natural history of ED in the population, age of the patient,
other confounding factors, and also the nocebo effect.
Ejaculatory dysfunction
The effect of nasteride on ejaculatory volume and other
semen parameters has not been reported in detail in the
literature. The ejaculatory dysfunction associated with
nasteride ranges from 2.1-7.7%.[22]
A randomized double-blind placebo-controlled study
assessed the effect of nasteride (5 mg/day), dutasteride
and placebo on the semen parameters of normal healthy
men. The individuals received any one of these drugs for
one year and semen analysis was performed at 26 weeks
and 52 weeks of treatment, and also after 24 weeks of
follow- up. The nasteride group showed statistically
signicant reduction in sperm count (34.3%), semen
volume (21.1%) and sperm concentration (21.5%) from
the baseline at 26 weeks of treatment. However, at
52 weeks of treatment and after 24 weeks follow-up,
the reduction of all the three semen parameters from
the baseline was no longer statistically significant.
Finasteride also resulted in significant reduction in
sperm motility of 6-12% from the baseline throughout
the study period. But there was no signicant change
in sperm morphology anytime during the study.[2] The
reduction in semen parameters in this study was slight
and did not fall below the pre-established threshold
levels to interfere with normal fertility. However, marked
sensitivity of some individuals to nasteride may result
in substantial reduction in semen quality leading to
infertility. Therefore, nasteride should be considered
as a possible etiological agent while evaluating men for
infertility.[2]
Recovery of semen parameters towards the baseline at
52 weeks of treatment and after 24 weeks of follow-up
in the presence of signicant decrease in DHT levels
(72.7%) suggests that DHT does not play a major role in
spermatogenesis and testosterone alone may be sufcient
to maintain spermatogenesis in normal healthy men.[2]
However, through its effect on size of prostate and
seminal vesicles, nasteride results in low semen or
ejaculatory volume. Finasteride causes significant
reduction in prostate size through inhibition of
conversion of testosterone to DHT by 5α-reductase
Type 2 enzyme which is expressed in both epithelial and
stromal cells of prostate but more predominantly in the
latter.[3] A 19-28% reduction in the prostate size from the
baseline has been reported after six months therapy with
nasteride 5 mg/day for BPH.[10,11,23-25] When used in the
dose of 1 mg day for one year, nasteride resulted in 18%
reduction in prostate size from the baseline.[10]
A similar situation has been observed in men with
congenital deciency of Type 2 5α-reductase enzyme.
In these patients, the prostate and seminal vesicles were
atrophic with resulting low semen volume.[26]
Thus the only causal relationship between nasteride and
sexual dysfunction is low semen or ejaculatory volume.
FINASTERIDE AND PROSTATE CANCER
Prostate cancer is one of the common causes of cancer
deaths in men. Most cancers develop in the peripheral
zone of the prostate, and cancers in this location
are palpable during digital rectal examination. The
management of prostate cancer should be focused on
early detection and treatment. However, prevention may
be a more effective approach.[27]
The prostate epithelial cells and the stromal cells express
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Journal of Cutaneous and Aesthetic Surgery - Jan-Jun 2009, Volume 2, Issue 1 15
Anitha, et al.: Finasteride
androgen receptors and depend on androgens for
growth.[27] Effectiveness of nasteride in the treatment of
BPH had led to a hypothesis that nasteride may have a
role in the prevention of prostate cancer.[6]
Finasteride was used in the Prostate Cancer Prevention
Trial (PCPT), a double-blind, randomized multicenter trial.
PCPT compared the ability of nasteride 5 mg versus
placebo in reducing the risk of prostate cancer. The study
reported that nasteride prevents or delays the appearance
of prostate cancer, thereby decreasing the overall
incidence of prostate cancer. Signicantly, it was also found
that there was an increase in the incidence of high-grade
prostate cancer with nasteride compared to placebo.
This may be due to the nasteride induced alteration of
intraprostatic androgen levels leading to morphologic
changes in low-grade tumors. Selective inhibition of
low-grade tumor by finasteride may also be another
explanation for the increase in high grade cancer.
[28] More
importantly, it is the effect of nasteride on levels of
PSA which is responsible for early detection of increased
number of high-grade prostate cancer. Finasteride (5 mg)
has been found to reduce the PSA level by 50% from the
baseline at the end of six months of therapy for BPH.
Therefore, for prostate cancer screening, a compensatory
adjustment of PSA level (multiplication by factor 2) is
recommended in men who are on nasteride 5 mg/ day
for BPH.[29] Similar reduction in PSA level has also been
demonstrated in men aged between 40-60 years receiving
nasteride 1 mg/ day for androgenetic alopecia.[30] Hence,
compensatory adjustment of PSA level should also be
applied for these patients during prostate cancer screening.
Higher PSA levels are usually associated with benign
conditions like BPH and prostatitis than prostate cancer.
Treatment with nasteride (5 mg/day) causes greatest fall
in PSA levels in patients with BPH than prostate cancer.
Patients receiving nasteride, who show persistent higher
levels of PSA, are more likely to have cancer than those
who are not on nasteride. The analysis of the PCPT study
demonstrated that nasteride signicantly increased the
sensitivity of PSA levels in the detection of all grades of
prostate cancer when compared to placebo. Thus increased
incidence of high-grade prostate cancer in the nasteride
group has been attributed to improved performance of
PSA screening in detection of prostate cancer. The patients
are more likely to have prostate cancer if nasteride does
not reduce PSA level by 50%.[31]
However, there is a concern over chronic use of
nasteride and development of prostate cancer. Through
its effect on hormonal (estrogens vs. androgens) balance
and immune surveillance of tumor cells, nasteride
increases the risk of prostate cancer. In many studies it
has been shown that the prostatic hyperplasia and cancer
develop frequently in the hormonal milieu of estrogen
excess over androgens. This hormonal imbalance is
normally seen in aging males. Finasteride increases the
circulating levels of testosterone which is peripherally
aromatized to estrogens. Thus the use of nasteride in
older males further shifts the hormonal balance towards
estrogen excess. The expression of aromatase is also
up- regulated in prostatic hyperplasia and cancer.
The immune competent cells possess androgen receptors
and androgens are known to affect the Th1/Th2 balance.
Finasteride alters the immune surveillance of cancer in
aging males and may predispose them to the risk of
prostate cancer.[32]
The supplementation of DHT, a non-aromatizing
androgen, restores the estrogen-androgen balance by
decreasing the plasma levels of estradiol and testosterone.
It has been reported that DHT has a favorable effect on
sexual function and the cardiovascular system without
any adverse effects on prostate.[33] Paradoxically, the use
of DHT has been proposed as an alternative treatment
in the prevention of prostate cancer.[32] However, before
any further therapeutic intervention to prevent or treat
prostate cancer a clear understanding of androgen-
and/or non-androgen-dependent mechanisms in the
development prostate cancer is necessary.
CONCLUSION
Although a relationship has been established between
finasteride and sexual dysfunction in the literature,
the analysis of the role of androgens in male sexual
function and the evidences from large population-based
long-term placebo-controlled studies using validated
questionnaire and objective method for assessing sexual
function suggested no substantial evidence of ED in
men receiving nasteride. Low ejaculatory volume is the
only causal relationship between nasteride and sexual
dysfunction. Finasteride has been an effective drug in
preventing low-grade prostate cancer but its role in
increased incidence of high-grade prostate cancer has
been attributed to better performance of PSA screening
in prostate cancer detection. The effects of both doses of
nasteride (5 mg and 1 mg/day) on prostate and PSA
levels are almost similar. So, as dermatologists, we should
be aware of the potential risks and benets while treating
baldness in young men with long-term nasteride.
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Source of Support: Nil, Conict of Interest: None declared.
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