Just starting out. Advice is welcome and invited

[shocktop311]

Don't let the fear of oral finasteride get in the way of you starting it. Most sides are in people's head then they have a predisposition bias once started. Most people without sides aren't posting on these threads. The big 3 is crucial. Other medicines such as fut and shampoos like tsal are beneficial but the main thing is the big 3. You have to have an anti-dht medicine (finasteride) to actually stop the internal cause of male pattern baldness (dht), a growth stimulant for regrowth of hairs almost with nearly closed follicles (speeds up the effects of finasteride too), as well as a shampoo to keep the scalp clean and free of dandruff and itching (believe me, if you start the big 3 you'll see lots of both possibly. Dandruff and inflammation alone can hinder the effects of finasteride. I also would recommend a solid multivitamin and biotion (5000 mcg) .

 

[shocktop311]

And dutasteride*. Also, you will have ball ache and lowed Semene counf for like a week because of the hormone change. I even had an odd type of terrible migraine I used to get 6 years ago (very painful, loss of vision). But these sides go and the body adjusts EXTREMELY quick. The amount of reported sides is less than 3%. You have a 97% margin of safety with an 83% chance of maintaining your hair. I would say with a cost-benefit analysis you're in the clear. Are the smallest of percentages really stopping g you from actually keeping your hair?

 

[arcangel]

And dutasteride*. Also, you will have ball ache and lowed Semene counf for like a week because of the hormone change. I even had an odd type of terrible migraine I used to get 6 years ago (very painful, loss of vision). But these sides go and the body adjusts EXTREMELY quick. The amount of reported sides is less than 3%. You have a 97% margin of safety with an 83% chance of maintaining your hair. I would say with a cost-benefit analysis you're in the clear. Are the smallest of percentages really stopping g you from actually keeping your hair?

No, lack of information was. I didn't know the odds until now. :woot:

 

[israelite]

Yes u will have ball pains the first couple days on either finasteride or dutasteride. When I added dutasteride to my regimen my sex drive went through the roof.

 

[shocktop311]

And after that week the body adjustsand you are on a sincere path to getting your hair back. I think the actual Stat of people with sides is 1.4% I just wanted to make sure I was under at least. That's what I remember the derk saying. There's no way around it, no an Advertiser but get on finasteride.

 

[arcangel]

Is there an advantage to using finasteride vs dutasteride?

 

[arcangel]

I've made an appointment to see an MD and get a complete physical, too. Will research finasteride and dutasteride this weekend.

 

[gascoigne]

And dutasteride*. Also, you will have ball ache and lowed Semene counf for like a week because of the hormone change. I even had an odd type of terrible migraine I used to get 6 years ago (very painful, loss of vision). But these sides go and the body adjusts EXTREMELY quick. The amount of reported sides is less than 3%. You have a 97% margin of safety with an 83% chance of maintaining your hair. I would say with a cost-benefit analysis you're in the clear. Are the smallest of percentages really stopping g you from actually keeping your hair?

How can you be so sure about those % ?
In that case, no man would walk around bald, or at least not over NW3.

 

[arcangel]

And dutasteride*. Also, you will have ball ache and lowed Semene counf for like a week because of the hormone change. I even had an odd type of terrible migraine I used to get 6 years ago (very painful, loss of vision). But these sides go and the body adjusts EXTREMELY quick. The amount of reported sides is less than 3%. You have a 97% margin of safety with an 83% chance of maintaining your hair. I would say with a cost-benefit analysis you're in the clear. Are the smallest of percentages really stopping g you from actually keeping your hair?

How can you be so sure about those % ?
In that case, no man would walk around bald, or at least not over NW3.

Sounds too authoritative to me. Everyone thinks they're an expert, and my mistake was expecting to find one here. I'll try to find (and post) numbers from research papers this evening.

Edit: I haven't read the papers yet, but wanted to post the Research papers themselves. The abstracts are available here: http://tinyurl.com/fina-hair-research

 

[TravisB]

And dutasteride*. Also, you will have ball ache and lowed Semene counf for like a week because of the hormone change. I even had an odd type of terrible migraine I used to get 6 years ago (very painful, loss of vision). But these sides go and the body adjusts EXTREMELY quick. The amount of reported sides is less than 3%. You have a 97% margin of safety with an 83% chance of maintaining your hair. I would say with a cost-benefit analysis you're in the clear. Are the smallest of percentages really stopping g you from actually keeping your hair?

How can you be so sure about those % ?
In that case, no man would walk around bald, or at least not over NW3.

Yeah it's a mystery to me too why all these years when we had Finasteride for hairloss there are still so many bald/balding guys? Even actors and sports people. Wouldn't actors like to save their hair? The first thing for them to do would be to hop on Propecia, but still we see balding celebs that can't stop the process.

Now that there is Spring and warm weather, and people started to remove their caps, I see shitload of bald and balding people.

 

[arcangel]

All I'm worried about (at least right now) is the results on the "Top Back of the Head" at the 2 year mark, which shows, essentially, that 33% of men reached a point where they had No visible hair loss and only 1%:
66% showed improvement
33% no visible hair loss
1% visible hair loss

Supposedly you'll be able to assess your results in 6 months and it may be up to 12 months.

Here's the Original Propecia Study (byMerck):
The study was done to determine whether finasteride treatment leads to clinical improvement in men with male pattern hair loss. In two 1-year trials, 1,553 men (18 to 41 years of age) with male pattern hair loss received oral finasteride 1 mg daily or placebo, and 1,215 men continued in blinded extension
studies for a second year. Efficacy was evaluated by scalp hair counts, patient and investigator assessments, and review of photographs by an expert panel. Finasteride treatment improved scalp hair by all evaluation techniques at 1 and 2 years. Treatment with placebo resulted in progressive hair loss.
Patients’ self-assessment demonstrated that finasteride treatment slowed hair loss, increased hair growth, and improved appearance of hair. These improvements were corroborated by investigator assessments and assessments of photographs. In men with male pattern hair loss, finasteride 1 mg daily
slowed the progression of hair loss and increased hair growth in clinical trials over two years.

PROPECIA
®
(finasteride) is the first oral treatment for male pattern hair loss in MEN ONLY. Clinical
studies of up to two years established efficacy in men, 18 to 41, with mild to moderate hair loss of the
vertex and anterior mid-scalp area. Efficacy in bitemporal recession has not been established.
PROPECIA is contraindicated in women when they are or may potentially be pregnant. Women should
not handle crushed or broken PROPECIA tablets when they are pregnant or may potentially be pregnant
because of the possibility of absorption of finasteride and the subsequent potential risk to a male fetus.
PROPECIA tablets are coated and will prevent contact with the active ingredient during normal
handling, provided that the tablets have not been broken or crushed.
Stopping treatment with PROPECIA leads to gradual reversal of beneficial effects. If PROPECIA has
not maintained hair count or regrown visible hair within 12 months, further treatment is unlikely to be of
benefit.
Before prescribing PROPECIA and/or PROSCAR
®
(finasteride), please review the complete
Prescribing Information by clicking the links above.Androgenetic alopecia (male pattern hair loss)
occurs in men with an inherited sensitivity to the
effects of androgens on scalp hair.1,2
It is marked
by visible loss of hair in areas of the scalp caused
by progressive miniaturization of hair follicles.3-5
The condition does not occur in men with a genetic deficiency of the enzyme steroid 5?-reductase
(5?R) type II, which converts testosterone to dihydrotestosterone (DHT), implicating DHT in its
pathogenesis.6 Of two 5?R isoenzymes in
humans,7-9
type I predominates in skin, including
scalp,10,11 whereas type II is present in hair follicles,12
as well as the prostate.
11
Oral finasteride, a type II 5?R inhibitor, lowers
serum,13
prostate,
14
and scalp
15,16 DHT. DevelopTHERAPY
Finasteride in the treatment of men with
androgenetic alopecia
Background: Androgenetic alopecia (male pattern hair loss) is caused by androgen-dependent miniaturization of scalp hair follicles, with scalp dihydrotestosterone (DHT) implicated as a contributing cause. Finasteride, an inhibitor of type II 5?-reductase, decreases
serum and scalp DHT by inhibiting conversion of testosterone to DHT.
Objective: Our purpose was to determine whether finasteride treatment leads to clinical
improvement in men with male pattern hair loss.
Methods: In two 1-year trials, 1553 men (18 to 41 years of age) with male pattern hair loss
received oral finasteride 1 mg/d or placebo, and 1215 men continued in blinded extension
studies for a second year. Efficacy was evaluated by scalp hair counts, patient and investigator assessments, and review of photographs by an expert panel.
Results: Finasteride treatment improved scalp hair by all evaluation techniques at 1 and 2
years (P < .001 vs placebo, all comparisons). Clinically significant increases in hair count
(baseline = 876 hairs), measured in a 1-inch diameter circular area (5.1 cm2
) of balding
vertex scalp, were observed with finasteride treatment (107 and 138 hairs vs placebo at 1
and 2 years, respectively; P < .001). Treatment with placebo resulted in progressive hair
loss. Patients’ self-assessment demonstrated that finasteride treatment slowed hair loss,
increased hair growth, and improved appearance of hair. These improvements were corroborated by investigator assessments and assessments of photographs. Adverse effects
were minimal.
Conclusion: In men with male pattern hair loss, finasteride 1 mg/d slowed the progression
of hair loss and increased hair growth in clinical trials over 2 years.
From the Departments of Clinical Researcha
and Biostatistics,b Merck
Research Laboratories, Rahway; Duke University Dermatopharmacology Study Center, Durhamc
; Baylor Hair Research and
Treatment Center, Dallasd
; Savin Dermatology Center, New
Havene
; Division of Dermatology, University of Texas Health
Science Center, San Antoniof
; Department of Dermatology,
Cleveland Clinic Foundationg
; Department of Dermatology,
University of California, San Franciscoh
; Skin Study Center,
Tournai
i
; Northwest Cutaneous Research Specialists, Portlandj
;
Department of Dermatology, University of Minnesota Twin Cities,
Minneapolisk
; Department of Dermatology, University of British
Columbia, Vancouver
l
; and Clinical Development, US Medical
and Scientific Affairs, Merck & Co, Inc, Horsham.m
Reprint requests: Keith D. Kaufman, MD, Merck Research
Laboratories (RY33-500), 126 E Lincoln Ave, Rahway, NJ 07065.
*
Participants in the Finasteride Male Pattern Hair Loss Study Group
are listed at the end of this article.
Copyright © 1998 by the American Academy of Dermatology, Inc.
0190-9622/98/$5.00 + 0 16/1/92149in 1 year, use of drugs with androgenic or antiandrogenic
properties, use of finasteride or other 5?R inhibitors, or
alopecia from other causes. Men were instructed not to
alter their hair style or dye their hair during the studies.
We conducted 2 replicate, 1-year, double-blind,
placebo-controlled, randomized, multicenter studies,
which continued as 1-year, double-blind, placebocontrolled, randomized, extension studies to determine
the effect of treatment for 2 years, the effect of withdrawal of treatment after 1 year, and the natural history
of male pattern hair loss in men seeking treatment.
Investigators at 33 US sites (US study) and 27 sites in
15 non-US countries (international study) participated.
Institutional review board approval and written
informed consent were obtained before patients were
entered into each study.
ed for treatment of benign prostatic hyperplasia
(BPH) at a dose of 5 mg/d, finasteride has an
excellent safety profile.
13
Early studies showed
that 1 mg/d was effective in men with male pattern
hair loss.
16-19
METHODS
Study population (Tables IA and IB)
Men 18 to 41 years of age, with mild to moderately
severe vertex male pattern hair loss according to a modified Norwood/Hamilton classification scale (II vertex,
III vertex, IV or V),
20,21 were enrolled. The principal
exclusions were significant abnormalities on screening
physical examination or laboratory evaluation, surgical
correction of scalp hair loss, topical minoxidil use withTable IA. Baseline characteristics of men randomized in initial studies
International phase III
US phase III initial study initial study
Finasteride 1 mg Placebo Finasteride 1 mg Placebo
(n = 471) (n = 462) (n = 308) (n = 312)
Age (y, mean ± SE) 33 ± 0.2 34 ± 0.2 31 ± 0.3 31 ± 0.3
Age at which hair loss began (y, mean ± SE) 24 ± 0.2 25 ± 0.2 24 ± 0.3 24 ± 0.3
No. (%) of patients with family history*
373 (80) 363 (80) 227 (74) 239 (77)
Baseline hair count (mean ± SE)
†
864 ± 11 856 ± 12 916 ± 15 924 ± 14
No. (%) of patients with hair loss pattern
‡
II vertex 63 (13) 63 (14) 56 (18) 59 (19)
III vertex 150 (32) 129 (28) 76 (25) 75 (24)
IV 112 (24) 141(30) 83 (27) 84 (27)
V 146 (31) 129 (28) 93 (30) 94 (30)
*
Family history: Parents or siblings with androgenetic alopecia.
†Measured in a 1-inch diameter circular area (5.1 cm2
) at anterior leading edge of vertex balding scalp.
‡According to a modified Norwood-Hamilton scale.
Table IB. Baseline characteristics of men randomized in extension studies
US and International phase III extension studies combined
finasteride?finasteride finasteride?Pbo Pbo?finasteride Pbo?Pbo
(n = 547) (n = 65) (n = 543) (n = 60)
Age (y, mean ± SE) 33 ± 0.2 33 ± 0.7 33 ± 0.2 32 ± 0.7
Age at which hair loss began (y, mean ± SE) 24 ± 0.2 24 ± 0.2 24 ± 0.2 24 ± 0.6
No. (%) of patients with family history
*
425 (78) 47 (72) 431 (80) 49 (82)
Baseline hair count (mean ± SE)
†
876 ± 11 835 ± 26 878 ± 11 903 ± 27
No. (%) of patients with hair loss pattern‡
II vertex 84 (15) 5 (8) 79 (14) 9 (15)
III vertex 156 (28) 21 (32) 153 (28) 12 (20)
IV 140 (26) 16 (25) 155 (29) 19 (32)
V 167 (30) 23 (35) 156 (29) 20 (33)
*
Family history: Parents or siblings with androgenetic alopecia.
†Measured in a 1-inch diameter circular area (5.1 cm2
) at anterior leading edge of vertex balding scalp.
‡According to a modified Norwood-Hamilton scale.October 1998
Study protocols (Fig 1)
Initial studies. After a screening procedure, patients
entered a 2-week, single-blind placebo run-in. Patients
received a study shampoo (Neutrogena T/Gel) for standardization of shampoo used and for prophylaxis of
seborrheic dermatitis, which might affect scalp hair
growth.22
Patients (N = 1553) were then randomly
assigned to treatment with either finasteride 1 mg/d or
placebo for 1 year.
Patients visited the clinic every 3 months, where they
completed a hair growth questionnaire and investigators
completed assessments of scalp hair growth. Every 6
months, photographs of scalp hair were taken for hair
counts and for assessments of hair growth by an expert
panel. Reports of adverse events were collected
throughout the studies.
Extension studies. Patients completing the initial 1-
year studies were eligible to enroll in 1-year extension
studies. In the extension studies, patients (N = 1215)
were randomly assigned treatment to either finasteride 1
mg or placebo (9:1), as determined at initial randomization (Table II). The protocol for the extension studies was
similar to the initial studies, except that photography for
hair count was done only at month 24.
Fig 1. Trial profile. Main inclusion criteria and evaluation procedures, as well as the number of patients who were randomized, who completed the studies, and who discontinued
prematurely, are shown for both original and extension studies by treatment group.global photographs (see below) were provided to the
investigator for reference.
Global photographic assessment
Standardized color global photographs (Kodak KR-
64 35-mm slide film) of the vertex scalp were taken
with the head in a stereotactic positioning device.
23
Paired baseline and posttreatment slides were independently reviewed, with the use of the standardized 7-
point rating scale (see above), by a panel of three dermatologists (E. Olsen, R. Savin, D. Whiting) blinded as
to treatment and experienced in photographic assessments of hair growth. This technique has previously
been demonstrated to have excellent test-retest reproducibility and interrater agreement.
25
Safety measurements
Safety measurements included clinical and laboratory evaluations, adverse event reports, and patient body
hair assessment via a self-administered questionnaire
(US study only).
LABORATORY EVALUATION
Hematology, urinalysis, chemistry, and hormone measurements were performed at baseline and every 6 months.
Serum chemistry, including prostate-specific antigen
(PSA), and serum hormones, including testosterone, DHT,
luteinizing hormone, and follicle-stimulating hormone,
were assayed in central laboratories (Medical Research
Laboratories, Highland Heights, Ky, and Endocrine
Sciences, Calabasas Hills, Calif, respectively).
STATISTICAL ANALYSIS
A data analysis plan prespecified all primary and
secondary hypotheses, including combining data from
both initial studies, to improve precision of the estimates of treatment effect, and from both extension studies, because of the small size of the placebo groups in
the extension phase.
The primary hypothesis for hair counts was assessed
by the difference between the count at each time point
and the accompanying baseline count, and mean values
EVALUATION PROCEDURES
Four predefined efficacy end points provided a comprehensive assessment of changes in scalp hair from
baseline.
Hair counts (co-primary end point)
Hair counts were obtained from color macrophotographs of a 1-inch diameter circular area (5.1 cm2
) of
clipped hair (length, 1 mm) at the anterior leading edge
of the vertex thinning area, centered with a dot tattoo to
ensure reproducibility.23
Macrophotographs (Kodak KR-64 35-mm slide
film) were taken with dedicated preset camera systems23
at fixed focus, distance (primary magnification,
1:1.7), and exposure, with the use of a macroflash
mounted on a scalp template,
23 with enlargement into
8- × 10-inch (20.3- × 25.4-cm) color transparencies
(final magnification, 5.84:1). At the end of the initial
studies, the baseline, month 6, and month 12 transparencies for each patient, and subsequently at the end
of the extension studies the baseline and month 24
transparencies, were converted into dot maps of each
visible hair by technicians (Canfield Scientific, Inc
[CSI], Fairfield, NJ), who were blinded as to patient,
treatment, and time. Dot maps were converted into hair
counts by means of personal computer–based scanners
and imaging software.
Patient self-assessment (co-primary end point)
Patients assessed their scalp hair using a validated,
self-administered hair growth questionnaire,24
consisting of 4 questions in the patient’s language on treatment
efficacy and 3 questions on satisfaction with appearance
(Fig 2).
Investigator assessment
Investigators assessed patients at all time points,
using a standardized 7-point rating scale of hair growth
compared with baseline (–3 = greatly decreased, –2 =
moderately decreased, –1 = slightly decreased, 0 = no
change, +1 = slightly increased, +2 = moderately
increased, +3 = greatly increased). Baseline patient
Table II. Randomization of patients to treatment groups in original and extension studies
Original studies (first year) Extension studies (second year)
Treatment group % Subjects Treatment % Subjects Treatment group
? Finasteride 45 finasteride?finasteride
Finasteride 50
? Placebo 5 finasteride?Pbo
? Finasteride 45 Pbo?finasteride
Placebo 50
? Placebo 5 Pbo?PboOctober 1998
for each treatment group were determined by means of
SAS computed Least Mean Squares. The primary
hypothesis for patient self-assessment was assessed by
a global test across all 7 questions, by means of a generalized least squares procedure that accounts for different scales of, and covariance among, the questions.26,27
For investigator and global photographic
assessments, hypotheses were assessed by comparison
of mean rating scores for each treatment group at each
time point, based on the 7-point rating scale (minimum
value = –3.0; maximum value = 3.0). Hypothesis testing for hair counts, individual patient self-assessment
questions, and investigator and global photographic
assessments was performed by means of analysis of
variance (ANOVA).
Efficacy analyses were based on the intention-totreat principle; that is, analysis of the initial studies
included all men with at least one measurement postrandomization, and analysis of the extension studies
included all men with at least one measurement in the
second year. In each study, the last observation was carried forward where appropriate to impute missing data.
The focus of the safety analyses was on the biochemical parameters, with the use of ANOVA, and on
adverse event reports. Comparison of the proportion of
patients with an adverse event was done between
groups with Fisher’s exact test.
RESULTS
Patient accounting is summarized in Fig 1.
Hair counts
Initial studies. In each study, finasteride treatment produced progressive increases in hair count
at months 6 and 12, whereas treatment with placebo resulted in significant hair loss (all P values <
.001 vs baseline). At month 12, the difference
between groups (mean ± SE) was 106 ± 5.6 and
107 ± 7.0 hairs in the target area in the US and
international studies, respectively (both, P < .001).
Combining data from both studies (mean baseline
hair count = 876 hairs) demonstrated an increase
Fig 2. Male hair growth questionnaire used for patient self-assessment of changes in scalp
hair.Patient self-assessment
Initial studies. In each study, finasteride was
superior to placebo as early as month 3 (P < .05),
the first efficacy time point, and at all subsequent
timepoints (P < .001). For individual questions,
finasteride was superior to placebo for 6 of 7 questions (except Q5a) by month 6, and for all questions
at all subsequent time points (all P values < .001).
Extension studies. In the combined analysis,
continued treatment with finasteride (finasteride?finasteride)
was superior to continued treatment with placebo
(Pbo?Pbo) at each time point (P < .001), and the
treatment effect was significantly greater (P < .05)
at month 24 than at month 12. At month 24, the
finasteride?finasteride group demonstrated further improvement for each question (P < .05 vs month 12),
whereas the Pbo?Pbo group demonstrated a negative trend.
For the finasteride?Pbo group, partial or complete
loss of effect of finasteride was observed for 6 of 7
questions (except Q4), whereas the Pbo?finasteride
group demonstrated improvement for each question (P < .001 vs month 12).
Another way of demonstrating the treatment
effect is the percentage of patients who reported
improvement for each of the 7 questions (Table
III). For each question, a greater percentage of
finasteride-treated than placebo-treated patients
reported improvement, with the difference
between groups increasing with time.
of 86 ± 3.4 hairs (11% ± 0.5%) for finasteride, a
decrease of –21 ± 3.4 hairs (–2.7% ± 0.5%) for
placebo, and a difference of 107 ± 4.4 hairs (14%
± 0.6%) between groups (all P values < .001). By
month 12, 58% of patients receiving placebo had
fewer hairs than at baseline, compared with only
14% receiving finasteride.
Extension studies. For the two groups continued on the original study therapy (finasteride?finasteride and
Pbo?Pbo), the combined analysis (Fig 3) demonstrated a difference of 107 ± 11 hairs between
groups at month 12 (P < .001), which was identical to the result observed in all patients in the initial studies. At month 24, the finasteride?finasteride group
maintained the hair count observed at month 12,
whereas the Pbo?Pbo group demonstrated further hair loss (–37 ± 13 hairs vs month 12, P <
.01). The difference between groups (P < .001)
was 138 ± 16 hairs (16% ± 2.1%), which was significantly greater (P < .05) than the difference at
month 12. By month 24, 72% of patients continuing placebo had fewer hairs than at baseline, compared with only 17% continuing finasteride.
For the group switched from finasteride to
placebo at month 12 (finasteride?Pbo), reversibility of
the finasteride effect was demonstrated at month
24 (–117 ± 13 hairs vs month 12, P < .001), whereas the group switched from placebo to finasteride
(Pbo?finasteride) demonstrated improvement (76 ± 4.3
hairs vs month 12, P < .001).
Fig 3. Hair count mean change from baseline (± 1 SE) from the combined US and international studies for men who entered the extension studies.October 1998
Investigator assessment
Initial studies. In each study, finasteride was
superior to placebo at all time points (P < .001).
By month 12, 65% of finasteride-treated patients
were rated as improved by the investigators versus
37% of placebo-treated patients (Table III).
Extension studies. In the combined analysis
(Fig 4), continued treatment with finasteride
(finasteride?finasteride) was superior to continued treatment
with placebo (Pbo?Pbo) at each time point (P <
.001). At month 24, the finasteride?finasteride group demonstrated further improvement and, as anticipated,
the Pbo?finasteride group improved (both, P < .001 vs
month 12). In contrast to the other end points, neither the Pbo?Pbo nor the finasteride?Pbo groups significantly worsened. By month 24, the investigators rated as improved 80% of patients continuing
finasteride versus 47% continuing placebo (Table
III).
Global photographic assessment
Initial studies. In each study, finasteride was
Table III. Percentage of men with improvements in scalp hair
Original studies (month 12) Extension studies (month 24)
Finasteride Placebo Difference finasteride?finasteride Pbo?Pbo Difference
(n = 720-751) (n = 709-749) (± 95% CI) (n = 508-535) (n = 55-60) (± 95% CI)
Patient self-assessment (questionnaire)
Q1: Size of bald spot 42 21 21 (17, 26) 58 17 41 (31, 52)
Q2: Appearance of hair 58 35 23 (18, 28) 71 31 40 (28, 53)
Q3: Growth of hair 56 33 23 (18, 27) 69 27 42 (30, 54)
Q4: Slowing hair loss 68 45 23 (18, 28) 81 46 35 (22, 48)
Q5a: Satisfaction with frontal hairline 29 17 12 (8, 16) 36 12 24 (15, 33)
Q5b: Satisfaction with hair on top 36 20 16 (12, 21) 49 17 32 (21, 42)
Q5c: Satisfaction with hair overall 39 22 17 (12, 21) 51 25 26 (14, 37)
Investigator assessment
Increased hair growth 65 37 32 (23, 33) 80 47 33 (21, 47)
Global photographic assessment
Increased hair growth 48 7 41 (36, 45) 66 7 59 (51, 67)
Fig 4. Investigator assessment mean rating score (± 1 SE) from the combined US and
international studies for men who entered the extension studies.superior to placebo at all time points (P < .001).
By month 12, the expert panel rated as improved
48% of finasteride-treated patients (30% slightly
improved, 18% moderately or greatly improved)
versus 7% of placebo-treated patients (Table III).
Extension studies. In the combined analysis
(Fig 5), continued treatment with finasteride
(finasteride?finasteride) was superior to continued treatment
with placebo (Pbo?Pbo) at each time point (P <
.001), and the treatment effect at month 24 was
significantly greater (P < .001) than at month 12.
At month 24, the finasteride?finasteride group demonstrated
further improvement, whereas the Pbo?Pbo
group demonstrated further worsening (both P values < .01 vs month 12). For the finasteride?Pbo group,
the effect of finasteride was lost gradually over 12
months (P < .001, month 24 or month 18 vs month
12). As anticipated, the Pbo?finasteride group improved
(P < .001 vs month 12).
By month 24, two thirds of patients continuing
finasteride were rated as improved by the expert
panel (30% slightly improved, 36% moderately or
greatly improved) versus 7% continuing placebo
(Table III). Only 1% of patients continuing finasteride worsened versus one third continuing placebo. Figs 6 and 7 show baseline, month 12,
and month 24 global photographs of 2 representative finasteride-treated patients rated at 12 and
24 months as slightly, moderately, or greatly
improved.
Serum hormones and PSA
Finasteride markedly reduced serum DHT from
a median of 44.0 ng/dL at baseline (normal range =
30-85 ng/dL) to 14.0 ng/dL at month 12 (median
percent change ± SE = –68.4% ± 1.2%; P < .001 vs
placebo), and slightly increased serum testosterone
from a median of 510 ng/dL at baseline (normal
range = 350-1030 ng/dL) to 559 ng/dL at month 12
(median percent change ± SE = 9.1% ± 1.5%; P <
.001 vs placebo). Finasteride treatment had no significant effects on serum luteinizing hormone or
follicle-stimulating hormone, whereas serum PSA
(normal range < 4.0 ng/mL) fell slightly (baseline
mean ± SE = 0.78 ± 0.04 ng/mL; month 12 = 0.52
± 0.02 ng/mL; mean change vs placebo = –0.23 ±
0.04 ng/mL, P < .001).
ADVERSE EVENTS
Clinical adverse events considered by the investigator to be possibly, probably, or definitely drugrelated that occurred in 1% of men or more are
shown in Table IV. In the first year, a slightly higher proportion of finasteride-treated than placebotreated patients reported adverse events related to
sexual function (4.2% vs 2.2%, P < .05; see Table
IV for details). Only 11 men (1.4%) in the finasteride group and 8 (1.0%) in the placebo group discontinued the study because of sexual adverse
events, which resolved after discontinuation.
These adverse events also resolved in many of the
Fig 5. Global photographic assessment mean rating score (± 1 SE) from the combined US
and international studies for men who entered the extension studies.October 1998
patients who reported them but who remained on
the finasteride regimen and continued in the study.
An equal number (n = 4; 0.4%) of patients in each
treatment group reported adverse events related to
the breast. The adverse event profile for patients
continuing in the second year was similar. In each
treatment group, small increases, slightly greater
for placebo-treated than finasteride-treated
patients, were reported in nonscalp body hair by
patient body hair assessment.
Fig 6. Patient 1. A, Baseline. B, Month 12: Slightly increased hair growth. C, Month 24:
Moderately increased hair growth.
A B C
Fig 7. Patient 2. A, Baseline. B, Month 12: Moderately increased hair growth. C, Greatly
increased hair growth.
A B Cpatients indicated that therapy led to slowing of
further hair loss.
Assessment of hair growth by investigators also
demonstrated the benefit of finasteride treatment,
with a placebo effect also observed. Recall or other
bias by investigators appeared to obscure detection
of ongoing hair loss, documented by other end
points, in placebo-treated patients.
In contrast, the blinded comparison of paired
pretreatment and posttreatment global photographs by the expert panel, which also assessed
change from baseline but was not subject to recall
bias, demonstrated minimal, if any, placebo effect.
By this assessment, finasteride treatment produced
progressive improvement in hair growth for 2
years, whereas placebo-treated patients worsened.
Because significant improvement was observed in
finasteride-treated patients between months 12 and
24 while hair count was stable, the continued use
of finasteride appears to improve the quality (ie,
thickness, pigment, length and/or growth rate) of
hair.
The safety and excellent tolerability of finasteride at 5 times the dose used in the present studies has been abundantly documented through large
clinical trials and postmarketing surveillance for
more than 5 years in men with BPH.13,28 As
expected from this body of experience, a few men
in the current studies experienced reversible
impairment of sexual function, but only 11 men
receiving finasteride, compared with 8 men in the
placebo group, discontinued treatment for this reason, with resolution in all. No other significant
adverse effects of finasteride were observed.
Based on observations of men with 5?R deficienDISCUSSION
In these studies, finasteride treatment produced
significant improvements in scalp hair in men with
male pattern hair loss. The efficacy of finasteride
was evident within 3 months of therapy. Hair
count, first measured at 6 months, progressively
increased over 1 year in the finasteride group, and
the improvement was maintained through the second year. In contrast, the placebo group progressively lost hair, consistent with the miniaturization
process and the natural history of male pattern hair
loss. As is often observed in long-term studies,
finasteride-treated patients who entered the extension studies had a slight tendency toward greater
efficacy in hair count than those who did not (an
increase of 92 vs 86 hairs from baseline at 1 year).
Regardless, the net improvement for finasteride
compared with placebo for continuing patients
increased with time (107 hairs at 1 year and 138
hairs at 2 years).
Significantly more patients in the finasteride
group reported improvements in scalp hair growth
and appearance, as well as satisfaction with
appearance, compared with the placebo group.
Satisfaction with the frontal hairline was also
improved compared with placebo, although the
area of bitemporal recession was not specifically
assessed. As is typical of patient questionnaire
data, a placebo effect was observed, probably
caused in part by recall bias, as each question
assessed change from baseline. Nevertheless,
patients in the placebo group perceived the loss
documented by hair counts, as indicated by their
responses to the question on slowing hair loss.
Conversely, responses for finasteride-treated
Table IV. Adverse events occurring in 1% of patients or more
*
Original studies (first year) Extension studies (second year)
Finasteride Placebo finasteride?finasteride Pbo?finasteride finasteride?Pbo Pbo?Pbo
(n = 779) (n = 774) (n = 547) (n = 543) (n = 65) (n = 60)
Genitourinary system
Urinary frequency 0 0 0 0 0 1 (1.7)
Sexual function
Libido decreased 15 (1.9) 10 (1.3) 6 (1.1) 7 (1.3) 0 1 (1.7)
Erectile dysfunction 11 (1.4) 7 (0.9) 4 (0.7) 6 (1.1) 0 0
Decreased ejaculate volume 8 (1.0) 3 (0.4) 1 (0.2) 0 0 0
Skin and skin appendages
Body hair growth increased 7 (0.9) 7 (0.9) 1 (0.2) 4 (0.7) 0 3 (5.0)October 1998
cy, finasteride treatment might be expected to
decrease body hair,6
but no such effect was
observed based on the patient body hair assessment administered in this study. The reduction
observed in serum PSA is well understood, and for
men in whom serum PSA is used as part of a
screening evaluation for prostate cancer, guidelines have been published for interpretation in
patients receiving finasteride treatment.
29,30 An
ongoing 10-year study in 18,000 men
31 will test
the hypothesis that finasteride 5 mg/d will reduce
the risk of prostate cancer by reducing intraprostatic DHT.
As a type II 5?-reductase inhibitor, finasteride
is contraindicated in women who are or may
potentially be pregnant because of the risk that
inhibition of conversion of fetal testosterone to
DHT could impair virilization of a male fetus.
Finasteride treatment has recently been shown to
lack efficacy in postmenopausal women with
androgenetic alopecia in a 1-year, placebo-controlled trial.
32
Finasteride 1 mg/d improved scalp hair in men
with male pattern hair loss within 3 months, with
the benefit increasing with continued treatment. In
contrast, men receiving placebo lost hair. These
results confirm that DHT is a key factor in those
men genetically predisposed for development of
male androgenetic alopecia. Adverse events
caused by finasteride treatment were minimal.
Finasteride 1 mg represents a new oral therapy for
men with male pattern hair loss.
*
The Finasteride Male Pattern Hair Loss Study Group
includes (in alphabetical order) R. Asarch, N. Birchall, I.
H. Boersma, S. Brenner, K. Bruno, D. Buntin, G. Burg,
J. Cilliers, P. Cotterill, W. J. Cunliffe, D. Ferguson, V.
Fiedler, D. Fivenson, T. Funicella, C. Gencheff, D.
Gratton, W. He, S. Horwitz, J. Imperato-McGinley, F.
Jurado Santa-Cruz, I. Katz, A. P. Kelly, D. Kopera, P.
Kotey, J.-M. Lachapelle, M. Ling, E. Lopez-Bran, N.
Lowe, A. Lucky, S. MacDonald Hull, A. McDonagh, C.
Mork, G. Peck, E. Prens, P. Reygagne, R. Rietschel, R.
Rittmaster, E. Round, T. Rufli, N. Sadick, P. Saiag, P.
Sanchez-Pedreno, J. B. Schmidt, M. Sher, J. Shupack, D.
Steiner, D. Stewart, M. Stiller, D. Stough, J. Swinehart,
L. Swinyer, G. Todd, W. Unger, J. Waldstreicher, G.
Weinstein, D. Weiss, J. Weiss, S. E. Whitmore, and H.
Wolff.
We acknowledge the technical assistance of Mr.
Douglas Canfield, of Canfield Scientific, Inc, in the
development of photographic procedures used in these
clinical studies. We also thank Dr O’Tar Norwood for
permission to use drawings in the clinical study protocols that first appeared in his article “Male Pattern
Baldness: Classification and Incidence†(South Med J
1975;68:1359-65).
REFERENCES
1. Hamilton JB. Male hormone stimulation is prerequisite
and an incitant in common baldness. Am J Anat
1942;71:451-80.
2. Hamilton JB. Patterned loss of hair in man: types and
incidence. Ann N Y Acad Sci 1951;53:708-28.
3. Price VH. Testosterone metabolism in the skin. Arch
Dermatol 1975;111:1496-502.
4. Whiting DA. Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male pattern
androgenetic alopecia. J Am Acad Dermatol 1993;28:
755-63.
5. Olsen EA. Androgenetic alopecia. In: Olsen EA, editor.
Disorders of hair growth: diagnosis and treatment. New
York: McGraw-Hill; 1994. p. 257-83.
6. Imperato-McGinley J, Guerrero L, Gautier T, Peterson
RE. Steroid 5?-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science 1974;
186:1213-5.
7. Andersson S, Bishop RW, Russell DW. Expression
cloning and regulation of steroidal 5?-reductase, an
enzyme essential for male sexual differentiation. J Biol
Chem 1989;264:16249-55.
8. Jenkins EP, Andersson S, Imperato-McGinley J, Wilson
JD, Russell DW. Genetic and pharmacological evidence
for more than one human steroid 5?-reductase. J Clin
Invest 1992;89:293-300.
9. Russell DW, Wilson JD. Steroid 5?-reductase: two
genes/two enzymes. Annu Rev Biochem 1994;63:25-61.
10. Harris G, Azzolina B, Baginsky W, Cimis G, Rasmusson
GH, Tolman RL, et al. Identification and selective inhibition of an isozyme of steroid 5?-reductase in human
scalp. Proc Natl Acad Sci U S A 1992;89:10787-91.
11. Thigpen AE, Silver RI, Guileyardo JM, Casey ML,
McConnell JD, Russell DW. Tissue distribution and
ontogeny of steroid 5a-reductase isoenzyme expression.
J Clin Invest 1993;92:903-10.
12. Bayne EK, Flanagan J, Azzolina B, Einstein R, Mumford
J, Avala B, et al. Immunolocalization of type 2 5?-reductase in human hair follicles [abstract]. J Invest Dermatol
1997;108:651.
13. Gormley GJ, Stoner E, Bruskewitz RC, ImperatoMcGinley J, Walsh, PC, McConnell J, et al. The effect of
finasteride in men with benign prostatic hyperplasia. N
Engl J Med 1992;327:1185-91.
14. McConnell JD, Wilson JD, George FW, Geller J, Pappas
F, Stoner E. Finasteride, an inhibitor of 5?-reductase,
suppresses prostatic dihydrotestosterone in men with
benign prostatic hyperplasia. J Clin Endocrinol Metab
1992;74:505-8.
15. Dallob AL, Sadick NS, Unger W, Lipert S, Geissler LA,
Gregoire SL, et al. The effect of finasteride, a 5?-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. J Clin Endocrinol Metab 1994;79:703-6.
16. Waldstreicher J, Fiedler V, Hordinsky M, Swinehart JM,
Thiboutot D, Unger W, et al. Effects of finasteride on
dihydrotestosterone content of scalp skin in men with
male pattern baldness [abstract]. J Invest Dermatol 1994;
102:615.24. Barber BL, Kaufman KD, Kozloff RC, Girman CJ,
Guess HA. A hair growth questionnaire for use in the
evaluation of therapeutic effects in men. J Dermatol
Treat In press.
25. Kaufman K, Binkowitz B, Savin R, Canfield D.
Reproducibility of global photographic assessments of
patients with male pattern baldness in a clinical trial with
finasteride [abstract]. J Invest Dermatol 1995;104:659.
26. O’Brien PC. Procedures for comparing samples with
multiple endpoints. Biometrics 1984;40:1079-87.
27. Pocock SJ, Geller NL, Tsiatis AA. The analysis of multiple endpoints in clinical trials. Biometrics 1987;43:
487-98.
28. Moore E, Bracken B, Bremner W, Geller J, ImperatoMcGinley J, McConnell J, et al. Proscar®: five-year
experience. Eur Urol 1995;28:304-9.
29. Guess HA, Gormley GJ, Stoner E, Oesterling JE. The
effect of finasteride on prostate-specific antigen: review
of the available data. J Urol 1992;155:3-9.
30. Oesterling JE, Roy J, Agha A, Shown T, Krarup T,
Johansen T, et al. Biologic variability of prostate-specific antigen and its usefulness as a marker for prostate cancer: effects of finasteride. Urology 1997;50:13-8.
31. Thompson IM, Coltman CA, Crowley J. Chemoprevention of prostate cancer: the prostate cancer prevention
trial. Prostate 1997;33:217-21.
32. Roberts J, Hordinsky M, Olsen E, Savin R, Bergfeld W,
Price V, et al. The effects of finasteride on postmenopausal women with androgenetic alopecia
[abstract]. Hair Workshop, Brussels, Belgium, May 2-3,
1998. p. 16.
17. Kaufman KD, DeVillez R, Roberts J, Fiedler V, Olsen E,
Imperato-McGinley J, et al. A 12-month pilot clinical
study of the effects of finasteride on men with male pattern baldness [abstract]. J Invest Dermatol 1994;102:615.
18. Kaufman KD, Gormley GJ, Binkowitz B, Jacobsen CA,
Bruno K, the Finasteride Male Pattern Baldness Study
Group. The effects of oral finasteride on scalp hair
growth in men with male pattern baldness [abstract].
77th Annual Meeting of the Endocrine Society, Program
and Abstracts, Washington, DC, June 14-17, 1995.
Bethesda (MD): The Endocrine Society Press; 1995. p.
326.
19. Kaufman KD. Clinical studies on the effects of oral
finasteride, a type II 5?-reductase inhibitor, on scalp hair
in men with male pattern baldness. In: Van Neste D,
Randall VA, editors. Hair research for the next millennium. Proceedings of the First Tricontinental Meeting of
Hair Research Societies; Brussels, Belgium, Oct 8-10,
1995. Amsterdam (Netherlands): Elsevier Science BV;
1996. p. 363-5.
20. Norwood O. Male pattern baldness: classification and
incidence. South Med J 1975;68:1359-65.
21. Takashima I, Iju M, Sudo M. Alopecia androgenetica: its
incidence in Japanese and associated conditions. In:
Orfanos CE, Montagna W, Stüttgen G, editors. Hair
research: status and future aspects. New York: SpringerVerlag; 1981. p. 287-93.
22. Agache PG. Eczematous dermatitis of the scalp. In:
Zviak C, editor. The science of hair care. New York:
Marcel Dekker; 1986. p. 513-21.
23. Canfield D. Photographic documentation of hair growth
in androgenetic alopecia. Dermatol Clin 1996;14:
713-21.

 

[arcangel]

5 year long 1mg Finasteride Study

Long-term (5-year) multinational experience with finasteride 1 mg in the treatment of men with androgenetic alopecia

European Journal of Dermatology. Volume 12, Numéro 1, 38-49, January - February 2002, Thérapie


Summary
Auteur(s) : The Finasteride Male Pattern Hair Loss Study Group, Merck Research Laboratories, 126 East Lincoln Avenue, RY33-500, Rahway, NJ 07065, USA..

Androgenetic alopecia (male pattern hair loss, MPHL) occurs in men with an inherited sensitivity to the effects of androgens on scalp hair [1, 2]. The disorder is characterized by loss of visible hair over areas of the scalp due to progressive miniaturization of hair follicles [3-5]. MPHL does not occur in men with genetic deficiency of the Type 2 5alpha-reductase (5alphaR) enzyme, which converts testosterone (T) to dihydrotestosterone (DHT), implicating DHT in the pathogenesis of this condition [6]. Of the two 5alphaR isoenzymes in man [7-9], Type 1 predominates in sebaceous glands of the skin, including scalp [10, 11], while Type 2 is present in hair follicles [12], as well as the prostate [11].

Finasteride, a Type 2-selective 5alphaR inhibitor, lowers serum [13], prostate [14] and scalp [15, 16] DHT levels after oral administration. Developed for the treatment of men with benign prostatic hyperplasia (BPH) at a dose of 5 mg/day, finasteride has a well-established, excellent safety profile [13, 17]. Subsequent studies in men with MPHL showed that finasteride had utility in this disorder as well [18-20], and confirmed 1 mg/day as the optimal dose for treatment of this condition. Three randomized, placebo-controlled, multicenter Phase III trials in men with MPHL demonstrated that treatment with finasteride 1 mg/day produced significant improvements in scalp hair growth and led to increased patient satisfaction with the appearance of their scalp hair [19-21]. In contrast to its beneficial effects in men with MPHL, finasteride was shown to lack efficacy in postmenopausal women with androgenetic alopecia in a 1-year, randomized, placebo-controlled trial [22]. As a Type 2 5alphaR inhibitor, finasteride use is contraindicated in women who are or may potentially be pregnant because of the potential risk of under-virilization of a male fetus.

Because finasteride is used chronically for the treatment of men with MPHL, it was important to evaluate the long-term safety and efficacy of the drug in these men. The present analysis investigated the combined safety and efficacy data over five years from the two replicate, Phase III clinical trials in men with predominantly vertex MPHL. Both trials involved an initial 1-year placebo-controlled study period, followed by four consecutive, 1-year placebo-controlled extension study periods.

Materials and methods
Study population

Full methodological details of the two Phase III studies included in this analysis have been reported previously [19]. Men aged 18 to 41 years, with mild to moderately severe vertex MPHL according to a modified Norwood/Hamilton classification scale (II vertex, III vertex, IV or V) [23, 24], were enrolled. Principal exclusion criteria included significant abnormalities on screening physical examination or laboratory evaluation, surgical correction of scalp hair loss, topical minoxidil use within one-year, use of drugs with androgenic or antiandrogenic properties, use of finasteride or other 5alphaR inhibitors, or alopecia due to other causes. Men were instructed not to alter their hairstyle or dye their hair during the studies.

Study protocols

Two initial, 1-year, randomized, double-blind, placebo-controlled studies were initiated, and both were continued as four consecutive, 1-year, double-blind, placebo-controlled extension studies. The objectives of the controlled extension studies were to determine the effect of long-term (up to five years) treatment with finasteride 1 mg/day, the effect of withdrawing treatment after one year, the effect of delaying treatment by one year, and the progression of MPHL in men not receiving active treatment. Investigators participated at 33 sites in the US and 27 sites in 15 countries outside the US. Institutional review board approval and written informed consent were obtained each year prior to entering subjects into each study.

1-year initial studies

Following a screening procedure, study subjects entered a 2-week, single-blind, placebo run-in period. All men received study shampoo (Neutrogena T/Gel®) for standardization of shampoo used and for prophylaxis of seborrheic dermatitis, which might affect scalp hair growth [25]. Subjects (N = 1,553) were then randomized to finasteride 1 mg/day or placebo (1:1) for one year (Figs. 1 and 2).

Men visited the clinic every 3 months, where they completed a hair growth questionnaire and investigators completed assessments of scalp hair growth. Every 6 months, photographs of scalp hair were taken for hair counts and for the expert panel assessment of hair growth. Reports of adverse events were collected throughout the studies.

1-year extension studies

Men completing the initial 1-year, placebo-controlled studies were eligible to enroll in four consecutive, 1-year, placebo-controlled extension studies. In the first extension studies, men (N = 1,215) were randomly assigned (as determined at initial randomization) to treatment with either finasteride 1 mg or placebo (9:1), such that men were randomized to one of four treatment groups that allocated treatment to them during both the initial 1-year studies (year 1) and the first 1-year extension studies (year 2): finasteride => finasteride, finasteride => Pbo, Pbo => finasteride, or Pbo => Pbo (Figs. 1 and 2). In the three subsequent, 1-year extension studies (years 3 to 5), men continued on the same treatment they had received during the first extension studies (year 2) except for men in the finasteride => Pbo crossover group; those men were switched back to finasteride (finasteride => Pbo => finasteride) during the second extension studies (year 3) and remained on that therapy throughout the subsequent extension studies (years 4 and 5).

The procedures for the first 1-year extension studies (year 2) were similar to those for the initial 1-year studies, except that hair counts were obtained only once, at month 24. In the remaining three 1-year extension studies (years 3 to 5), all efficacy evaluations were performed once yearly.

Evaluation procedures

Efficacy measurements

Four predefined efficacy endpoints provided a comprehensive assessment of changes in scalp hair from baseline: (1) hair counts, obtained from color macrophotographs of a 1-inch diameter circular area (5.1 cm2) of clipped hair (length 1 mm), centered at the anterior leading edge of the vertex thinning area; (2) patient self-assessment of scalp hair, using a validated, self-administered hair growth questionnaire; (3) investigator assessment of scalp hair growth, using a standardized 7-point rating scale; and (4) independent assessment of standardized clinical global photographs of the vertex scalp by a panel of three dermatologists (E. Olsen, R. Savin, D. Whiting) who were blinded to treatment and experienced in photographic assessments of hair growth, using the standardized 7-point rating scale.

Safety measurements

Safety measurements included clinical and laboratory evaluations, and adverse experience reports.

Laboratory evaluation

Hematology and serum chemistries were performed at baseline and every 6 months up to month 24, then yearly thereafter. Hormone measurements were performed at baseline and every 6 months up to month 24, and then at the end of the last extension studies (month 60). Hematology was analyzed in the local laboratory at each study site while serum chemistries, including prostate-specific antigen (PSA), and serum hormones, including testosterone, DHT, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), were assayed in central laboratories (Medical Research Laboratories, Highland Heights, KY and Endocrine Sciences, Calabasas Hills, CA, respectively).

Statistical analysis

A data analysis plan pre-specified all primary and secondary hypotheses, including combining data from the two initial, 1-year, phase III studies to improve precision of the estimates of the treatment effect, as well as from each of the 1-year controlled extensions due to the small size of the placebo groups in those studies.

Hair counts were assessed by the difference between the count at each time point versus the baseline count, and mean hair count values for each treatment group were determined using SASâ„¢ Least Squares Means. Each of the seven questions in the patient self-assessment of hair growth was assessed separately, and the responses to each question at each time point were taken as assessments of changes from baseline. The investigator assessments of hair growth and the expert panel assessments of global photographs were assessed by comparison of mean rating scores for each treatment group at each time point, based on the 7-point rating scale (minimum value = - 3.0 [greatly decreased]; maximum value = 3.0 [greatly increased]). Hypothesis testing for hair counts, individual patient self-assessment questions, and investigator and global photographic assessments was performed using analysis of variance (ANOVA). The ANOVA model included terms for treatment and protocol. For analysis of serum testosterone and DHT, the Wilcoxon Rank Sum test and the associated Hodges-Lehmann estimator were used to determine the median differences and the associated confidence intervals and p-values.

The primary efficacy analysis population for this report was the intention-to-treat population, which included all subjects with at least one day of randomized therapy and with both baseline and at least one post-baseline efficacy assessment. For all efficacy analyses, missing data were estimated by carrying data forward from the previous visit. However, no data were carried forward from the baseline evaluation, or between the initial 1-year study and the first 1-year extension study, or between the extension studies. A secondary population for analysis of efficacy included only the data from the cohort of men who completed the 5-year study.

Safety analyses were based on all subjects with at least one day of randomized therapy. The safety analyses focused on the biochemical parameters, using ANOVA, and on adverse experience reports.

Results
Patient accounting and baseline characteristics

Patient accounting is summarized in Figure 1. A summary of baseline characteristics for men who entered the first extension study (year 2) is presented by treatment group in Table I. Demographics and baseline characteristics were comparable among the four treatment groups.

Hair counts

In the group that received finasteride for up to five years (finasteride => finasteride), there were significant increases in hair counts over five years (p < 0.001 versus baseline for all time points), which reached a maximal increase at month 12 (mean increase [95% CI] from baseline at month 12 = 91 [84, 98] hairs in the target area), declined somewhat thereafter but remained above baseline throughout, with a mean increase of 38 [21, 56] hairs at month 60 (Fig. 3). In contrast, in the group that received placebo for up to five years (Pbo => Pbo), there was a progressive decline in hair counts over five years (p < 0.001 versus baseline for months 24-60), culminating in a mean decrease from baseline of - 239 [- 304, - 173] hairs at month 60 (Fig. 3). Taken together, the hair counts measured in the finasteride => finasteride and Pbo => Pbo groups over five years resulted in a progressive increase in the difference between these two groups over time (mean differences [95% CI] in the changes from baseline): 107 [85, 130] hairs at month 12, 138 [107, 170] hairs at month 24, 146 [106, 185] hairs at month 36, 216 [161, 271] hairs at month 48, and 277 [209, 345] hairs at month 60 (p < 0.001 for all between-group comparisons). Similar results were observed based on an analysis of hair count data for the cohort of men who completed the 5-year study (Fig. 4). Sixty-five per cent (143/219) of finasteride-treated men (finasteride => finasteride) had increased in hair counts at five years, compared to none (0/15) of the placebo-treated (Pbo => Pbo) men. Conversely, hair loss by hair count was demonstrated in all men in the Pbo => Pbo group (15/15) at five years, in contrast to 35% of men (76/219) in the finasteride => finasteride group. Furthermore, the decrease in hair count for the minority of men who lost hair while receiving finasteride for five years was less (- 84 [- 101, - 67] hairs from baseline) than the decrease observed in men receiving placebo over the same time period (- 239 [- 304, - 173] hairs from baseline).

For the group crossed over from placebo to finasteride after one year (Pbo => finasteride), there was a decrease in hair count during the year of placebo treatment (mean change from baseline = - 20 [- 27, - 12] hairs at month 12; p < 0.001). This initial loss of hair on placebo was followed by significant increases in hair count during treatment with finasteride through month 60 (p < 0.001 versus month 12 for months 24-48; p < 0.050 versus month 12 for month 60), with maximal improvement observed at month 24 (12 months on finasteride) (Fig. 3). Increases in hair count during finasteride treatment in this group were generally sustained over time, although the increases compared to baseline were consistently less than those observed in the finasteride => finasteride group at comparable time points, with the difference being similar in magnitude to the amount of hair loss sustained during the year of placebo treatment. For the group that received finasteride for one year, was crossed over to placebo for one year, and was then switched back to finasteride (finasteride => Pbo => finasteride), the beneficial effect on hair count seen during the first year of finasteride treatment was reversed after one year of placebo treatment. Benefit was restored after resumption of therapy with finasteride through month 60 (Fig. 3).

Patient self-assessment

For each of the seven questions in the patient self-assessment questionnaire, treatment with finasteride (finasteride => finasteride) was superior to treatment with placebo (Pbo => Pbo) at each time point (p < 0.001 for all between-group comparisons). The finasteride => finasteride group demonstrated significant (p < 0.001) improvement from baseline at each time point for each question, with the exception that there was no significant difference from baseline at the month 12 time point for Question 5a (assessment of satisfaction with appearance of the frontal hairline), whereas the Pbo => Pbo group generally demonstrated deterioration from baseline over time. For each of the seven questions, a greater proportion of finasteride- versus placebo-treated subjects reported an improvement from baseline, with the difference between groups increasing over time (Fig. 5 and Table II).

In the Pbo => finasteride group, there was generally sustained improvement following one year of placebo treatment for each question during the period of finasteride treatment (p < 0.001 versus month 12 for months 24-60), although, as with hair counts, this improvement was less than that seen in the finasteride => finasteride group at comparable time points. For the finasteride => Pbo => finasteride group, partial to complete reversibility of the beneficial effect of finasteride was observed for six of the seven questions after one year of placebo treatment, with the beneficial effect being partially restored following resumption of finasteride treatment.

Investigator assessment

Based on the investigator assessment, treatment with finasteride (finasteride => finasteride) was superior to treatment with placebo (Pbo =>Pbo) at each time point (p < 0.001, all comparisons) (Fig. 6). By month 60, the investigators rated 77% of subjects in the finasteride => finasteride group as having improved compared to 15% in the Pbo => Pbo group (Table II). As anticipated, the Pbo => finasteride group showed improvement during the period of finasteride therapy through month 60 (p < 0.001 versus. month 12 for months 24-60), although as with hair counts and patient self-assessment the magnitude of this improvement was less than that seen in the finasteride => finasteride group at comparable time points (Fig. 6). In contrast to the other endpoints, the investigator assessment did not demonstrate worsening from baseline for the Pbo => Pbo group until month 36, after which time point further deterioration through month 60 was observed (Fig. 6). For the finasteride => Pbo => finasteride group, there was initial improvement during the first year of finasteride treatment, followed by a plateau during the year of placebo treatment and then restoration of improvement following resumption of finasteride treatment.

Global photographic assessment

Based on the global photographic assessment, treatment with finasteride (finasteride => finasteride) was superior to treatment with placebo (Pbo => Pbo) at each time point (p < 0.001, all comparisons) (Fig. 7). At month 60, 48% of finasteride-treated subjects were rated as slightly, moderately, or greatly improved compared to 6% of placebo-treated subjects. Viewed in the context of maintaining visible hair from baseline, 90% of subjects treated with finasteride demonstrated no further visible hair loss by this assessment, compared to 25% of patients on placebo. Conversely, 75% of men treated with placebo demonstrated further visible hair loss at five years, compared to 10% of men on finasteride (Table II and Fig. 8). For the finasteride => finasteride group, maximal improvement by global photographic assessment was observed at month 24, declined somewhat thereafter, but remained above baseline throughout (p < 0.001 versus baseline for all time points) (Fig. 7). In contrast, the Pbo => Pbo group demonstrated progressive worsening by global photographic assessment through month 60 (p < 0.010 versus baseline for month 24; p < 0.001 versus baseline for months 36-60) (Fig. 7). The Pbo => finasteride group also demonstrated sustained improvement in mean score during the period of finasteride treatment from month 12 to month 60 (p < 0.001 versus month 12 for months 24-60), although, as with the three other efficacy measures, the magnitude of improvement was less than that seen in the finasteride => finasteride group for comparable time points (Fig. 7). For the finasteride => Pbo => finasteride group, the beneficial effect of finasteride was reversed after 12 months of placebo treatment (p < 0.001, month 24 versus month 12), with the beneficial effect partially restored upon resumption of finasteride therapy (Fig. 7).

Global photographs of representative subjects from the Pbo => Pbo and finasteride => finasteride groups who were rated by the expert panel as having decreased or increased hair growth from baseline are shown in Figure 9.

Serum hormones and PSA

As anticipated, treatment with finasteride produced a marked and sustained reduction in serum DHT. For the cohort of men in the finasteride => finasteride and Pbo => Pbo groups with month 60 data, the median baseline serum DHT levels were identical (44.0 ng/dL; normal range = 30-85 ng/dl) and median serum testosterone levels were similar (510 and 496 ng/dl, respectively; normal range = 350-1,030 ng/dl). At month 60, treatment with finasteride led to a median difference between the treatment groups of - 55% [- 68.6, - 45.3] (p < 0.001) for serum DHT and 7.0% [- 6.8, 21.6] (p = 0.315) for serum testosterone. Finasteride treatment had no significant effect on serum LH or FSH compared to placebo, while serum PSA was slightly decreased from a mean baseline of 0.7 ng/ml [normal range < 4.0 ng/mL] to 0.5 ng/ml at month 60 [p < 0.010 versus baseline], leading to a mean difference [95% CI] between the finasteride => finasteride and Pbo => Pbo groups of - 0.3 ng/ml [- 0.5, -0.2] at month 60 (p < 0.001).

Adverse events

Clinical adverse experiences that were considered by the investigator to be possibly, probably or definitely drug-related and that occurred in at least 1% of men are summarized in Table III. As reported previously, in the first year a slightly higher proportion of finasteride than placebo subjects reported drug-related adverse experiences related to sexual function (4.4% versus 2.2%, p = 0.030) (Table III), and only 11 men (1.4%) treated with finasteride and 8 (1.0%) treated with placebo discontinued the studies due to these side effects. These side effects resolved after discontinuation and also resolved in most men who reported them but remained on therapy with finasteride. The adverse experience profile for men continuing in the extension studies was similar to that of the initial studies, and only 7 (1.3%) of the 547 men in the finasteride => finasteride group who continued in the extension studies were withdrawn due to drug-related sexual adverse experiences over the ensuing four years (Table III).

Discussion
The data from these two replicate Phase III studies and their long-term extensions represent the longest reported controlled observations in men with MPHL. The combined analysis demonstrated that long-term treatment with finasteride led to significant and durable improvements, compared to both baseline and placebo, in scalp hair in men with MPHL. Hair counts increased over the first year of treatment with finasteride, with improvement above baseline maintained over five years. In contrast, the placebo group progressively lost hair over five years, confirming the natural progression of hair loss in this disorder due to the continued miniaturization of scalp hair. Thus, the treatment effect of finasteride on hair count relative to placebo increased progressively over time, leading to a net improvement for finasteride-treated men of 277 hairs compared to placebo at five years. Most (65%) finasteride-treated men had increases in hair count at five years, compared to none of the placebo-treated men, but even for those finasteride-treated men with less hair by hair count at five years, the magnitude of loss was less than that observed in the placebo group. These data support that the progression of hair loss observed in placebo-treated men was significantly reduced by treatment with finasteride.

Based on the predefined endpoints utilizing photographic methods (hair counts and global photographic assessment), peak efficacy was observed at one to two years of treatment with finasteride. This observation of an apparent peaking effect is likely due, in part, to the previously-reported beneficial effects of finasteride on the hair growth cycle based on a phototrichogram study [26]. In that study, initiation of finasteride treatment was shown to increase the number of anagen-phase hairs and to increase the anagen to telogen ratio, consistent with normalization of the growth cycles of previously miniaturized hairs due to the release of hair follicles from the inhibitory effects of DHT [26]. Consistent with these results, finasteride treatment was also shown to increase the growth rate and/or thickness of hairs, based on analysis of serial hair weight measurements [27]. Because these beneficial changes in the hair growth cycle are dependent on when therapy with finasteride is initiated and occur rapidly, the affected hairs are driven to cycle in a synchronous manner. If these hairs have somewhat similar anagen phase durations, they would enter telogen phase as the anagen (and catagen) phase ended, followed by subsequent shedding, in a partially synchronized fashion. This would be expected to produce a gradual decline from peak hair count after a period of time equal to the average anagen phase duration. Eventually, as subsequent growth cycles recurred, these hairs would be expected to become increasingly independent, thereby losing their synchronous character as their growth cycles further normalized over time, leading to a sustained increase in hair count at a plateau above baseline, as suggested by the 5-year data presented here.

Patient self-assessment of hair growth provides a mechanism for each subject to judge the benefits of treatment under controlled and blinded conditions. This questionnaire asks specific questions about the patient's hair growth or loss and his degree of satisfaction with the appearance of his hair compared to study start. While a placebo effect was observed with this instrument, as is typical of patient questionnaire data, results consistently demonstrated that men treated with finasteride had a more positive self-assessment of their hair growth and satisfaction with their appearance than men treated with placebo, with the majority of finasteride-treated men reporting satisfaction with the overall appearance of their scalp hair at 5 years. Consistent with the findings of another study in which finasteride was evaluated in men with predominantly frontal MPHL [20], patients' satisfaction with the appearance of their frontal hairline was improved by treatment with finasteride in the present studies.

The investigators' assessments are based on observations of subjects seen in the clinic and provide a clinically relevant assessment of the patient's hair growth or loss since study start. These assessments demonstrated a sustained benefit of finasteride treatment over five years. Although there was no change in the improvements reported for finasteride-treated subjects between month 24 and month 60, there was significant deterioration reported for placebo-treated subjects during the same time period. Thus, the treatment effect as assessed by the investigators increased between months 24 and 60, indicating further separation between the treatment groups over time. As with the patient self-assessment, the investigator assessment had a greater placebo effect than the more objective endpoints of hair count and global photographic assessment. Such an effect is not unusual in double-blind, placebo-controlled studies, and is often due to a general expectation bias on the part of the patient's treating physician. Despite this apparent placebo effect, the beneficial effects of finasteride were demonstrated by the clinical assessments made by the investigators in these studies. In contrast to the investigator assessment, the blinded comparison of paired pre- and post-treatment global photographs by the expert panel, which also assessed change from baseline, demonstrated minimal, if any, placebo effect. Based on this assessment, finasteride treatment led to maintenance of improvement above baseline in scalp hair growth and scalp coverage over five years, while placebo subjects progressively worsened. Treatment with finasteride for five years led to sustained protection against further visible hair loss in nearly all (90%) subjects, while further visible hair loss was evident in most (75%) subjects treated with placebo over the same time period.

While the number of patients remaining in the study declined over time and the size of the placebo group was limited in the extension studies, the results of analyses that included either all available patients at each time point or only the cohort of patients with data at month 60 were consistent and supported a sustained benefit in hair growth for men receiving finasteride 1 mg compared with placebo. Additionally, examination of data from placebo-treated men in all cohorts demonstrated the continued loss of scalp hair that occurs in untreated men with MPHL. Thus, regardless of the cohort examined, the long-term data from these studies consistently demonstrated a beneficial effect of finasteride compared with placebo for men with MPHL. Moreover, this beneficial effect increased over time due to the progressive increase in the net treatment effect of finasteride compared with placebo.

The safety data from the five years of controlled observations in the current studies provide reassurance that long-term use of finasteride 1 mg in men with MPHL is not associated with an increase in the incidence of adverse experiences or any new safety concerns. As in all clinical studies with finasteride, a marked and persistent suppression of serum DHT levels was observed in finasteride-treated subjects, but this was not associated with significant changes in serum gonadotropins (LH and FSH). These data are consistent with previous data on the lack of effect of finasteride on the hypothalamic pituitary-gonadal axis in young men [21, 28]. As expected, based on the previously reported experience with finasteride, a few men in the current studies experienced reversible impairment of sexual function. However, less than 2% of men receiving finasteride discontinued treatment for this reason, compared with 1% of men in the placebo group, with resolution occurring after discontinuation of drug. No other significant adverse effects of finasteride were observed in the patient population evaluated in the current studies. This excellent safety profile of long-term use of finasteride is consistent with the experience with the drug at five times the dose used in the present studies that has been well-documented in large clinical trials and post-marketing surveillance over nine years in men with BPH [13, 17, 29]. In light of the well known inhibitory effect of finasteride on growth of the prostate gland, the modest reduction in serum PSA observed in finasteride-treated subjects over five years was not unexpected. For men in whom serum PSA is used as part of a screening evaluation for prostate cancer, guidelines have been published for interpretation of PSA levels in men receiving finasteride treatment [29-31].

In summary, treatment with finasteride 1 mg/day over five years increased scalp hair as determined by scalp hair counts, patient self-assessment, investigator assessment, and global photographic assessment, when compared with placebo. In contrast, data from the placebo group confirmed that without treatment progressive reductions in hair count and continued loss of visible hair occurs. Long-term treatment with finasteride 1 mg/day was generally well tolerated. The results of these studies demonstrate that chronic therapy with finasteride leads to durable improvements in hair growth in men with MPHL and slows the further progression of hair loss that occurs without treatment.



* The Finasteride Male Pattern Hair Loss Study Group includes (in alphabetical order, by country):

AUSTRIA

D. Kopera, Graz

J. Schmidt, Vienna

BELGIUM

J.-M. Lachapelle, Jumet

D. Van Neste, Tournai

BRAZIL

D. Steiner, Sao Paulo

CANADA

P. Cotterill, Toronto

D. Gratton, Montreal

P. Reardon, Halifax

J. Shapiro, Vancouver

W. Unger, Toronto

FRANCE

P. Reygagne, Paris

P. Saiag, Billancourt

GERMANY

H. Wolff, Munich

ISRAEL

S. Brenner, Tel-Aviv

MEXICO

F. Jurado Santa-Cruz, Mexico City

NETHERLANDS

I. Boersma, Zwijndrecht

E. Prens, Vlissingen

NEW ZEALAND

N. Birchall, Auckland

NORWAY

C. Mork, Oslo

SOUTH AFRICA

J. Cilliers, Tygerberg

M. Sher, Johannesburg

G. Todd, Capetown

SPAIN

E. Lopez-Bran, Madrid

P. Sanchez-Pedreno, El Palmar

SWITZERLAND

G. Burg, Zurich

T. Rufli, Basel

UK

W. Cunliffe, Leeds

S. MacDonald-Hull, Pontefract

A. McDonagh, Bradford

USA

W. Bergfeld, Cleveland, OH

D. Buntin, Hermitage, TN

R. DeVillez, San Antonio, TX

L. Drake, Boston, MA

V. Fiedler, Chicago, IL

D. Fivenson, Detroit, MI

T. Funicella, Austin, TX

C. Gencheff, Madison, WI

M. Hordinsky, Minneapolis, MN

S. Horwitz, Miami Beach, FL

J. Imperato-McGinley, New York, NY

I. Katz, Fridley, MN

A. Kelly, Los Angeles, CA

R. Langley, Boston, MA

N. Lowe, Santa Monica, CA

A. Lucky, Cincinnati, OH

C. McCall, Atlanta, GA

E. Olsen, Durham, NC

G. Peck, Washington, DC

V. Price, San Francisco, CA

R. Rietschel, New Orleans, LA

J. Roberts, Portland, OR

N. Sadick, New York, NY

S. Savage, Denver, CO

R. Savin, New Haven, CT

J. Shupack, New York, NY

D. Stewart, Clinton Township, MI

D. Stough, Hot Springs, AR

J. Swinehart, Denver, CO

L. Swinyer, Salt Lake City, UT

K. Washenik, New York, NY

G. Weinstein, Irvine, CA

D. Weiss, Fairlawn, NJ

J. Weiss, Snellville, GA

D. Whiting, Dallas, TX

E. Whitmore, Baltimore, MD

and

B. Binkowitz, W. He, M. Sanchez

Dept. of Biostatistics

K. Kaufman, E. Round, P. Ruane

Dept. of Clinical Research

Merck Research Laboratories, Rahway, NJ

CONCLUSION

Acknowledgements

This study was supported by a grant from Merck & Co., Inc. The authors wish to acknowledge the technical assistance of Mr. Douglas Canfield, of Canfield Scientific, Inc., in the development of photographic procedures used in these clinical studies. The authors also wish to thank Dr. Alan Meehan, Merck & Co., Inc. for his assistance in preparing this paper for publication.

Article accepted on 15/11/01

REFERENCES

1. Hamilton JB. Male hormone stimulation is prerequisite and an incitant in common baldness. Am J Anat 1942; 71: 451-80.

2. Hamilton JB. Patterned loss of hair in man: types and incidence. Ann NY Acad Sci 1951; 53: 708-28.

3. Price VH. Testosterone metabolism in the skin. Arch Dermatol 1975; 111: 1496-502.

4. Whiting DA. Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male pattern androgenetic alopecia. J Am Acad Dermatol 1993; 28: 755-63.

5. Olsen EA. Androgenetic alopecia. In: Olsen EA, ed. Disorders of hair growth: diagnosis and treatment. New York: McGraw-Hill, Inc., 1994: 257-83.

6. Imperato-McGinley J, Guerrero L, Gautier T, Peterson RE. Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science 1974; 186: 1213-5.

7. Andersson S, Bishop RW, Russell DW. Expression cloning and regulation of steroidal 5alpha-reductase, an enzyme essential for male sexual differentiation. J Biol Chem 1989; 264: 16249-55.

8. Jenkins EP, Andersson S, Imperato-McGinley J, Wilson JD, Russell DW. Genetic and pharmacological evidence for more than one human steroid 5alpha-reductase. J Clin Invest 1992; 89: 293-300.

9. Russell DW, Wilson JD. Steroid 5a-reductase: two genes/two enzymes. Annu Rev Biochem 1994; 63: 25-61.

10. Harris G, Azzolina B, Baginsky W, Cimis G, Rasmusson GH, Tolman RL, Raetz CR, Ellsworth K. Identification and selective inhibition of an isozyme of steroid 5alpha-reductase in human scalp. Proc Natl Acad Sci USA 1992; 89: 10787-91.

11. Thigpen AE, Silver RI, Guileyardo JM, Casey ML, McConnell JD, Russell DW. Tissue distribution and ontogeny of steroid 5alpha-reductase isoenzyme expression. J Clin Invest 1993; 92: 903-10.

12. Bayne EK, Flanagan J, Azzolina B, Einstein R, Mumford J, Avala B, Chang B, Thiboutot D, Singer II, Harris G. Immunolocalization of type 2 5alpha-reductase in human hair follicles. J Invest Dermatol 1997; 108: 651 (abstract).

13. Gormley GJ, Stoner E, Bruskewitz RC, Imperato-McGinley J, Walsh, PC, McConnell J, Andriole GL, Geller J, Bracken BR, Tenover JS, Vaughn ED, Pappas F, Taylor A, Binkowitz B, Ng J. The effect of finasteride in men with benign prostatic hyperplasia. N Engl J Med 1992; 327: 1185-91.

14. McConnell JD, Wilson JD, George FW, Geller J, Pappas F, Stoner E. Finasteride, an inhibitor of 5alpha-reductase, suppresses prostatic dihydrotestosterone in men with benign prostatic hyperplasia. J Clin Endocrinol Metab 1992; 74: 505-8.

15. Dallob AL, Sadick NS, Unger W, Lipert S, Geissler LA, Gregoire SL, Nguyen HH, Moore EC, Tanaka WK. The effect of finasteride, a 5alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. J Clin Endocrinol Metab 1994; 79: 703-6.

16. Drake L, Hordinsky M, Fiedler V, Swinehart J, Unger WP, Cotterill PC, Thiboutot DM, Lowe N, Jacobson C, Whiting D, Stieglitz S, Kraus SJ, Griffin EI, Weiss D, Carrington P, Gencheff C, Cole GW, Pariser DM, Epstein ES, Tanaka W, Dallob A, Vandormael K, Geissler L, Waldstreicher J. The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia. J Am Acad Dermatol 1999; 41: 550-4.

17. US product circular for PROSCAR® (finasteride 5 mg tablets). In: Physicians' Desk Reference. 55th ed. Montvale, NJ: Medical Economics Company, Inc., 2001: 2012-6.

18. Roberts JL, Fiedler V, Imperato-McGinley J, Whiting D, Olsen E, Shupack J, Stough D, DeVillez R, Rietschel R, Savin R, Bergfeld W, Swinehart J, Funicella T, Hordinsky M, Lowe N, Katz I, Lucky A, Drake L, Price VH, Weiss D, Whitmore E, Millikan L, Muller S, Gencheff C, Carrington P, Binkowitz B, Kotey P, He W, Bruno K, Jacobsen C, Terranella L, Gormley GJ, Kaufman KD. Clinical dose ranging studies with finasteride, a type 2 5alpha-reductase inhibitor, in men with male pattern hair loss. J Am Acad Dermatol 1999; 41: 555-63.

19. Kaufman KD, Olsen EA, Whiting D, Savin R, DeVillez R, Bergfeld W, Price VH, Van-Neste D, Roberts JL, Hordinsky M, Shapiro J, Binkowitz B, Gormley GJ. Finasteride in the treatment of men with androgenetic alopecia. J Am Acad Dermatol 1998; 39: 578-88.

20. Leyden J, Dunlap F, Miller B, Winters P, Lebwohl M, Hecker D, Kraus S, Baldwin H, Shalita A, Draelos Z, Markou M, Thiboutot D, Rapaport M, Kang S, Kelly T, Pariser D, Webster G, Hordinsky M, Rietschel R, Katz I, Terranella L, Best S, Round E, Waldstreicher J. Finasteride in the treatment of men with frontal male pattern hair loss. J Am Acad Dermatol 1999; 40: 930-7.

21. US product circular for PROPECIA® (finasteride 1 mg tablets). In: Physicians' Desk Reference. 55th ed. Montvale, NJ: Medical Economics Company, Inc., 2001: 2009-12.

22. Price VH, Roberts JL, Hordinsky M, Olsen EA, Savin R, Bergfeld W, Fiedler V, Lucky A, Whiting DA, Pappas F, Culbertson J, Kotey P, Meehan A, Waldstreicher W. Lack of efficacy of finasteride in postmenopausal women with androgenetic alopecia. J Am Acad Dermatol 2000; 43: 768-76.

23. Norwood O. Male pattern baldness: classification and incidence. South Med J 1975; 68: 1359-65.

24. Takashima I, Iju M, Sudo M. Alopecia androgenetica - its incidence in Japanese and associated conditions. In: Orfanos CE, Montagna W, Stüttgen G, eds. Hair research. Status and future aspects. New York: Springer-Verlag, 1981: 287-93.

25. Agache PG. Eczematous dermatitis of the scalp. In: Zviak C, ed. The Science of Hair Care. New York: Marcel Dekker, 1986: 513-21.

26. Van Neste D, Fuh V, Sanchez-Pedreno P, Lopez-Bran E, Wolff H, Whiting D, Roberts J, Kopera D, Stene J, Calvieri S, Tosti A, Prens E, Guarrera M, Kanojia P, He W, Kaufman KD. Finasteride increases anagen hair in men with androgenetic alopecia. Br J Dermatol 2000; 143: 804-10.

27. Price VH, Menefee E, Sanchez M, Ruane P, Kaufman KD. Changes in hair weight and hair count in men with androgenetic alopecia after treatment with finasteride 1 mg daily. J Am Acad Dermatol 2001 (in press).

28. Rittmaster RS, Lemay A, Zwicker H, Capizzi T, Winch S, Moore E, Gormley GJ. Effect of finasteride, a 5alpha-reductase inhibitor, on serum gonadotropins in normal men. J Clin Endocrinol Metab 1992; 75: 484-8.

29. Moore E, Bracken B, Bremner W, Geller J, Imperato-McGinley J, McConnell J, Roy J, Tenover L, Vaughn D, Pappas F, Cook T, Gormley G, Stoner E. Proscar®: five-year experience. Eur Urol 1995; 28: 304-9.

30. Guess HA, Gormley GJ, Stoner E, Oesterling JE. The effect of finasteride on prostate-specific antigen: Review of the available data. J Urol 1992; 155: 3-9.

31. Oesterling JE, Roy J, Agha A, Shown T, Krarup T, Johansen T, Lagerkvist M, Gormley G, Bach M, Waldstreicher J. Biologic variability of prostate-specific antigen and its usefulness as a marker for prostate cancer: Effects of finasteride. Urol 1997; 50: 13-8.



Copyright © 2007 John Libbey Eurotext - Tous droits réservés

 

[shocktop311]

The 83% is from a five year independent study, not from merck. The reason people are still walking around bald are because 1.)started on a regimen too late. 2.)don't treat their regimen seriously and miss days or don't take treatments exactly as they're to be taken. 3.) Have incomplete regimens, such as y'all who are timid to take propecia. If you don't believe me on the 83 %, solely for propecia, then look it up. Not only that but most other studies have all concluded around 80% chance of maintaining. That with rogaine and nizoral makes it near the 95% mark. You can continue to search for all of these other treatments and waste time and money or you could simply do what has proven to work. The 2% sides Stat is also from the independent study. It's a simple equation: anti-dht agent, regrowth stimulant, scalp cleaning shampoo as well as anti amdrogen. I know there's many dumb people on these forums but most all of the success stories and mods will tell the big 3 is the only for sure way to make a difference. Keep debating internally and keep losing your hair. I'm on the big 3 and have had awesome results.

 

[arcangel]

The 83% is from a five year independent study, not from merck...

I found only one paper which says something similar to the claimed 83% number, except that it is slightly different:

"... 83% of finasteride versus 28% of placebo recipients had no further hair loss compared with baseline after 2 years."

That quote is referenced by other research papers, and (as far as I can tell) the original "83%" quote is from "Finasteride: A Review of its Use in Male Pattern Hair Loss"
Authors: McClellan K.J.; Markham A.
Source: Drugs, Volume 57, Number 1, January 1999 , pp. 111-126(16)

I may be wrong, but a Pubmed search for "(((83%) AND hair) AND propecia) OR finasteride" yields no other research, and a google scholar search is also fruitless so as far as I can tell, everyone is just repeating what they've been told or what they've read on forums. Please provide a direct link to any research that backs up your claims, because I'm tired of searching.

 

[shocktop311]

Obviously not every study is going to be a perfect 83% but they're all over 80%. As I said earlier, you can try all of those medications or you can do the full big 3 and get your hair back. The longer you wait and more products you try the more hair you'll lose and the more money you'll waste. The 2% of sides was also reported by my derm when I first came in for a prescription. Do what you want.

 

[shocktop311]

Go to your derm and let him tell you yourself. The 5 year study is sufficient enough evidence for most people. You can try to find as many studies as you want but when are you finally going to look at the numbers as well as success stories on the forum and realize propecia is effective. I think you have a mild case of physics envy.

 

[arcangel]

I don't know WTF "physics envy" even is. I am comfortable searching Pubmed because I work in the medical field and I am skeptical of forum posts because many people regurgitate false information (especially numbers) without caring if the info is true or not, if it sounds good enough to back up their preconceptions. I will use Fina or Dutasteride because the odds of experiencing side effects are low, but your 83% number is nothing but hearsay - to put it politely. As for reported results on forums, if they're all similar but no proof is offered, then Confirmation Bias can account for a good portions of the results. See http://en.wikipedia.org/wiki/Confirmation_bias

I'll document my hair loss / attempt at regrowth with photos.

 

[shocktop311]

Nice verbiage with the undergrad psychology term You posted a study with the 83% success rate so it's somewhat odd that you're immediately denying their results. My doctor told me of the same rate which I verified for myself by researching the 5 year study. The study is posted all over the forums, isn't too hard to find. I've been skeptical, as are you, because of previous products that wasted my time. I first decided to start finasteride and minoxidil 7 months ago because they ARE THE ONLY 2 FDA APPROVED PRODUCTS for hairloss. If that doesn't speak any sense to you then I don't know what does.

As for physics envy, here's a link for yourself. Make sure to read close Mr. Medical field. It would help explain the irrational nature of humans. http://en.wikipedia.org/wiki/Physics_envy

 

[arcangel]

Why are you pointing out an article on the "Physics Envy" of soft sciences after quoting an "83% success rate" that isn't in any research that I can find? What does that have to do with soft sciences? Are you just trolling me, Mister "I-know-what-confirmation-bias-is-you-b**ch"? "Mr. Medical field" still disputes your numbers because he can't find an independent (non-Merck) study to back them up. I apologize if I'm wrong, I've looked at so many papers that I may have overlooked this legendary 83% figure - but I simply don't see an 83% success rate published by independent researchers anywhere. In fact, if you look at the 2 year long (Merck sponsored) study regarding the "top back of the head" results, then the success rate is 99% if you consider not losing anymore hair to be "success". The success rate is 66% if you are looking for improvement, and 33% if you are shooting for "no visible hair loss".

66% showed improvement
33% no visible hair loss
1% visible hair loss

This study is by Merck itself. If it were reproduced by independent researchers I wouldn't be as skeptical, but I would still be leery because confirmation bias is more than a mere "undergrad" psych term.

http://www.plosmedicine.org/article/inf ... ed.0020124 states "...for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias."

At some point you do have to accept the value of research, but right now I'm simply hoping for the best and putting all my trust in the positive results reported by forum members (including Mister "I-know-what-confirmation-bias-is-you-b**ch"). I don't feel like I have a choice, so not having independent research to back them up just makes me nervous.