pmoll 14.0, 7.5, 9.0; and 12.0, 5.2, 7.5; for SHBG 10.8, 64, 116 nmoll, 3.1, 5.3, 6.9; and 2.8, 3.0, 3.6.
DHT also was determined by RIA, after extraction of samples with a mixture of n-exane and ethanol 98
exane; 2 ethanol, employing a commercial kit from Diagnostic Products Corporation Los Angeles, CA.
Minimum detection limit was 0.01 nmoll. Inter-assay and intra-assay coefficients of variation for three con-
centrations 0.33, 1.00, 2.36 nmoll were respectively: 8.5, 2.3, 8.4 and 6.2, 4.5, 3.1.
On the same occasion of blood sample collection, a standardised interview was performed to exclude any
possible substantial modification of lifestyle, in particu- lar smoking habits and exercise, and dietary habits,
assessed by self-reported alcohol intake and 24-h recall. Nutrient intake was estimated by 24-h recall, using
computerised food tables Dieta 2000, Computek s.r.l. Verona, Italy.
In addition, an assessment of body composition was performed by both anthropometry and bio-impedance
analysis BIA. The following anthropometric measure- ments were taken: weight and height; skinfold thick-
ness, measured in triplicate to the nearest 1 mm at triceps, biceps, subscapular and suprailiac sites with a
Harpender skinfold caliper; circumferences, measured at waist, hip and thigh. From anthropometry the fol-
lowing indexes were calculated: body mass index BMI, kgm
2
as the ratio between weight and height; fat mass percent FMSKF, from four skinfold thickness, by
Durnin and Womersley [33] and Siri equations [34]; the ratio of waist to hip circumferences WHR. In addi-
tion, whole body bioelectric resistance R was mea- sured at 800 mA and 50 kHz with a portable impedance
analyser type BIA, Akern, Firenze, Italy. Resistance R, reactance X and the angular transformation of
the ratio of R to X, the phase angle PA were regis- tered. From bioelectric parameters, fat mass percent
was estimated by the equations developed by Segal et al. [35] or Deurenberg et al. [36], according to age
under or over 62 years FMBIA.
Statistical analysis was performed by a computer employing the SPSS-X program Statistical Package for
the Social Sciences, University of Pittsburgh. For each parameter, the normality of distribution by
Lilliefors test was assessed, which showed a normal distribution for all variables with the exception of TG
and Lpa. For these variables, statistical analysis was performed by both non-parametric tests and parametric
tests on log-transformed values. So, the differences from baseline during treatment were tested for signifi-
cance by ANOVA for repeated measures, as well as Friedman test when appropriate. However, results were
represented by non-transformed values.
Bivariate correlation analysis and stepwise multiple regression analysis were used to study the association
among the absolute changes in lipid, hormone and body composition.
Finally, agglomerative hierarchical cluster analysis was employed to identify patient subsets according to
their different responses in HDL subclasses. Also, the distance between cases was measured as the squared
Euclidean distances and clusters were combined by the average linkage method.
3. Results
Table 1 shows baseline characteristics of patients with BPH, such as age, body composition parameters,
lifestyle self-reported smoking habits and exercise and dietary habits self-reported alcohol and nutrient in-
take, estimated by 24-h recall. Some differences in dietary habits, especially in lipid intake, and activity
Table 1 Baseline characteristics of patients with benign prostatic hyperplasia
BPH M 9 S.D.: age, body composition, lifestyle, alcohol intake and dietary habits
a
Finasteride Controls
N 13
15 64.4 9 6.3
63.5 9 6.0 Age range
55–74 54–74
BMI kgm
2
27.2 9 2.53 26.8 9 2.44
27.84 9 2.56 28.81 9 3.19
FMSKF 0.95 9 0.05
0.95 9 0.05 WHR cmcm
5.68 9 0.79 5.38 9 1.04
PA 32.1 9 1.86
31.13 9 3.23 FMBIA
Smoking cigarettesday
:
85.6 84.2
15.4 B
20 15.8
] 20
Alcohol intake gday
N 2 15.4
2 15.8 5 38.5
B 20
5 31.6 6 46.1
20–40 8 52.6
Acti6ity le6el hweek
N
:
10 76.9 7 47.4
Inactive 6 42.1
Some physical activity 2 3 23.1
hrweek 0 0
2 12.3 Regular physical activity
Dietary intake
:
Calories 2011 9 804
1829 9 640 252 9 71 50.5
Carbohydrates gr 225 9 63 49.2
53 9 21 10 Proteins gr
74 9 26 16.2 Fats gr
74 9 29 33 56 9 17 28.5
Alcohol gr 19 9 10.4 6.5
16 9 9.2 6.1 0.4 9 0.1
0.6 9 0.1 PS ratio
191 9 67 Cholesterol mg
157 9 63
a
Comparison between treated and control patients were made by Mann–Whitney U test and the x
2
test, when appropriate. BMI, body mass index; FMSKF, fat mass percent by anthropometry; WHR,
waist to hip ratio; PA, phase angle; FMBIA, fat mass percent by Bio-impedance analysis.
Table 2 Hormone levels M 9 S.D. at baseline and after 3 and 6 months of
treatment with finasteride 3 months
6 months Baseline
DHT nmoll
0.76 9 0.32 0.63 9 0.19
Finasteride 1.52 9 0.65
1.52 9 0.65 1.54 9 0.70
1.55 9 0.32 Controls
fT pmoll
Finasteride 61.1 9 10.5
58.4 9 13.0 56.6 9 13.4
56.6 9 14.8 Controls
58.8 9 12.5 57.6 9 12.0
E
2
pmoll Finasteride
96.3 9 31.7 103 9 50.0
96.32 9 45.9 94.5 9 17.6
91.4 9 20.9 95.3 9 11.3
Controls SHBG
nmoll 52.39 9 20.2
Finasteride 52.98 9 24.8
53.00 9 17.4 69.02 9 30.2
68.9 9 33.4 68.5 9 33.9
Controls PB0.01 vs. baseline.
for unpaired data and x
2
test, as appropriate excluded that these differences were significant. As for lipo-
proteins, baseline concentrations in treated and un- treated patients are represented in Table 3. No
significant differences were apparent between treated and control subsets, although control patients showed
slightly higher total and LDL-C levels. As expected, distribution of Lpa serum concentrations was typi-
cally skewed toward the lower values. Overall, there were no differences between patients with BPH and free
living control subjects of similar age data not shown.
After 3 and 6 months of treatment with finasteride, a significant decrease of DHT concentration was ob-
served, respectively of 52 and 56. On the contrary, no significant changes in fT, E2 and SHBG concentrations
were found Table 2.
Therapy was associated with consistent changes in lipoproteins Table 3, with a significant HDL-C in-
crease of 9.6 at 3 months and of 24 at 6 months vs. no changes in control group. As a consequence, LDL
HDL-C ratio significantly decreased by 19. Also Lpa concentrations were significantly increased by
27 after 6-month therapy with finasteride.
No significant changes were apparent in most body composition parameters, especially in BMI and FM,
assessed by both anthropometry and BIA Table 4 in both treated and control patients. Accordingly, no sig-
nificant changes in smoking habits, activity level and dietary habits were detected data not shown. How-
ever, a slight but significant decrease of the bioelectric index PA became apparent after 6-month treatment
with finasteride.
With the aim of further characterising the increase in HDL-C found after Finasteride, HDL2 and HDL3
Table 3 Lipoprotein levels M 9 S.D. at baseline and after 3 and 6 months of
treatment with finasteride
a
Baseline 3 months
6 months TC
mmoll 5.03 9 1.07
5.00 9 0.79 Finasteride
5.25 9 1.27 Controls
5.21 9 1.02 5.24 9 0.83
5.16 9 0.9 LDL-C
mmoll 3.36 9 0.71
3.27 9 1.01 Finasteride
3.39 9 1.04 3.50 9 0.76
Controls 3.49 9 1.04
3.43 9 1.0 HDL-C
mmoll 1.01 9 0.20
1.12 9 0.22 1.27 9 0.26
,
Finasteride 0.98 9 0.20
1.00 9 020 Controls
0.98 9 0.21 LDLHDL-C
3.38 9 0.70 Finasteride
3.08 9 1.30 2.74 9 0.89
3.75 9 1.12 3.72 9 1.58
Controls 3.63 9 1.53
TG mmoll
1.36 9 0.56 Finasteride
1.42 9 0.63 1.44 9 0.55
1.38 1.26
1.04 Controls
1.66 9 0.58 1.45 9 0.53
1.65 9 0.64 1.52
1.46 1.32
Lp a
mgl 221.9 9 239
,
182.8 9 197 Finasteride
174.7 9 203 129.5
147.5 112.5
Controls 119 9 125
130 9 148 110 9 104
63.7 65.8
64.3
a
For triglyceride TG and lipoprotein a Lpa also median values are represented in brackets
PB0.01 vs. baseline. PB0.05 vs. baseline.
PB0.01 vs. 3 months. PB0.05 vs. 3 months.
Table 4 Body composition indexes at baseline and after 3 and 6 months of
treatment with finasteride 6 months
Baseline 3 months
BMI kgm
2
Finasteride 27.2 9 1.6
27.2 9 1.6 27.1 9 1.5
25.8 9 1.4 25.7 9 1.4
Placebo 25.8 9 1.3
FM SKF
Finasteride 28.81 9 3.19
28.38 9 2.79 27.99 9 2.70
Placebo 27.84 9 2.56
27.28 9 1.71 27.18 9 1.58
WHR cmcm
0.96 9 0.05 0.95 9 0.05
Finasteride 0.97 9 0.05
0.96 9 00.4 Placebo
0.97 9 0.03 0.95 9 0.05
PA 5.68 9 0.89
Finasteride 5.30 9 0.73
5.68 9 0.79 Placebo
5.46 9 0.77 5.48 9 1.04
5.52 9 0.55 FM
BIA Finasteride
32.10 9 1.86 32.3 9 1.56
32.31 9 1.90 31.13 9 3.23
30.48 9 4.1 Placebo
30.6 9 3.6 PB0.05 vs. baseline.
level, were apparent at baseline between treated and control groups, suggesting that they were not well
matched. However, statistical analysis Student’s t-test
Fig. 1. High density lipoprotein-cholesterol HDL-C subclasses M 9 S.E. after 3 and 6 months of finasteride treatment.
changes, documented both at 3 and 6 months were entered into the analysis. Also some body composition
indexes were entered into analysis, as independent co- variates; as for FM, estimates from BIA were used
instead of FMSKF, since BIA is generally considered as more accurate than anthropometry to estimate fat
mass in aged people [37]. The analysis did not show any association of total HDL-C and Lpa increases to
hormones or nutritional status Table 5. However, an association of HDL subfractions with fT and E2
changes, positive for HDL2-C and negative for HDL3- C, was found. Multiple regression analysis stepwise
confirmed the lack of any associations between lipo- protein increase and DHT declines, as well as the slight
but significant contribution of E2 to HDL2 and HDL3 changes respectively of 36 and 19. On the contrary,
the association of HDL subfractions with fT apparent at bivariate correlation analysis was no more significant
Table 6.
However, considering individual responses to ther- apy, some variability was found in HDL subclass re-
sponses to
finasteride. Therefore,
agglomerative hierarchical cluster analysis was performed. Two differ-
ent classes of patients were identified: seven patients cluster I showed a prevalent increase in HDL2-C,
while in the others cluster II, an increase of HDL3-C associated with a decrease in HDL2-C was apparent.
Relative changes in DHT were not different between the two clusters Table 7, but some differences in E2
and fT were found: in patients showing an increase of HDL2-C Cluster I, an increase of fT and E2 was
apparent, while the preferential increase of HDL3-C, with its accompanying decline in HDL2-C Cluster II,
was associated with a decrease of both fT and E2.
4. Discussion
