Page 9-11

Based on table 4.3, the mean systolic blood pressure obtained in the prostate volume
group <40 mL and ≥ 40 mL was 128.20 ± 13.38 and 131.09 ± 19.83; prostate volume <40
mL and ≥ 40 mL were 78.00 ± 5.00 and 82.63 ± 11.76. In the analysis of the Independent t-
test and Mann-Whitney obtained no significant difference between the two groups with a
value of p = 0.679 for systolic blood pressure and p = 0.125 for diastolic blood pressure.
According to Hwang's research in 2013, getting a total IPSS (22.9 ± 7.8 vs 21.2 ± 7.3, p =
0.01) and obstructive symptom scores (13.3 ± 5.2 vs 11.9 ± 4,7, p = 0.01) significantly
different between men with hypertension and without cardiovascular risk factors. There were
no significant differences between subjects with DM, smoking or dyslipidemia and without
cardiovascular risk factors. In the Pearson corelation, systolic and diastolic blood pressure is
related to prostate volume (r = 0.138, p = 0.040; r = 0.163, p = 0.020), total IPSS (r = 0.139, p
= 0.043; r = 0.138, p = 0.043) , and Obstructive symptom scores (r = 0.168, p = 0.014; r =
0.143, p = 0.037), respectively. The relationship between hypertension and LUTS can
influence disease management due to the pathophysiology correlated with the postulated
disease entity due to increased plasma catecholamine levels associated with urine production
or reduced nighttime bladder capacity. It has been approved by patients with hypertension
that represent an increase in renal arteries, which encourages increased urine output.8
The mean abdominal girth in the prostate volume group <40 mL and ≥ 40 mL was
83.70 ± 9.94 and 96.02 ± 10.99. In the Independent t-test analysis test it was found that there
were differences in mean abdominal circumference between the two prostate volume groups
with a value of p = 0.005. Research conducted by Lee in 2012 also found that abdominal
circumference was associated with an increase in BPH symptoms.9,10
There are many hypotheses that have been suggested for the effects of obesity on
BPH. Central obesity has several systemic effects. Obesity will increase intraabdominal
pressure, which can increase bladder pressure and intravesic pressure, with the potential to
worsen and cause BPH symptoms. Another mechanism is changing endocrine status. The
increase in the ratio of estrogen to androgens due to the P450 aromatase enzyme is expressed
by fat tissue. Therefore, adipose tissue mass will increase aromatase activity and the
conversion of androgens to estrogens (testosterone to estradiol and androstenedione to
estrone). Increased fat mass and aromatase activity reduce testosterone concentrations and
allow deposition of abdominal adipose tissue/VAT preferences as a positive calorie balance
which results in an obese cycle of hypogonadism. The continuous production of estradiol
caused by accumulation of fat mass can result in suppression of gonadotropin, with a further
reduction in testosterone levels and the development of a progressive state of hypogonadism
so that it is beneficial in the development of BPH. Increased sympathetic nerve activity in
central obesity has been known to influence the development of BPH and the severity of
obstructive urinary symptoms. However, difficulties in measuring sympathetic nerve activity
and heterogeneity in characterizing obesity can cause a lack of a conclusive relationship
between sympathetic nerve activity and obesity.9,10
The mean HDL in the prostate volume group <40 mL and ≥ 40 mL was 41.20 ± 10.03
and 44.59 ± 24.16; the mean blood glucose in the prostate volume group <40 mL and ≥ 40
mL was 93.20 ± 19.30 and 107.18 ± 18.59; the mean triglycerides in the prostate volume
group <40 mL and ≥ 40 mL were 109.90 ± 31.30 and 119.63 ± 34.28. In the Independent t-
test and Mann-Whitney analysis it was found that there were no significant mean differences
between the two groups with p = 0.951 for HDL, p = 0.061 for blood glucose and p = 0.329
for triglycerides.
In the Parsons study, there was no significant relationship of total cholesterol (p =
0.520), HDL cholesterol (p = 0.560), triglycerides (p = 0.300), or triglycerides to HDL ratio
(p = 0.130) with the risk of BPH. In a subset analysis in men with diabetes, those in the
highest quartile (> 133 mg/dL) of LDL cholesterol, compared with those in the lowest
quartile (<110 mg/dL), were 4 times more likely to experience BPH (OR 4.00, 95% CI 1.27-
12.63, p = 0.02) .11
Although the variables in this study did not find statistically significant mean
differences, descriptively it can be seen that the mean systolic/diastolic blood pressure,
abdominal circumference, blood glucose, triglycerides were higher in the group with prostate
volume ≥ 40 mL, but the mean HDL was found high in groups with prostate volume ≥ 40
mL.
Based on table 4.5, it was found that there were 70.0% of subjects without metabolic
syndrome and 30.0% of subjects with metabolic syndrome in the prostate volume <40 mL,
while there were 22.7% of subjects without metabolic syndrome and 77.3% of subjects
without metabolic syndrome in the prostate group ≥ 40 mL. In the Fisher's Exact analysis test
found that there is a significant relationship between metabolic syndrome and prostate
volume with a value of p = 0.018.
The results of this study are the same as the results of Hyun's study in 2012 which
found that patients with central obesity (p ＜ 0,0001, ＜ 0,0001), high systolic blood pressure
(p = 0.021, p = 0.003), high diastolic blood pressure ( p = 0.001, p ＜ 0.0001), high
triglycerides (p = 0.001, p ＜ 0.0001), low HDL-C (p = 0.012, p ＜ 0.0001), and high fasting
blood sugar (p = 0.0001, p ＜ 0.0001 ) had significantly higher serum PSA levels and greater
prostate volume than patients without metabolic syndrome. Therefore, the presence of a
metabolic component in these patients is significantly associated with higher serum PSA
levels and greater prostate volume.5
Metabolic syndrome can cause prostate growth by various mechanisms.
Hyperinsulinemia has a stimulant effect on the sympathetic nervous system. It increases
glucose intake to the hypothalamic ventromedial neurons, which regulate the sympathetic
nervous system. Prostate obstruction is not only caused by static obstruction caused by the
prostate gland; The adrenergic smooth muscle cell tone present in the prostate capsule and
bladder neck also has a role in this process, which is called dynamic union. Increased
sympathetic activity caused by hyperinsulinemia can be attributed to the pathophysiology of
BPH. Hyperinsulinemia contributes to activation of the sympathetic nervous system and
causes increased levels of catecholamines in the tissues. This can also contribute to the
5-
development of BC and increase prostate smooth muscle tone, which causes severe LUTS.
7,12

One more pathway that explains the increased risk of BPH in hyperinsulinemia is
insulin like growth factor (IGF). IGF-1 is a powerful mitogen and increases cell proliferation
and inhibits apoptosis in many tissues including prostate and epithelial stroma. The systemic
use of IGF-1 in mice for a short period increased prostate weight by 29%. Acromegaly
patients with high levels of growth hormone and IGF-1 have prostate enlargement despite
low levels of testosterone.5-7.12
Based on table 4.4, it was found that the mean systolic blood pressure in the moderate
and severe IPSS groups was 129.53 ± 18.31 and 140.00; the mean diastolic blood pressure in
the moderate and severe IPSS groups was 83.00 ± 4.24 and 81.33 ± 10.52; the mean
abdominal girth in the moderate and severe IPSS group was 80.00 ± 2.82 and 92.98 ± 11.95;
the mean HDL in the moderate and severe IPSS group was 37.50 ± 6.36 and 43.93 ± 21.28;
the mean blood glucose in the moderate and severe IPSS group was 101.50 ± 36.06 and
102.90 ± 19.16; the mean triglycerides in the moderate and severe IPSS groups were 82.50 ±
2.12 and 118.86 ± 33.04. In the Independent t-test and Mann-Whitney analysis, it was found
that only triglycerides had a mean difference in value between the two groups with a value of
p = 0.043, but no mean difference was obtained for other metabolic syndrome variables.