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Prostatic Hyperplasia: An Unknown Feature
of Acromegaly
ANNAMARIA COLAO, PAOLO MARZULLO, DIEGO FERONE, STEFANO SPIEZIA,
GAETANA CERBONE, VALERIA MARINO
`, ANTONELLA DI SARNO,
BARTOLOMEO MEROLA, AND GAETANO LOMBARDI
Department of Clinical and Molecular Endocrinology and Oncology, University Federico II (A.C., P.M.,
D.F., G.C., V.M., A.D.S., B.M., G.L.), and Emergency Unit, Ospedale Incurabili (S.S.), 80131 Naples,
Italy
ABSTRACT
This study was designed to investigate whether GH and insulin-
like growth factor I (IGF-I) excess could lead to the development of
benign prostatic hyperplasia and/or prostatic carcinoma. Prostatic
diameters and volume as well as the occurrence of prostatic diseases
were studied by ultrasonography in 10 untreated acromegalic pa-
tients less than 40 yr of age and 10 age- and body mass index-matched
healthy males. Serum GH, IGF-I, PRL, testosterone, dihydrotestos-
terone, prostate-specific antigen, and prostatic acid phosphatase lev-
els were assessed. All patients had secondary hypogonadism, as di-
agnosed by low testosterone levels, and 4 of 10 patients had
hyperprolactinemia. After 1 yr of treatment with octreotide (0.3–0.6
mg/day), ultrasound scan and hormone parameters were repeated.
The 4 hyperprolactinemic acromegalics were treated with octreotide
and cabergoline (1–2 mg/week) to suppress PRL levels.
Symptoms due to prostatic, seminal vesicle, and/or urethral dis-
orders or obstruction were experienced by neither acromegalics nor
controls. Digital rectal examination revealed no occurrence of pros-
tatic nodules or other abnormalities. Compared to healthy subjects,
a remarkable increase in transversal prostatic diameter and volume
was observed in acromegalics. In healthy subjects, prostate volume
ranged from 15.1–21.8 mL, whereas in acromegalics it ranged from
21.8–41.8 mL. Similarly, an increased median lobe was observed. In
fact, the transitional zone diameter was just detectable in 5 of 10
controls, whereas it was measurable in all acromegalics (18 61.2 vs.
2.8 60.3 mm; P,0.001). The prevalence of periurethral calcifications
was more than doubled in acromegalics (50%) compared to that in
controls (20%). Treatment with octreotide for 1 yr produced normal-
ization of circulating GH and IGF-I levels in 7 of 10 patients. In these
7 patients, ultrasound evaluation showed a significant reduction of
the antero-posterior diameter (26.1 61vs. 28.9 61.6 mm; P,0.01),
the transversal diameter (44.9 62vs. 48 62 mm; P,0.01), and the
cranio-caudal diameter (36.5 61vs. 41.3 61.5 mm; P,0.001),
whereas the transitional zone diameter was unchanged (16.4 61.5 vs.
17.4 61.7 mm). As a consequence, a significant decrease in prostate
volume was recorded (22.1 61.1 vs. 29.8 62.5 mL; P,0.001).
Prostate volume increased in 2 of the 3 patients who did not achieve
normalization of GH and IGF-I after octreotide treatment. Finally,
after treatment, serum testosterone levels were significantly in-
creased (from 1.5 60.3 to 3.5 60.3
m
g/L), whereas dihydrotestos-
terone, dehydroepiandrosterone sulfate, D
4
-androstenedione, 17
b
-es-
tradiol, prostate-specific antigen, and prostatic acid phosphatase
were unchanged. Serum PRL levels were suppressed after cabergo-
line treatment in all 4 hyperprolactinemic patients throughout the
study period.
In conclusion, prostate enlargement occurs in young acromegalics
with a higher than expected prevalence of micro- and macrocalcifi-
cations. This suggests that a careful prostate screening should be
included in the work-up and follow-up of acromegalic males. (J Clin
Endocrinol Metab 83: 775–779, 1998)
ACROMEGALY, a pituitary disorder caused in most
cases by a GH-secreting adenoma, is characterized by
progressive skeleton abnormalities and visceromegaly,
which lead to a stepwise disfigurement of the patient (1–3).
Whereas thyroid, heart, liver, and bone changes, strictly GH
and insulin-like growth factor I (IGF-I) targeted, have been
widely investigated, no study has been performed until now
to assess the prevalence of prostate hyperplasia in conditions
of chronic excess of GH and IGF-I. In humans, prostate en-
largement starts approximately at the age of 40 yr and rises
from 23% to 88% by the ninth decade. Prostate cancer rep-
resents one of the most common malignancies in adult men
(4).
This study was designed to investigate whether GH and
IGF-I excess could lead to the development of benign pros-
tatic hyperplasia and/or prostatic carcinoma in acromegalic
patients. Prostatic diameters and volume as well as the oc-
currence of prostatic diseases were studied by ultrasonog-
raphy in 10 untreated acromegalic patients less than 40 yr of
age. Serum dihydrotestosterone (DHT) and prostate-specific
antigen (PSA) levels were assessed to evaluate the partici-
pation of this regulatory factors in prostatic growth. After 1
yr of treatment with octreotide (OCT), ultrasound scan and
hormone measurements were repeated to evaluate volume
changes after suppression of GH/IGF-I levels had been
achieved.
Subjects and Methods
Patients
Ten acromegalic patients, less than 40 yr of age (range, 26–39 yr),
and 10 age- and body mass index-matched healthy males entered this
study after their informed consent had been obtained. Acromegaly
was diagnosed on the basis of clinical features, elevated GH serum
levels (36.9 66.9
m
g/L) not suppressible below 2
m
g/L by oral
glucose administration, and elevated IGF-I plasma levels (682.4 6
67.4
m
g/L). Four patients presented with coexistent hyperprolactine-
mia (from 55.5–250
m
g/L; Table 1), whereas all patients suffered from
Received September 10, 1997. Revision received November 21, 1997.
Accepted December 2, 1997.
Address all correspondence and requests for reprints to: Annamaria
Colao, M.D., Ph.D., Department of Clinical and Molecular Endocrinol-
ogy and Oncology, University Federico II, Via S. Pansini 5, 80131 Naples,
Italy.
0021-972X/98/$03.00/0 Vol. 83, No. 3
Journal of Clinical Endocrinology and Metabolism Printed in U.S.A.
Copyright © 1998 by The Endocrine Society
775
hypogonadism and showed reduced serum concentrations of FSH,
LH (data not shown), and testosterone (1.5 60.3
m
g/L; Table 1).
Computed tomography and/or magnetic resonance imaging docu-
mented the presence of macroadenoma in 8 patients and microad-
enoma in 2 patients. At study entry, 4 acromegalic patients and 4
control subjects were smokers; none of the study subjects was a high
alcohol consumer, and all had normal diet intake. None of the patients
who were included in the study had previously received any andro-
gen replacement therapy. The patients’ profiles at study entry are
shown in Tables 1 and 2.
Study design
Circulating GH, IGF-I, PRL, FSH, LH, 17
b
-estradiol, testosterone,
DHT, D
4
-androstenedione (D
4
), dehydroepiandrosterone sulfate
(DHEA-S), PSA, and prostatic acid phosphatase (PAP) were assessed at
least twice at study entry and quarterly during treatment with OCT.
Ultrasound examination was performed at study entry and after treat-
ment with OCT. All patients were treated with OCT (Sandostatina,
Novartis, Milan, Italy) for 1 yr. OCT was initially administered at a daily
dose of 0.15 mg in six patients and 0.3 mg in four patients, according to
patients’ compliance during the acute test (0.1 mg, sc), as previously
reported (5). Subsequently, the dose of 0.3 mg/day was maintained
throughout the follow-up in six patients, whereas it was increased up
to 0.6 mg daily in four patients to obtain GH/IGF-I suppression, im-
provement of clinical signs and symptoms and/or tumor shrinkage. In
the four hyperprolactinemic acromegalics, a combined treatment with
OCT plus cabergoline (Dostinex, Pharmacia and Upjohn, Milan, Italy) at
a dose of 1–2 mg/week was given to suppress serum PRL levels. At
study entry, plasma IGF-I levels were assayed twice in a single sample,
whereas serum GH was calculated as the mean of a 6-h blood sampling
(0800–1400 h, 30-min sampling). During treatment, the final GH level
was calculated as the average value from at least three blood samples
collected at 15-min intervals 2 h after OCT administration. At this time
point, plasma IGF-I concentrations were assayed as single sampling.
Hormone normalization after OCT treatment was considered when
basal and oral glucose tolerance test-suppressed GH values were below
TABLE 2. Ultrasonographic evaluation of prostate parameters in acromegalics and controls at study entry
Subject no.,
age (yr)
Body mass
index
Antero-posterior
diameter (mm)
Transversal
diameter (mm)
Cranio-caudal
diameter (mm)
Transitional
zone (mm) Vol (mL) Ultrasonographic and
power doppler findings
Acromegalic patients
1. 26 25.3 24 51.5 36.4 15 23.4 Single 8-mm MC in RL
2. 28 24.8 31.4 42.1 39.8 20 27.3 Periurethral mC
3. 29 26.3 23.1 43 42.3 19 21.8 Periurethral mC
4. 30 25.5 24.6 52.8 41.4 12 27.9 Normal
5. 31 23.9 32.2 41.5 39.4 19 27.3 Normal
6. 32 24.7 28 42 36.2 14 22.1 Periurethral diffused mC
7. 35 27.0 32.8 40.1 47.8 23.1 32.7 Periurethral MC
8. 37 26.6 34.9 53.6 43 22.2 41.8 Normal
9. 38 27.5 32.1 47.2 41.9 20.5 33 Normal
10. 39 29.4 26 49.2 42.1 15.3 28 Single uthricular cyst
Mean 6SEM 26.1 60.5 28.9 61.3 46.3 61.6
a
41 61.1 18 61.2
a
28.5 61.9
a
Healthy subjects
1. 26 23.3 24.1 34.2 35.4 ND 15.1 Normal
2. 28 25.1 28.1 36.1 41.1 3 21.6 Normal
3. 28 25.7 25.2 40.4 39.1 ND 20.7 Periurethral mC
4. 31 24.2 28.1 34.6 34.9 2 17.6 Normal
5. 31 22.1 28.2 38.9 38.2 ND 21.8 Normal
6. 32 25.1 25.4 36.4 43.9 4 19.2 Normal
7. 35 26.4 24.8 39.1 37.3 3 18.8 Normal
8. 36 27.1 25.6 34.9 40.9 3 19 mC at LL
9. 38 27.3 27.4 35.3 38.1 ND 19.1 Normal
10. 39 27.9 26.1 35 39.4 2 18.7 Normal
Mean 6SEM 25.4 60.6 26.3 60.5 36.5 60.7 38.8 60.9 2.8 60.3 18.2 60.6
MC, Macrocalcification; mC, microcalcification; RL, right lobe; LL, left lobe.
a
P,0.001 vs. controls.
TABLE 1. Hormone profile of the 10 patients at study entry
Patient no.,
age (yr)
Disease
duration
(yr)
Serum GH
(
m
g/L)
Plasma IGF-I
(
m
g/L)
Serum PRL
(
m
g/L)
Serum T
(
m
g/L)
Serum DHT
(nmol/L)
Serum PSA
(
m
g/L)
Serum PAP
(IU/L)
1. 26 6 30 850 12.2 2.2 1.0 1.8 0.8
2. 28 5 65 1120 55.5 1.1 1.0 2.1 1.1
3. 29 7 44 600 250 0.9 0.3 3.5 1.2
4. 30 4 16.5 670 4.4 1.8 0.8 4.8 0.1
5. 31 10 71.2 864 95.2 1.9 0.9 4.1 1.6
6. 32 15 18.9 600 84 0.1 0.1 0.9 1.8
7. 35 15 55 625 10.1 0.1 0.2 1.2 1.6
8. 37 7 16.7 725 3.5 2.1 0.8 3.1 1.5
9. 38 15 9.5 600 10 3.7 0.8 2.0 1.5
10. 39 10 42 570 12.1 1.3 1.0 2.2 1.6
Mean 6SEM 9.4 61.4 36.9 66.9 722.4 655.3 53.7 624.4 1.5 60.3 0.7 60.1 2.6 60.4 1.3 60.2
Normal ranges: GH, less than 5
m
g/L; IGF-I, 110 –502 and 100– 494
m
g/L for patients aged 20 –30 and 31–40 yr, respectively; PRL, 5–15
m
g/L;
testosterone, 3.5–9
m
g/L; DHT, 0.4–1.6 nmol/L; PAP, 0–2.6 U/L; PSA, 0–10
m
g/L.
776 COLAO ET AL. JCE&M•1998
Vol 83 •No 3
5 and 2
m
g/L, respectively, and IGF-I values were within the normal
ranges.
Hormonal assessment
GH, PRL, testosterone, and 17
b
-estradiol were measured by RIA;
IGF-I, FSH, LH, PSA, and DHT were determined by immunoradiometric
assay; PAP was measured by autoanalyzer. The normal ranges were:
GH, 0–5
m
g/L; IGF-I, 110–502 and 100–494
m
g/L, respectively for
patients aged 20–30 and 31–40 yr; PRL, 5–15
m
g/L; FSH and LH, 5–18
mU/mL; testosterone, 3.5–9
m
g/L; DHT, 0.4–1.6 nmol/L; D
4
, 1–3.5
m
g/L; DHEA-S, 60–560
m
g/L; 17
b
-estradiol, 20–70
m
g/L; PAP, 0–2.6
U/L; and PSA, 0–10
m
g/L. All assessments were age adjusted.
Ultrasound examination
All of the patients received a preliminary enema with 120 mL sodium
acid phosphate (Clismalax, Sofar, Milan, Italy) not later than 1 h before
the examination to favor rectal cleanliness. Before ultrasonography,
patients underwent a preliminary digital rectal exploration. Prostate
ultrasonography was carried out with ATL Apogee 800 (Advanced
Technology Laboratories, Bothell, WA) by means of a 9.0-megahertz
end-fire transrectal transducer (2-cm external diameter) and a Power
Echo Color Doppler Advanced Technology module that displays the
total integrated Doppler power in color, to obtain angiographic micro-
maps (6). The transducer, preliminarily covered with ultrasound trans-
mission gel (Acquasonic, Parker Laboratory, Newark, NJ) and a dis-
posable rubber sheat, was lubricated and gradually inserted about 3 cm
into the rectum, then directed toward the anterior rectal wall. The fol-
lowing prostate diameters and features were evaluated in B-mode: an-
tero-posterior, transversal, cranio-caudal, and that including the tran-
sitional zone (TZD); morphology of gland boundary; occurrence of
microcalcifications (#3 mm) and/or macrocalcifications (.3 mm); de-
tection and sizing of intraprostatic nodules; evaluation of seminal ves-
icles; and occurrence of local inflammatory events. Reconstruction by a
standard ellipsoid formula (0.52 3length 3height 3width) allowed the
measurement of total prostate volume. All scans were performed by a
single examiner (S.S.). In agreement with previous findings (7), normal
prostate volume was considered as less than 30 mL.
Statistical analysis
Data are expressed as the mean 6sem. ANOVA, Student’s ttest for
paired data, and linear correlation analysis were applied where appro-
priate. Statistical significance was set at 5%.
Results
Patients with acromegaly showed significantly decreased
serum testosterone levels (Table 1), whereas FSH, LH,
DHEA-S, 17
b
-estradiol (data not shown), DHT, PSA, and
PAP (Table 1) were in the normal range. All patients had
secondary hypogonadism, as diagnosed by low testosterone
levels, and 4 of 10 patients had hyperprolactinemia (no. 2, 3,
5 and 6; Table 1).
Ultrasonographic findings at study entry
Symptoms due to prostatic, seminal vesicle, and/or ure-
thral disorders or obstruction were not experienced by either
acromegalics or controls. Digital rectal examination revealed
no occurrence of prostatic nodules or other abnormalities.
Compared to healthy subjects, a remarkable increase in
transversal diameter and volume of the prostate gland was
observed in acromegalics (Table 2). In healthy subjects, pros-
tate volume ranged from 15.1–21.8 mL, whereas in acrome-
galics, it ranged from 21.8– 41.8 mL. In 3 patients (no. 7–9;
Table 2), prostate volume was greater than 30 mL, which was
considered a normal threshold value (7). Similarly, an in-
creased median lobe was observed. In fact, TZD was just
detectable in 5 of 10 controls, whereas it was measurable in
all acromegalics (18 61.2 vs. 2.8 60.3 mm; P,0.001). The
prevalence of periurethral calcifications was more than dou-
bled in acromegalics (50%) compared to that in controls (20%;
Table 2). Among the 10 acromegalics, calcifications in the
periurethral zone were detected in 4 patients (no. 2, 3, 6, and
7), and calcifications within the lobes were found in 1 patient
(no. 1), whereas in another patient (no. 10) a diffuse hypere-
chogenity of prostatic tissue with a single uthricolar cyst was
detected (Table 2). No sign of vesicle inflammation was
shown. No significant difference in prostatic volume (24.6 6
1.5 vs. 31.1 62.6 mL) or serum testosterone levels (1 60.4
vs. 1.9 60.5
m
g/L) was found between hyperprolactinemic
and normoprolactinemic acromegalics. A significant corre-
lation was found only between prostate volume and patient
age (Table 3).
Effect of long term OCT treatment on prostate parameters
and hormone levels
Treatment with OCT for 1 yr induced normalization of
circulating GH and IGF-I levels in 7 of 10 patients (Fig. 1). In
these 7 patients, ultrasound evaluation showed a significant
reduction of antero-posterior diameter (26.1 61vs. 28.9 61.6
mm; P,0.01), transversal diameter (44.9 62vs. 48 62 mm;
P,0.01), and cranio-caudal diameter (36.5 61vs. 41.3 61.5
mm; P,0.001), whereas TZD was unchanged (16.4 61.5 vs.
17.4 61.7 mm). As a consequence, a significant decrease in
prostate volume was recorded (22.1 61.1 vs. 29.8 62.5 mL;
P,0.001). The individual data of the 10 patients are shown
in Fig. 1. Prostate volume increased in 2 (no. 3, from 21.8 to
29.9 mL; no. 5, from 27.3 to 33.5 mL; Tables 1 and 2) of the
3 patients who did not achieve normalization of GH and
TABLE 3. Results of the linear correlation analysis between
prostate volume and clinical and hormone parameters in
acromegalic patients
rP
Age 0.6 0.04
Disease duration 0.09 0.8
Serum GH ;0.2 0.5
Plasma IGF-I ;0.054 0.8
Serum PRL ;0.5 0.09
Serum testosterone 0.3 0.3
Serum DHT 0.14 0.7
FIG. 1. Serum GH profile (left) and prostate volume measured by
ultrasonography (right) in the 10 acromegalics before and after 1 yr
of octreotide treatment.
PROSTATIC DISORDERS IN ACROMEGALY 777
IGF-I after OCT treatment (Fig. 1). In the remaining patient
(no. 2), prostate volume decreased from 27.3 to 20.5 mL
despite evidence that GH decreased from 65 to 11.3
m
g/L, but
was not normalized. In 1 patient (no. 4) of the 7 who nor-
malized GH and IGF-I levels after OCT treatment, a hypo-
echoic nodular zone was detected within the left lobe without
a distinct boundary and with an irregular intralesional echoic
pattern (Fig. 2). The Power Echo Color Doppler evaluation
revealed high intra- and perilesional vascular flow. Fine nee-
dle biopsy revealed nodular hyperplasia. After OCT treat-
ment, calcifications were still detected in the periurethral
zone in 3 patients (no. 2, 5, and 6), whereas in 1 patient they
disappeared. Calcifications within the lobes were visualized
in 2 other patients (no. 4 and 8). In 2 patients, 1 presenting
with single macrocalcification within the right lobe (no. 1)
and 1 with uthricular cyst before therapy (no. 10), the ex-
amination performed 1 yr after OCT treatment showed mi-
crocalcifications in the former and no further detection of the
cyst in the latter patient. Lastly, after OCT treatment, serum
testosterone levels were significantly increased (from 1.5 6
0.3 to 3.5 60.3
m
g/L), whereas DHT, DHEA-S, D
4
, and
17
b
-estradiol levels were unchanged. In the 4 patients with
hyperprolactinemia, serum PRL levels were suppressed
throughout the study (data not shown).
Discussion
In acromegaly, prolonged hypersecretion of GH and IGF-I
constantly causes enlargement of most internal body organs
(1, 2). Thyroid, heart, liver, and bone seem to be strictly GH
and IGF-I targeted, but recent reports suggest a proliferating
effect of GH/IGF-I on colonic mucosa, as demonstrated by
an increased prevalence of colonic polyps detected at pan-
colonoscopy (8, 9). To date, no study has been performed to
assess the prevalence of benign prostate hyperplasia and/or
prostate cancer in acromegaly. In humans, prostate enlarge-
ment seems to begin at the age of 40 yr (10) and develops
almost exclusively in the transitional and periurethral zones
(11). Although evidence for direct or indirect regulatory ef-
fects of androgens on prostatic cell growth and differentia-
tion have been provided (10, 12), their action alone appears
to be insufficient to explain prostatic diseases. Acromegalic
patients can be considered as a peculiar study model, as they
often present low testosterone levels. In the current study,
prostatic enlargement, particularly that affecting the median
lobe, was recorded in all patients despite the evident hy-
pogonadism. In addition, an increased incidence of calcifi-
cations, suggestive of regressive events within the gland, was
observed in the patients (50%) compared to that in healthy
subjects (20%). To prevent volume changes associated with
aging, this study was performed in patients under 40 yr of
age, which is supposed to be the age limit for developing
benign prostatic hyperplasia (10). The normal prostate vol-
ume was reported as 30 mL in a normal population of 181
men, aged 40–79 yr. (7). No data are available in normal men
less than 40 yr of age. Taking into account the threshold of
30 mL, 3 of 10 acromegalic patients had clear-cut prostate
hypertrophy. However, in our series of healthy subjects,
prostate volume ranged from 15.1–21.8 mL, with a mean
value of 18.2 60.6 mL. In comparison with that in age-
matched controls, prostate volume was greater than ex-
pected in all patients but 1. Thus, it could be argued that the
prostate is a primary target tissue of GH and IGF-I. In none
of the patients were PSA levels, digital rectal exploration, or
transrectal ultrasound (TRUS) able to detect the occurrence
of prostatic cancer. This could be due both to the relatively
young age of the patients and to a protective effect that
reduced levels of androgens might exert. In fact, testosterone
acts on prostate growth directly and indirectly, through the
conversion to DHT by 5
a
-reductase (12). A physiological
decrease in testosterone in the elderly seems to be followed
by accumulation of DHT within the gland, because of re-
duced catabolism and enhanced intracellular binding (12).
Therefore, different results of prostatic ultrasound evalua-
tion in older patients could not be excluded. Although the
involvement of several growth factors, such as PRL, epider-
mal growth factor, fibroblast growth factor, and transform-
ing growth factor-
a
and -
b
, has been demonstrated both in
vitro and in vivo (13, 14), little is known about the direct
involvement of GH in prostate development. However, GH
receptors have been demonstrated in the rat prostate (15),
and increased messenger ribonucleic acid transcription for
androgen receptors has been detected after GH and PRL
administration in immature rat prostate (16).
The possibility that prostatic enlargement was actually
due to the chronic excess of GH and IGF-I was supported by
the significant decrease in prostate volume obtained after 1
yr of treatment with OCT in all patients who achieved GH/
IGF-I suppression. As further support, in two of three acro-
megalics who did not achieve hormone suppression after
OCT treatment, prostate volume was increased. As far as the
prevalence of micro- and macrocalcifications was concerned,
the 1-yr treatment with OCT led to the disappearance of
microcalcifications and uthricular cyst in two patients, but
caused the occurrence of microcalcifications in two other
patients. On the basis of the detection of somatostatin re-
ceptors, primarily subtypes 1 and 2, in stromal cells of benign
and malignant prostate (17–19), it is arguable that chronic
OCT administration could regulate the GH/IGFs/IGF-bind-
ing protein paracrine-autocrine pathways within the gland.
OCT could act on prostate size with different mechanisms.
First, it can induce a decrease in prostate dimension by a
direct antiproliferative effect (20) and indirectly by suppress-
ing circulating levels of GH/IGF-I. Second, it may prevent
FIG. 2. Prostate ultrasonographic imaging in patient 4 before (left)
and after (right) 1 yr of octreotide treatment at a dose of 0.3 mg/day.
On the left, the transversal diameter measured at study entry is
shown without any distinct nodular lesion. On the right, a clear-cut
nodule (0.97 31.03 cm) was found after treatment. At cytology per-
formed on a specimen collected by fine needle biopsy, the nodule was
diagnosed as simple hyperplasia.
778 COLAO ET AL. JCE&M•1998
Vol 83 •No 3
prostate enlargement by inducing apoptotic processes of the
mesenchymal tissue and by modifying the hemodynamics of
local blood circulation (21). The positive effect of OCT treat-
ment on prostate volume and morphology was observed
despite a significant increase in testosterone levels and a
significant improvement of spermatogenic activity (data not
shown).
In conclusion, prostate enlargement occurs in young ac-
romegalics with a higher than expected prevalence of micro-
and macrocalcifications. These findings seem to be related to
the GH/IGF-I excess, as they occur in the presence of evident
hypogonadism. This suggests that a careful prostate screen-
ing, supported by transrectal ultrasound evaluation, should
be included in the work-up of acromegalic males. Androgen
replacement should be carefully monitored to avoid adding
to prostate growth. Long term treatment with OCT can re-
verse prostate enlargement. The occurrence of micro- and
macrocalcifications and even prostate nodules during OCT
treatment indicates that monitoring of prostate size is also
advisable in the follow-up of acromegalic patients.
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