Discussion
Atypical small acinar proliferation is a pathology that should be
re-evaluated with a second biopsy in cases where small foci cannot be
clearly defined histopathologically and in cases where differential
diagnosis of PCa cannot be definitively performed. Detection rate of
patients with ASAP in our biopsy cohort was 11.28%. This rate has
increased especially in the past few years. We think that these rates
have increased as a result of decreasing the tPSA threshold value from 4
to the 2.5 ng/mL in recent years. Our re-biopsy rate was 53.78%. In the
literature, there are second biopsy rates varying between 47-63%16 and it was compatible with the literature. The
question that should be responsed is the reasons why the patients avoid
from the second biopsy. It is difficult to convince patients who need a
second biopsy due to psychological or physical difficulties of the
biopsy procedure. This rate reflects the public’s approach to prostate
biopsy, especially in Muslim countries. Therefore, the necessity of a
second prostate biopsy is always scrutinized. Considering that it causes
additional cost and morbidity, this decision should be made carefully.
In our patients with ASAP, PCa was occured 39.84% of the second
prostate biopsy. In the literature, the diagnosis rate of PCa in
patients with ASAP in the second biopsy ranges from 39 to 42%17,18. The relationship between ASAP and PCa has been
evaluated for many years. Currently, there is no published algorithm for
patients with ASAP to avoid unnecessary biopsy, and a second prostate
biopsy is routinely applied to all patients diagnosed with ASAP in line
with the recommendations of the guidelines. There are many studies in
the literature focused on the diagnosis of PCa as a result of the second
biopsy of patients diagnosed with ASAP and the predictive values of the
all PSA forms were evaluated to explain relationship between ASAP and
PCa in these studies.
Several nomograms have been reported in the literature to increase
detection rates of PCa in recurrent prostate biopsies. In a study by
Sakura et al., a new repeat biopsy nomogram was developed, including
patients’ age, f/tPSA rate, PV, etc 19. However,
patients diagnosed with ASAP were not included in the study. Yanke et
al. and Moussa et al. were reported a nomogram that contains PSA slopen
and history of high grade intraepithelial neoplasm or ASAP20,21. A study by Corona et al. was reported a
nomogram that the cumulative number of negative cores obtained, PSA
slope, history of high grade prostatic intraepithelial neoplasia and
history of ASAP were associated with repeat biopsy findings22.
These studies created nomograms with many parameters but were not enough
to be routinely recommended in the guidelines. In addition, evaluating
some parameters meant an extra cost increase. For example to evaluate
PSA slope at least 3 measurements are required. All the nomograms were
not examined specifically for patients with ASAP. It also does not point
the alteration of tPSA between two biopsies. In ASS-RT, we have defined,
used 4 benchmarks that can be measured effectively in prostate biopsy
decision. Another difference of ASS-RT from the others is that it
divides the patients into risk groups according to the score they
received. When the number of patients in both groups is compared, we
think that the risk group classification is extremely important and
statistically significant (Table 4). A study on the classification of
patients with ASAP as low and high risk by risk group was published in
2005 by Scattoni et al. and they showed there is no difference of
getting cancer between these two groups after repeated biopsies23. There was no difference between risk groups in
terms of detection of PCa. Contrary to this study, the use of “ASAP
Scoring System and risk table “increases the predictability of PCa
diagnosis in our study. As a result of the second biopsy in our study,
8% of the patients with benign prostate pathology were in the high-risk
group, while 50.98% (26/51) of the patients with PCa were in the
high-risk group. However, Gleason score of the most of the patients with
PCa (70.58%) was 3+3 and the rate of clinically significant PCa was
found as 29.42% in group 2. Unfortunately, the parameter that would
provide sufficient distinction could not be obtained in the intermediate
risk group.
Considering the relationship between ASAP and clinically insignificant
PCa, too high tPSA levels are not expected in patients with ASAP. The
mean tPSA level of the cohort in our study ranged from 4.0 to 10.0
ng/ml, known as the gray zone. In a previous study, it was reported that
the rate of PCa detection in the first biopsy was 25.1% and the rate of
clinically significant PCa detection was lower in men with PSA levels of
4.0-10.0 ng/ml 24. As mentioned before, this rate is
approximately 40% in patients diagnosed with ASAP. However, our
clinically significant PCa rate was 11.71% in all patients with ASAP.
Therefore, in patients with ASAP, the rate of clinically significant PCa
as a result of the second biopsy is less than feared and we think that
the best way to prevent high costs with increased morbidity in re-biopsy
is to better identify to high risk patients by using of ASS-RT.
The main limitation of the study was retrospective planning.
Unfortunately, the number of patients with data loss prevented more
patients in the cohort. In fact, another factor that is not a limitation
but it may increase the effectiveness of the current ASS-RT is the time
elapsed between two biopsies and this factor was not examined in detail
in our study. The time between two biopsies is perhaps an effective
factor in the formation of the final pathology in patients diagnosed
with ASAP.