Case 1 -
St. Louis, MO
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The patient is an asymptomatic 55 year old man with an elevated serum prostate specific antigen of 6.5 ng/ml. He underwent ultrasound-guided prostate needle biopsy.
Pertinent Laboratory Data:
Elevated PSA (7 ng/mL)
Pathological/Microscopic Findings and any Immunohistochemical or Other Studies:
Sections show prostate needle core tissue with a single, small, detached tissue fragment. This
fragment is completely occupied by a crowded small gland process. It is not feasible to assess the
overall architectural configuration of these glands. It is difficult to assess for basal cells in these
glands, which do show cytoplasmic volume loss. Some nuclei appear hyperchromatic but obvious
nucleomegaly and prominent nucleoli are not present.
- Benign atrophy
- Adenosis (atypical adenomatous hyperplasia)
- Crowded normal glands
- Mesonephric hyperplasia
- Nephrogenic adenoma
This is a case of post-atrophic hyperplasia that was initially misdiagnosed as adenocarcinoma of the
prostate. Atrophy is one of the benign conditions most commonly diagnosed as adenocarcinoma. In this
particular case, as is true for cases of post-atrophic hyperplasia in general, there is a crowded small
acinar architectural arrangement. Diagnostic difficulty is encountered in this case since it is not
possible to ascertain whether this a lobular/circumscribed type of growth. The small glands occupy
completely a single and separate, small detached core fragment, without adjacent benign tissue available
for evaluation of boundary relationships. In some cases of post-atrophic hyperplasia in needle biopsy
one can appreciate a rounded architectural profile that would provide a clue as to the non-infiltrative
nature of the glands, but not in this case. The crowding of the small glands also figured prominently in
the misinterpretation as adenocarcinoma, but the many types of small benign glands can be crowded
including atrophy, adenosis (atypical adenomatous hyperplasia), sclerosing adenosis, crowded normal
glands, basal cell hyperplasia, and verumontanum gland hyperplasia. In small foci such as this, nuclear
atypia is extremely important in the diagnostic distinction of benign crowded small acini from
adenocarcinoma. The separation of this small fragment from the rest of the core may have led to a
failure to compare the nuclear features of these small acini to those of clearly benign glands elsewhere
in the core. Had this been done, one could appreciate the bland nuclear cytology in this case in the
atrophy. Finally, immunohistochemistry was not performed in this case, since this was case from 1990,
when immunostains for basal cells were just being introduced into diagnostic surgical pathology of the
prostate. Immunostains for alpha- methylacyl coenzyme A racemase (AMACR), a selective but not entirely
specific marker of prostatic neoplastic epithelial cells, were not available until recently.
Immunostains may have been helpful in this case if basal cells were identified using 34βE12 and/or
p63 immunostains. However, as discussed below, there are pitfalls in use of basal cell and AMACR
immunostains in the diagnostic separation of atrophy from adenocarcinoma. In particular basal cell loss
may be seen in atrophy, although the loss, when present in atrophy, is usually partial. Also, AMACR
overexpression may be seen in atrophy, as discussed below. Overall, though, this case should have been
readily diagnosed on the H and E slide only, without employment of immunohistochemistry.
Atrophy in the prostate continues to be one of the most common benign histological entities to be
misdiagnosed as carcinoma. Diagnostic awareness of the different types of prostatic atrophy and their
appearance in limited tissue samples, such as small needle core fragments, is vital to avoid a false
positive diagnosis of maligancy.
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