PATHOLOGY

Focal prostatic atrophy: mimicry of prostatic cancer on TRUS and 3D-MRSI studies
Prando A, Billis A
Radiology, Hospital Vera Cruz, Campinas, SP, Brazil
Abdom Imaging. 2009; 34: 271-5

• Prostatic atrophy which represents a form of adaptive response to injury most commonly to inflammation and/or chronic ischemia is a histological abnormality frequently found in prostate biopsies and autopsies. Although commonly found, this lesion is rarely reported in the prostatic biopsy reports. It is well known that histologically focal prostatic atrophy (FPA) is one of the most frequent mimics of prostatic adenocarcinoma. On conventional and color Doppler transrectal ultrasound and on magnetic resonance spectroscopic imaging studies (MRSI), FPA may also simulate prostate cancer. Thus, this entity should be considered together with prostatitis as an important cause of false-positive results in MRSI of the prostate. It has been shown that there is a positive and significant association between extent of FPA in biopsies and serum total or free PSA elevation. For this reason, pathologists should include the presence of FPA in the pathology report of a prostatic biopsy, particularly in those patients with absence of cancer. When extensive FPA is the only finding in patients with several negative prostatic biopsies, this lesion may be the source for PSA elevation.

• Editorial Comment
  Prostatic atrophy is one of the most frequent microscopic mimics of prostatic adenocarcinoma (1). In the study reviewed, the lesion is also an important mimicker of adenocarcinoma on conventional and color Doppler transrectal ultrasound and on magnetic resonance spectroscopic imaging studies MRSI). It occurs most frequently in the peripheral zone and gained importance with the increasing use of needle biopsies for the detection of prostatic carcinoma. The frequency of the lesion in autopsies is 85% and increases with age. Inflammation, radiation, antiandrogens and chronic ischemia due to local arteriosclerosis are all considered causes of the lesion although many examples of atrophy are still considered idiopathic in nature. The histological subtypes of prostatic atrophy do not represent distinct entities but a morphologic continuum of acinar atrophy and most of the times are seen concomitantly. The most common subtype that causes difficulty for pathologists is partial atrophy due to the pale cytoplasm lateral to the nuclei giving rise to pale staining glands that more closely mimic cancer.
  Some reports suggest that focal atrophy may be causally linked to prostate cancer and to other pre-neoplastic lesions (2). However, other studies do not support this hypothesis (3). An intriguing finding is the association of extent of atrophy to serum PSA elevation (4). What would be a possible pathogenesis for the serum PSA elevation associated to focal prostatic atrophy? It is intriguing that cells of the secretory compartment of atrophic acini may produce higher levels of PSA. It is speculated that injurious stimuli causing focal prostatic atrophy may interfere in the physiologic barrier that prevents the escape of any significant amounts of PSA to the general circulation.
  Prostate-specific antigen is a single chain glycoprotein with proteolytic enzyme activity mainly directed against the major gel-forming protein of the ejaculate (semenogelin). PSA induces liquefaction of semen with release of progressively motile spermatozoa. There are several efficient physiologic barriers to prevent the escape of any significant amounts of PSA from the prostatic ductal system: basement membrane of the acini, basal cells lining the acini, prostatic stroma, basement membrane of capillary endothelial cells, and endothelial cells. These barriers normally prevent PSA from entering the general circulation at concentrations of more than 3 ng/mL.
  Focal prostatic atrophy represents a form of adaptive response to injury most commonly to inflammation and/or local ischemia. Inflammation and/or ischemia are injurious stimuli resulting in diminished oxidative phosphorilation, membrane damage, influx of intracellular calcium, and accumulation of oxygen-derived free radicals (oxidative stress). Studies showing elevated levels of glutathione S-transferase P1, glutathione S-transferase A1, and Cox-2 in prostatic atrophic epithelial cells suggest a stress-induced response (5,6). We do not know which mechanisms are involved in the physiologic barrier that prevents the escape of any significant amounts of PSA to the general circulation, however, all these stress-induced responses may affect this barrier. Inflammation and particularly ischemia may have also a field effect affecting the physiologic barrier of normal acini close to atrophic acini.

References

1. Billis A: Prostatic atrophy: an autopsy study of a histologic mimic of adenocarcinoma. Mod Pathol. 1998; 11: 47-54.
2. De Marzo AM, Marchi VL, Epstein JI, Nelson WG: Proliferative inflammatory atrophy of the prostate: implications for prostatic carcinogenesis. Am J Pathol. 1999; 155: 1985-92.
3. Postma R, Schröder FH, van der Kwast TH: Atrophy in prostate needle biopsy cores and its relationship to prostate cancer incidence in screened men. Urology. 2005; 65: 745-9.
4. Billis A, Meirelles LR, Magna LA, Baracat J, Prando A, Ferreira U: Extent of prostatic atrophy in needle biopsies and serum PSA levels: is there an association? Urology. 2007; 69: 927-30.
5. Parsons JK, Nelson CP, Gage WR, Nelson WG, Kensler TW, De Marzo AM: GSTA1 expression in normal, preneoplastic, and neoplastic human prostate tissue. Prostate. 2001; 49: 30-7.
6. Zha S, Gage WR, Sauvageot J, Saria EA, Putzi MJ, Ewing CM, et al.: Cyclooxygenase-2 is up-regulated in proliferative inflammatory atrophy of the prostate, but not in prostate carcinoma. Cancer Res. 2001; 61: 8617-23.

Dr. Athanase Billis
Full-Professor of Pathology
State University of Campinas, Unicamp
Campinas, São Paulo, Brazil
E-mail: athanase@fcm.unicamp.br