PATHOLOGY

Atrophy in prostate needle biopsy cores and its relationship to prostate cancer incidence in screened men
Postma R, Schroder FH, van der Kwast TH
Department of Urology, Josephine Nefkens Institute, Erasmus Medical Center, Rotterdam, The Netherlands
Urology 2005; 65: 745-9

• Objectives: To evaluate whether the incidence of atrophy reported on sextant biopsies is associated with subsequent prostate cancer detection and to obtain a more thorough analysis of the different categories and extent of atrophy, we performed a review of benign biopsy cores.
• Methods: In the Rotterdam section of the European Randomized Study of Screening for Prostate Cancer, 4117 and 1840 men underwent sextant biopsy in the first and second screening round (4-year interval), respectively. Sextant biopsy was prompted by elevated prostate-specific antigen levels. For review, randomly taken benign sextant biopsies (n = 202) with a follow-up of at least 8 years were chosen.
• Results: Before review, atrophy was reported in the biopsies of 11.4% and 8.7% of the first and second round, respectively. The prostate cancer incidence during 8 years of follow-up after an initial diagnosis of atrophy was 10.4%, which was not significantly different than the 12.3% of cancers detected after a benign diagnosis without reference to atrophy. After review, the incidence of simple atrophy, post-atrophic hyperplasia, and sclerotic atrophy in sextant biopsies was 91%, 47%, and 9%, respectively. Extensive atrophy was observed in 5% of biopsies. Only 2 men (4.7%) in the reviewed group had a subsequent diagnosis of prostate cancer in the 8 years of follow-up. Additionally, prostatic intraepithelial neoplasia was diagnosed in 3 men (7.0%) in the second screening round.
• Conclusions: Atrophy, especially its simple form, is a very common lesion in prostate biopsy cores (94%). Atrophy in an asymptomatic population undergoing screening was not associated with a greater prostate cancer or prostatic intraepithelial neoplasia incidence during subsequent screening rounds.
  
  
• Editorial Comment
  Prostatic atrophy is one of the most fequent histologic mimics of prostatic adenocarcinoma. It occurs most frequently in the posterior lobe or peripheral zone and gained importance with the increasing use of needle biopsies for the detection of prostatic carcinoma. Chronic inflammation of longstanding duration has been linked to the development of carcinoma in several organ systems. In the prostate, chronic inflammation is associated with both hyperplastic atrophy (or postatrophic hyperplasia) and simple atrophy. De Marzo et al. (1) from Johns Hopkins propose combining these lesions into a category called proliferative inflammatory atrophy (PIA). The authors suggest that there are morhological transitions within the same acinar/duct unit, between high-grade prostatic intraepithelial neoplasia (HGPIN) and PIA which occur frequently. This finding supports a model whereby the proliferative epithelium in PIA may progress to GHPIN and subsequently to adenocarcinoma of the prostate.
  This hypothesis is contested by others. In an autopsy study done by us, no association was found between atrophy and either HGPIN or histologic carcinoma (2). In a subsequent study also in autopsies, we did not found any association between atrophy with inflammation (PIA) and either HGPIN or histologic carcinoma (3). Anton et al. (4) studying radical prostatectomies concluded that hyperplastic atrophy (or postatrophic hyperplasia) is a relatively common lesion present in about one-third of prostates, either with or without carcinoma. The authors found no association between the presence of postatrophic hyperplasia and the likelihood of cancer and no topographic association between postatrophic hyperplasia and prostate foci.
  The findings of Postma et al. of the present survey, are similar to Bakshi et al. (5). The latter authors studied 79 consecutive prostate biopsies: 54% of initial biopsies were benign, 42% of the cases showed cancer, and 4% HGPIN or atypia. Postatrophic hyperplasia was seen in 17% of benign initial biopsies with available follow-up. Of these, 75% had associated inflammation. There was no significant difference in the subsequent diagnosis of prostate cancer for groups with postatrophic hyperplasia, partial atrophy, atrophy, or no specific abnormality. The authors conclude that the subcategories of atrophy do not appear to be associated with a significant increase in the risk of diagnosis of prostate cancer subsequently.

References
1. 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.
2. Billis A: Prostatic atrophy: An autopsy study of a histologic mimic of adenocarcinoma. Mod Pathol. 1998; 11: 47-54.
3. Billis A, Magna LA: Inflammatory atrophy of the prostate. Prevalence and significance. Arch Pathol Lab Med. 2003; 127: 840-4.
4. Anton RC, Kattan MW, Chakraborty S, Wheeler TM: Postatrophic hyperplasia of the prostate: lack of association with prostate cancer. Am J Surg Pathol. 1999; 23: 932-6.
5. Bakshi NA, Pandya MW, Schervish EW, Wojno KJ: Morphologic features and clinical significance of post-atrophic hyperplasia in biopsy specimens of prostate. Mod Pathol. 2002; 15: 154A (abst).

Dr. Athanase Billis
Full-Professor of Pathology
State University of Campinas, Unicamp
Campinas, São Paulo, Brazil