speculate that using combination therapy at our center would reduce the incidence of sepsis after TRUS biopsy even further. Cycling through multiple regimens of ef- fective prophylactic combinations would be preferable to ensure that a single regimen is not “overused,” which would result in an increase in resistance to that particular combination. The comments and example of the trial performed by the authors indicate that the alteration of a pro- phylactic regimen from single to multiple antibiotics works well clinically and is an effective method to decrease the incidence of sepsis after TRUS biopsy. Their choice of antibiotic prophylaxis was guided by an examination of local resistance patterns and illus- trates the point that whatever course of antibiotic therapy is chosen, it must be chosen with one’s par- ticular region in mind. Dirk Lange, Ph.D. Ryan F. Paterson, M.D. S. Larry Goldenberg, M.D. Ben H. Chew, M.D., M.Sc. Department of Urologic Sciences University of British Columbia Vancouver, British Columbia, Canada Re: Billis et al.: Does the Type of Prostatic Atrophy Influence the Association of Extent of Atrophy in Needle Biopsies and Serum Prostate-specific Antigen Levels? (Urology 2009;74:1111-1115) TO THE EDITOR: We read with great interest the article by Billis et al, 1 who based on their older findings 2 of a positive/signifi- cant association between the extent of prostatic atrophy and serum prostate-specific antigen (PSA) levels in pa- tients with biopsies revealing only atrophy, assessed pos- sible correlation with the type of atrophy. They con- cluded that there was no correlation to the type of atrophy; that is, partial atrophy, simple atrophy, hyper- plastic atrophy (postatrophic hyperplasia), and sclerotic atrophy. Our main argument is on the exclusion of study- ing separately the entity of proliferative inflammatory atrophy (PIA), a type of atrophy described a decade ago. 3 We believe that our argument is justified by the fact that the authors reported inflammation in 77% of the biop- sies. The authors hypothesize that stress-induced re- sponse by inflammation may interfere in the physiologi- cal barrier that prevents PSA to enter the general circulation. If the authors could scrutinize their database relatively an association might arise between serum PSA levels and PIA. PIA cells have a low frequency of apoptosis, a high proliferative index, and share molecular and genetic markers with PCa. In the human prostate, PIA lesions are predominantly found in the peripheral zone where most of the PCa arise. 4 Recently, direct morphologic transition of PIA to coexisting HGPIN and/or PCa was demonstra- ted. 5 The atrophic cells in these merging lesions were highly proliferative with an intermediate phenotype, in- cluding increased expression for CK5, GSTP1, c-MET, and C/EBP. Prostate biopsies may reveal several precursor lesions of PCa, and therefore we should become more familiar with relevant pathologist interpretation. To attenuate prostate carcinogenesis driven by prostate inflammation and PIA lesions, rational chemoprevention has thus far featured anti-inflammatory drugs and antioxidants. 4 However, re- sults from clinical trials of these approaches have been controversial, emphasizing the need for further relevant research. Furthermore, the authors could clarify the basis setting a PSA level of 8.2 ng/mL as a cut-off point between group A and B, because in their previous study the median value was 7.5 ng/mL. Probably, they refer to different median values according to the different number of bi- opsies. Another interesting issue is the term “extended” biopsies that the authors use for performing a median number of 8 core biopsies. This is because nowadays there is a shift from classical sextant biopsies to standard 8-12 core biopsies and saturation repeat biopsies. Finally, the authors could clarify the basis of grading only inactive inflammation as slight, moderate, or intense. Athanasios Papatsoris, M.D. Stefanos Albanis, M.D. Charalambos Deliveliotis, M.D. 2nd Department of Urology Sismanoglio General Hospital University of Athens Athens, Greece References 1. Billis A, Meirelles L, Freitas LL, et al. Does the type of prostatic atrophy influence the association of extent of atrophy in needle biopsies and serum prostate-specific antigen levels? Urology. 2009; 74:1111-1115. 2. Billis A, Meirelles LR, Magna LA, et al. Extent of prostatic atrophy in needle biopsies and serum PSA levels: is there an association? Urology. 2007;69:927-930. 3. De Marzo AM, Marchi VL, Epstein JI, et al. Proliferative inflamma- tory atrophy of the prostate: implications for prostatic carcinogene- sis. Am J Pathol. 1999;155:1985-1992. 4. Bardia A, Platz EA, Yegnasubramanian S, et al. Anti-inflammatory drugs, antioxidants, and prostate cancer prevention. Curr Opin Phar- macol. 2009;9:419-426. 5. Wang W, Bergh A, Damber JE. Morphological transition of prolif- erative inflammatory atrophy to high-grade intraepithelial neoplasia and cancer in human prostate. Prostate. 2009;69:1378-1386. UROLOGY 75 (5), 2010 1239