The influence of chronic inflammation in prostatic carcinogenesis: A 5-year followup study

被引:113
|
作者
MacLennan, Gregory T.
Eisenberg, Rosana
Fleshman, Ranleigh L.
Taylor, J. Michael
Fu, Pingfu
Resnick, Martin I.
Gupta, Sanjay [1 ]
机构
[1] Case Western Reserve Univ, Dept Urol, James & Eilleen Dicke Res Lab, Sch Med,Univ Hosp Cleveland, Cleveland, OH 44106 USA
[2] Case Western Reserve Univ, Univ Hosp Cleveland, Dept Epidemiol & Biostat, Cleveland, OH 44106 USA
[3] Case Western Reserve Univ, Univ Hosp Cleveland, Dept Urol, Cleveland, OH 44106 USA
[4] Case Comprehens Canc Ctr, Cleveland, OH USA
来源
JOURNAL OF UROLOGY | 2006年 / 176卷 / 03期
关键词
prostate; inflammation; biopsy; adenocarcinoma; prostate-specific antigen;
D O I
10.1016/j.juro.2006.04.033
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Purpose: We investigated an association between chronic prostatic inflammation and prostate carcinogenesis. Materials and Methods: Initial prostate needle biopsies from 177 patients with clinical parameters suspicious for malignancy were examined. We evaluated them for the presence and extent of chronic inflammation and other pathological findings. Findings in followup biopsies during the next 5 years were reviewed and correlated with the initial results. Results: Two patients subset were identified, including 144 patients with and 33 without chronic inflammation in the initial biopsies. Additional pathological findings in some cases in each group included simple atrophy, high grade prostatic intraepithelial neoplasia, adenocarcinoma and atypical small acinar proliferation. Post-atrophic hyperplasia and proliferative inflammatory atrophy were noted only in patients with chronic inflammation. A significant association between serum prostate specific antigen and the degree of inflammation was observed in needle biopsies. In repeat biopsies within 5 years in patients with chronic inflammation 29 new cancers were diagnosed, representing a new cancer incidence of 20%. Of these cancers 6 occurred in patients in whom initial biopsies showed only chronic inflammation, 15 occurred in patients with initial post-atrophic hyperplasia/proliferative inflammatory atrophy lesions, 7 occurred in patients with initial high grade prostatic intraepithelial neoplasia and chronic inflammation, and 1 occurred in a patient with initial atypical small acinar proliferation and chronic inflammation. High grade prostatic intraepithelial neoplasia was newly discovered in 9 patients in the initial chronic inflammation group, of whom 7 had post-atrophic hyperplasia/proliferative inflammatory atrophy and 2 had simple atrophy and chronic inflammation in the initial biopsies. In contrast, in 33 patients initially showing no inflammation adenocarcinoma was subsequently found in 2 (6%). One of these patients had high grade prostatic intraepithelial neoplasia and the other had atypical small acinar proliferation on initial biopsies. Conclusions: Chronic inflammation may be a significant risk factor for prostatic adenocarcinoma.
引用
收藏
页码:1012 / 1016
页数:5
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