Racial differences in the relationship between clinical prostatitis, presence of inflammation in benign prostate and subsequent risk of prostate cancer.
Racial differences in the relationship between clinical prostatitis, presence of inflammation in benign prostate and subsequent risk of prostate cancer.
复制标题
DOI：
10.1038/pcan.2015.54
复制
发表时间：
2016-06
影响因子：
4.8
通讯作者：
Tang D
中科院分区：
文献类型：
--
作者：
Rybicki BA;Kryvenko ON;Wang Y;Jankowski M;Trudeau S;Chitale DA;Gupta NS;Rundle A;Tang D
主要针对白人男性的流行病学研究表明，临床诊断为前列腺炎的病史会增加患前列腺癌的风险，但组织学上的前列腺炎症会降低患前列腺癌的风险。前列腺炎的临床病史和组织学炎症之间的关系，即前列腺炎症的这两种表现如何共同促进前列腺癌的风险，以及这种关系中是否存在种族差异尚不确定。我们对574对前列腺癌病例对照（345例白人，229例非裔美国人）的临床诊断前列腺炎（NIH分类I-III）和组织学炎症进行了分析，并采用巢式设计对具有良性前列腺组织标本的男性队列进行了研究。在整个样本中，临床前列腺炎与前列腺癌风险增加无关，但在非裔美国人中显示与前列腺癌呈负相关(优势比(OR) = 0.47；95%置信区间(CI) = 0.27-0.81)。在白人中，临床前列腺炎增加了40%的风险，但只有在没有组织学炎症证据的情况下，前列腺癌风险才会显著增加（OR = 3.56; 95% CI = 1.15-10.99）。此外，PSA检测速度（P = 0.008）和PSA检测频率（P = 0.003）是风险的显著调节因子。临床前列腺炎使PSA速度低的白人男性患前列腺癌的风险增加近3倍（OR = 2.97; 95% CI = 1.40-6.30），而PSA检测频率高的白人男性患前列腺癌的风险增加约2倍（OR = 1.91; 95% CI = 1.09-3.35）。在我们的男性良性前列腺标本队列中，种族和组织学炎症是临床前列腺炎和前列腺癌之间关系的重要辅助因素。临床前列腺炎与非裔美国男性患前列腺癌的风险略有降低有关。在白人男性中，临床前列腺炎和前列腺癌风险之间的关系被组织学前列腺炎、PSA速度和PSA检测频率所改变，这表明前列腺炎的这些指征和前列腺癌检测之间存在复杂的相互作用。
Epidemiologic studies, primarily done in white men, suggest that a history of clinically-diagnosed prostatitis increases prostate cancer risk, but that histological prostate inflammation decreases risk. The relationship between a clinical history of prostatitis and histologic inflammation in terms of how these two manifestations of prostatic inflammation jointly contribute to prostate cancer risk and whether racial differences exist in this relationship is uncertain. Using a nested design within a cohort of men with benign prostate tissue specimens, we analyzed the data on both clinically-diagnosed prostatitis (NIH categories I–III) and histological inflammation in 574 prostate cancer case-control pairs (345 white, 229 African American). Clinical prostatitis was not associated with increased prostate cancer risk in the full sample, but showed a suggestive inverse association with prostate cancer in African Americans (odds ratio (OR) = 0.47; 95% confidence interval (CI) = 0.27–0.81). In whites, clinical prostatitis increased risk by 40%, but was only associated with a significant increased prostate cancer risk in the absence of evidence of histological inflammation (OR = 3.56; 95% CI = 1.15–10.99). Moreover, PSA velocity (P = 0.008) and frequency of PSA testing (P = 0.003) were significant modifiers of risk. Clinical prostatitis increased risk of prostate cancer almost three-fold (OR = 2.97; 95% CI = 1.40–6.30) in white men with low PSA velocity and about twofold in white men with more frequent PSA testing (OR = 1.91; 95% CI = 1.09–3.35). In our cohort of men with benign prostate specimens, race, and histological inflammation were important cofactors in the relationship between clinical prostatitis and prostate cancer. Clinical prostatitis was associated with a slightly decreased risk for prostate cancer in African American men. In white men, the relationship between clinical prostatitis and prostate cancer risk was modified by histological prostatic inflammation, PSA velocity, and frequency of PSA testing—suggesting a complex interplay between these indications of prostatic inflammation and prostate cancer detection.