Association of nonsteroidal anti-inflammatory drugs, prostate specific antigen and prostate volume.
Association of nonsteroidal anti-inflammatory drugs, prostate specific antigen and prostate volume.
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DOI：
10.1016/j.juro.2009.01.031
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发表时间：
2009-05
期刊：
影响因子：
--
通讯作者：
Byerly S
中科院分区：
文献类型：
--
作者：
Fowke JH;Motley SS;Smith JA Jr;Cookson MS;Concepcion R;Chang SS;Byerly S
像阿司匹林这样的非甾体抗炎药可以预防心血管疾病，之前的一些研究表明，非甾体抗炎药还可以降低前列腺炎症和前列腺癌的风险。我们调查了非甾体抗炎药使用、PSA和前列腺体积之间的关系，并假设使用非甾体抗炎药时PSA和体积水平较低。纳什维尔男性健康研究采用多中心、快速招募方案，收集1277名40岁以上男性的临床、生物学、行为和身体测量数据，并计划进行前列腺活检诊断。通过调查和临床访谈确定非甾体抗炎药的使用情况，并回顾医疗图表以确定当前PSA水平、前列腺体积和活检后的临床诊断。大约46%的受试者报告服用非甾体抗炎药，主要是阿司匹林（37%）。在调整了年龄、种族和其他因素后；阿司匹林服用者和非服用者的前列腺体积相似（47.6 ml vs 46.0 ml, p=0.16）。相比之下，阿司匹林使用者的PSA显著降低（7.3对8.0 ng/ml, p=0.01）。PSA与阿司匹林的相关性在潜伏性前列腺癌患者中显著（6.1 vs. 7.3 ng/ml, p<0.01），在PIN患者中不显著（5.0 vs. 5.9 ng/ml, p=0.09），而在活检阴性患者中不显著（5.6 vs. 5.7 ng/ml, p=0.64）。前列腺体积大于或等于60 ml的癌症患者psa与阿司匹林的相关性最强（7.3 vs 12.7 ng/ml, p<0.01）。患有潜伏性癌症的阿司匹林使用者的PSA水平明显较低。前列腺体积与非甾体抗炎药的使用无关。结果提示阿司匹林可能影响前列腺癌的检测，并提示在未来的非甾体抗炎药和前列腺癌预防研究中可能存在检测偏差。
NSAIDs such as aspirin prevent CVD, and several prior studies suggest NSAIDs also reduce prostate inflammation and prostate cancer risk. We investigated the association between NSAID use, PSA, and prostate volume, hypothesizing lower PSA and volume levels with NSAID use. The Nashville Men’s Health Study utilizes a multi-centered, rapid-recruitment protocol to collect clinical, biological, behavioral, and body measurement data from 1,277 men over age 40 years and scheduled for diagnostic prostate biopsy. NSAID use was ascertained by survey and clinical interview, and medical charts were reviewed to ascertain current PSA levels, prostate volume, and clinical diagnoses following biopsy. Approximately 46% of subjects reported taking NSAIDs, primarily aspirin (37%). After adjusting for age, race, and other factors; prostate volume was similar between aspirin users and non-users (47.6 vs. 46.0 mls, p=0.16). In contrast, PSA was significantly lower among aspirin users (7.3 vs. 8.0 ng/ml, p=0.01). The association between PSA and aspirin was significant among men with latent prostate cancer (6.1 vs. 7.3 ng/ml, p<0.01), marginal among PIN patients (5.0 vs. 5.9 ng/ml, p=0.09), while nonsignificant with a negative biopsy (5.6 vs. 5.7 ng/ml, p=0.64). The strongest PSA-aspirin association was among cancer cases with a prostate volume of 60 mls or more (7.3 vs. 12.7 ng/ml, p<0.01). PSA levels were significantly lower among aspirin users with latent cancer. Prostate volume was not associated with NSAID use. Results suggest aspirin may affect prostate cancer detection, and suggests a potential detection bias in address in future studies of NSAIDs and prostate cancer prevention.
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