Diabetes and Prostate Cancer Outcomes in Obese and Nonobese Men After Radical Prostatectomy.

Diabetes and Prostate Cancer Outcomes in Obese and Nonobese Men After Radical Prostatectomy.
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DOI:
10.1093/jncics/pkab023
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发表时间:
2021-06
影响因子:
4.4
通讯作者:
Csizmadi I
Csizmadi I
中科院分区:
其他
文献类型:
--
作者:
Kelkar S;Oyekunle T;Eisenberg A;Howard L;Aronson WJ;Kane CJ;Amling CL;Cooperberg MR;Klaassen Z;Terris MK;Freedland SJ;Csizmadi I

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糖尿病和前列腺癌进展之间的联系知之甚少,并因肥胖而复杂化。我们研究了接受根治性前列腺切除术(RP)的肥胖和非肥胖男性中糖尿病与前列腺癌特异性死亡率(PCSM)、去势抵抗性前列腺癌(CRPC)和转移瘤之间的关系。我们纳入了1988年至2017年接受RP的共享平等获取区域癌症医院男性队列的4688名男性。糖尿病前RP,人体测量,临床数据从6退伍军人事务部医疗中心的电子病历中提取。主要和次要结局分别为PCSM、转移和CRPC。估计糖尿病和PCSM、CRPC和转移的多变量校正风险比(adj-HR)和95%置信区间(CI)。在按肥胖分层的分析中也估计了校正的风险比(体重指数:非肥胖<30 kg/m2;肥胖≥30 kg/m2)。所有统计检验均为双侧检验。在所有男性中,糖尿病与PCSM(adj-HR = 1.38,95% CI = 0.86至2.24)、CRPC(adj-HR = 1.05,95% CI = 0.67至1.64)或转移(adj-HR = 1.01,95% CI = 0.70至1.46)无关。在PCSM、CRPC和转移的多变量模型中,糖尿病和肥胖的相互作用项具有统计学显著性(P ≤ .04)。在分层分析中,在肥胖男性中,糖尿病与PCSM(adj-HR = 3.06,95% CI = 1.40至6.69)、CRPC(adj-HR = 2.14,95% CI = 1.11至4.15)和转移(adj-HR = 1.57,95% CI = 0.88至2.78)相关,但转移无统计学意义。在非肥胖男性中,糖尿病和前列腺癌的结果呈负相关,但没有达到统计学意义。糖尿病与肥胖男性前列腺癌进展和死亡率的风险增加相关,但与非肥胖男性无关,这突出了积极减少前列腺癌幸存者中肥胖患病率增加的重要性。
The link between diabetes and prostate cancer progression is poorly understood and complicated by obesity. We investigated associations between diabetes and prostate cancer–specific mortality (PCSM), castrate-resistant prostate cancer (CRPC), and metastases in obese and nonobese men undergoing radical prostatectomy (RP). We included 4688 men from the Shared Equal Access Regional Cancer Hospital cohort of men undergoing RP from 1988 to 2017. Diabetes prior to RP, anthropometric, and clinical data were abstracted from 6 Veterans Affairs Medical Centers electronic medical records. Primary and secondary outcomes were PCSM and metastases and CRPC, respectively. Multivariable-adjusted hazard ratios (adj-HRs) and 95% confidence intervals (CIs) were estimated for diabetes and PCSM, CRPC, and metastases. Adjusted hazard ratios were also estimated in analyses stratified by obesity (body mass index: nonobese <30 kg/m2; obese ≥30 kg/m2). All statistical tests were 2-sided. Diabetes was not associated with PCSM (adj-HR = 1.38, 95% CI = 0.86 to 2.24), CRPC (adj-HR = 1.05, 95% CI = 0.67 to 1.64), or metastases (adj-HR = 1.01, 95% CI = 0.70 to 1.46), among all men. Interaction terms for diabetes and obesity were statistically significant in multivariable models for PCSM, CRPC, and metastases (P ≤ .04). In stratified analyses, in obese men, diabetes was associated with PCSM (adj-HR = 3.06, 95% CI = 1.40 to 6.69), CRPC (adj-HR = 2.14, 95% CI = 1.11 to 4.15), and metastases (adj-HR = 1.57, 95% CI = 0.88 to 2.78), though not statistically significant for metastases. In nonobese men, inverse associations were suggested for diabetes and prostate cancer outcomes without reaching statistical significance. Diabetes was associated with increased risks of prostate cancer progression and mortality among obese men but not among nonobese men, highlighting the importance of aggressively curtailing the increasing prevalence of obesity in prostate cancer survivors.