Karen Curtin, Lisa A Cannon-Albright, James VanDerslice, Zhe Yu, Kimberly A Herget, Ramya Thota, Deborah W Neklason
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Tobacco and alcohol exposures before case diagnosis were identified from International Classification of Diseases codes in statewide medical records and from self-reported data captured at patient encounters beginning in 1996. Multivariate logistic regression was used to estimate risk of SINT associated with tobacco and alcohol in cases compared with controls.</p><p><strong>Results: </strong>An increased risk of SINT was observed in tobacco-exposed individuals compared with unexposed [OR, 1.44; 95% confidence interval (CI), 1.11-1.86; <i>P</i> = 0.006]. Those who were exposed to alcohol exhibited an increased risk of SINT (OR, 1.62; 95% CI, 1.05-2.49; <i>P</i> = 0.03).</p><p><strong>Conclusions: </strong>This study supports tobacco and alcohol use as risk factors for SINT, independent of family history. However, low rates of smoking and alcohol use in Utah coupled with higher rates of SINT suggest other factors may contribute to development of these tumors.</p><p><strong>Impact: </strong>Although tobacco and alcohol modestly contribute to risk, our study suggests in addition to greater detection of tumors, other as-of-yet undefined exposures may drive rising SINT incidence.</p>","PeriodicalId":39340,"journal":{"name":"NASSP Bulletin","volume":"17 1","pages":"1998-2004"},"PeriodicalIF":0.0000,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6961822/pdf/","citationCount":"0","resultStr":"{\"title\":\"Associations of Tobacco and Alcohol Use with Risk of Neuroendocrine Tumors of the Small Intestine in Utah.\",\"authors\":\"Karen Curtin, Lisa A Cannon-Albright, James VanDerslice, Zhe Yu, Kimberly A Herget, Ramya Thota, Deborah W Neklason\",\"doi\":\"10.1158/1055-9965.EPI-19-0465\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Incidence of small-intestine neuroendocrine tumors (SINT) has been increasing in the United States over the past 40 years, with higher incidence in Utah than elsewhere. As information about how these tumors arise is limited, elucidating lifestyle factors associated with SINT in a statewide cohort could potentially identify those at risk to help mitigate their effects.</p><p><strong>Methods: </strong>Cases of SINT with a carcinoid histology (8240 or 8241) diagnosed in Utah from 1996 to 2014 with no prior history of cancer within 5 years (<i>n</i> = 433) were matched to population controls (1:10 ratio). Tobacco and alcohol exposures before case diagnosis were identified from International Classification of Diseases codes in statewide medical records and from self-reported data captured at patient encounters beginning in 1996. Multivariate logistic regression was used to estimate risk of SINT associated with tobacco and alcohol in cases compared with controls.</p><p><strong>Results: </strong>An increased risk of SINT was observed in tobacco-exposed individuals compared with unexposed [OR, 1.44; 95% confidence interval (CI), 1.11-1.86; <i>P</i> = 0.006]. 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引用次数: 0
摘要
背景:过去40年来,小肠神经内分泌肿瘤(SINT)的发病率在美国不断上升,犹他州的发病率高于其他地区。由于有关这些肿瘤发生原因的信息有限,在全州范围内对与小肠神经内分泌肿瘤相关的生活方式因素进行阐释,有可能发现高危人群,从而帮助减轻这些肿瘤的影响:方法: 将 1996 年至 2014 年在犹他州确诊的类癌组织学 SINT 病例(8240 或 8241)(n = 433)与人群对照组(1:10)进行配对。根据全州医疗记录中的国际疾病分类代码和 1996 年开始的患者就诊时采集的自我报告数据,确定了病例诊断前的烟草和酒精暴露情况。与对照组相比,采用多变量逻辑回归法估算病例与烟酒相关的 SINT 风险:与未接触烟草者相比,接触烟草者患 SINT 的风险增加[OR,1.44;95% 置信区间 (CI),1.11-1.86;P = 0.006]。接触酒精的人患 SINT 的风险增加(OR,1.62;95% 置信区间,1.05-2.49;P = 0.03):本研究支持吸烟和饮酒是SINT的风险因素,与家族史无关。然而,犹他州的低吸烟率和低酗酒率以及较高的 SINT 患病率表明,其他因素也可能导致这些肿瘤的发生:尽管烟草和酒精对风险的影响不大,但我们的研究表明,除了肿瘤的检测率更高之外,其他尚未确定的暴露因素也可能导致 SINT 发病率的上升。
Associations of Tobacco and Alcohol Use with Risk of Neuroendocrine Tumors of the Small Intestine in Utah.
Background: Incidence of small-intestine neuroendocrine tumors (SINT) has been increasing in the United States over the past 40 years, with higher incidence in Utah than elsewhere. As information about how these tumors arise is limited, elucidating lifestyle factors associated with SINT in a statewide cohort could potentially identify those at risk to help mitigate their effects.
Methods: Cases of SINT with a carcinoid histology (8240 or 8241) diagnosed in Utah from 1996 to 2014 with no prior history of cancer within 5 years (n = 433) were matched to population controls (1:10 ratio). Tobacco and alcohol exposures before case diagnosis were identified from International Classification of Diseases codes in statewide medical records and from self-reported data captured at patient encounters beginning in 1996. Multivariate logistic regression was used to estimate risk of SINT associated with tobacco and alcohol in cases compared with controls.
Results: An increased risk of SINT was observed in tobacco-exposed individuals compared with unexposed [OR, 1.44; 95% confidence interval (CI), 1.11-1.86; P = 0.006]. Those who were exposed to alcohol exhibited an increased risk of SINT (OR, 1.62; 95% CI, 1.05-2.49; P = 0.03).
Conclusions: This study supports tobacco and alcohol use as risk factors for SINT, independent of family history. However, low rates of smoking and alcohol use in Utah coupled with higher rates of SINT suggest other factors may contribute to development of these tumors.
Impact: Although tobacco and alcohol modestly contribute to risk, our study suggests in addition to greater detection of tumors, other as-of-yet undefined exposures may drive rising SINT incidence.