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Cancer Epidemiol Biomarkers Prev. 2019 Dec;28(12):1998-2004. doi: 10.1158/1055-9965.EPI-19-0465. Epub 2019 Sep 26.

Associations of Tobacco and Alcohol Use with Risk of Neuroendocrine Tumors of the Small Intestine in Utah.

Author information

1
Division of Epidemiology, Department of Internal Medicine, University of Utah, Salt Lake City, Utah. karen.curtin@hsc.utah.edu.
2
Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.
3
Division of Epidemiology, Department of Internal Medicine, University of Utah, Salt Lake City, Utah.
4
George E. Wahlen Department of Veterans Affairs Medical Center, Salt Lake City, Utah.
5
Division of Public Health, Department of Family and Preventive Medicine, University of Utah, Salt Lake City, Utah.
6
Utah Cancer Registry, University of Utah, Salt Lake City, Utah.
7
Hematology/Oncology, Intermountain Healthcare, Salt Lake City, Utah.

Abstract

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.

PMID:
31558509
PMCID:
PMC6961822
[Available on 2020-06-01]
DOI:
10.1158/1055-9965.EPI-19-0465

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