Smoke exposure is associated with a lower prevalence of serum thyroid autoantibodies and thyrotropin concentration elevation and a higher prevalence of mild thyrotropin concentration suppression in the third national health and nutrition examination survey (NHANES III)

被引:199
作者
Belin, RM
Astor, BC
Powe, NR
Ladenson, PW
机构
[1] Johns Hopkins Med Inst, Div Endocrinol & Metab, Baltimore, MD 21287 USA
[2] Johns Hopkins Med Inst, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD 21287 USA
关键词
D O I
10.1210/jc.2004-0431
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Few modifiable exposures influencing autoimmune thyroid disease have been identified. Studies evaluating cigarette smoke and thyroid disorders have yielded conflicting results. The relationship between smoking and thyroid abnormalities was evaluated in the 1988-1994 Third National Health and Nutrition Examination Survey (NHANES III), a cross-sectional study that used a complex, multistage, stratified, clustered sampling approach to reflect the entire noninstitutionalized United States population. Among 18,148 persons who underwent thyroid testing, data regarding age, gender, iodine status, smoke exposure, and thyroid tests were complete for 16,046 persons. After excluding those taking thyroid-altering medications, 15,592 remaining subjects were analyzed. Subjects with serum cotinine levels greater than 15 ng/ml were classified as smokers. Outcome measures included the presence of 1) antithyroperoxidase antibody levels of 0.5 IU/ml or more or antithyroglobulin antibody levels of 1.0 IU/ml or more, 2) TSH concentration greater than 4.5 mU/liter, 3) TSH concentration less than 0.1 mU/liter, and 4) TSH concentration of 0.1-0.4 mU/liter. Fewer smokers (11%, 95% confidence interval (CI) = [10-13%]) had thyroid autoantibodies compared with nonsmokers (18%, 95% CI = [17-19%]). Prevalence in smokers after adjustment for age, gender, race-ethnicity, and iodine status was 13%, 95% CI = [12-15%]. Fewer smokers (2.6%, 95% CI = [2.0-3.2%]) had elevated TSH compared with nonsmokers (5.5%, 95% CI = [4.7-6.3%]). The adjusted rate in smokers was 3.4%, 95% CI = [2.6-4.3%]). Among persons with thyroid autoantibodies, smokers had 40% lower odds of TSH elevation compared with nonsmokers (adjusted odds ratio [95% CI] = 0.6 [0.4-0.97]). Among persons without TSH elevation, smoke exposure was associated with 200% greater odds of low normal TSH 0.1-0.4 mU/liter (adjusted odds ratio [ 95% CI] = 2.0 [1.3-2.9]). Smoking appears to be negatively associated with serological evidence of thyroid autoimmunity and hypothyroidism and positively associated with mild TSH decreases. Eliminating smoke exposure may help prevent the low normal TSH measurements that are characteristic of mild hyperthyroidism. Understanding the underlying mechanism could help identify potential pathways for the prevention of autoimmune thyroid disease.
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页码:6077 / 6086
页数:10
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