Belin Ruth M, Astor Brad C, Powe Neil R, Ladenson Paul W
Division of Endocrinology and Metabolism, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287, USA.
J Clin Endocrinol Metab. 2004 Dec;89(12):6077-86. doi: 10.1210/jc.2004-0431.
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.
已确定的影响自身免疫性甲状腺疾病的可改变暴露因素很少。评估香烟烟雾与甲状腺疾病的研究结果相互矛盾。在1988 - 1994年第三次全国健康和营养检查调查(NHANES III)中评估了吸烟与甲状腺异常之间的关系,这是一项横断面研究,采用复杂的多阶段、分层、整群抽样方法以反映整个非机构化的美国人群。在接受甲状腺检测的18148人中,16046人的年龄、性别、碘状态、吸烟暴露和甲状腺检测数据完整。在排除服用改变甲状腺药物的人后,对其余15592名受试者进行了分析。血清可替宁水平大于15 ng/ml的受试者被归类为吸烟者。结果指标包括:1)抗甲状腺过氧化物酶抗体水平≥0.5 IU/ml或抗甲状腺球蛋白抗体水平≥1.0 IU/ml;2)促甲状腺激素(TSH)浓度>4.5 mU/L;3)TSH浓度<0.1 mU/L;4)TSH浓度为0.1 - 0.4 mU/L。与不吸烟者(18%,95%置信区间(CI) = [17 - 19%])相比,吸烟者中甲状腺自身抗体阳性的比例更低(11%,95% CI = [10 - 13%])。在对年龄、性别、种族和碘状态进行调整后,吸烟者中的患病率为13%,95% CI = [12 - 15%]。与不吸烟者(5.5%,95% CI = [4.7 - 6.3%])相比,吸烟者中TSH升高的比例更低(2.6%,95% CI = [2.0 - 3.2%])。吸烟者的调整后比例为3.4%,95% CI = [2.6 - 4.3%])。在患有甲状腺自身抗体的人群中,与不吸烟者相比,吸烟者TSH升高的几率低40%(调整后的优势比[95% CI] = 0.6 [0.4 - 0.97])。在TSH未升高的人群中,吸烟暴露与TSH处于低正常水平0.1 - 0.4 mU/L的几率高200%相关(调整后的优势比[95% CI] = 2.0 [1.3 - 2.9])。吸烟似乎与甲状腺自身免疫和甲状腺功能减退的血清学证据呈负相关,与轻度TSH降低呈正相关。消除吸烟暴露可能有助于预防轻度甲状腺功能亢进特征性的低正常TSH测量值。了解潜在机制有助于确定预防自身免疫性甲状腺疾病的潜在途径。