European journal of epidemiology · 2007
Smoking and environmental iodine as risk factors for thyroiditis among parous women.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Galanti Maria Rosaria, Cnattingius Sven, Granath Fredrik, Ekbom-Schnell Annika, Ekbom Anders
Аннотация
OBJECTIVE: To elucidate whether exposure to some environmental factors, i.e. cigarette smoking and iodine deficiency influence the risk of thyroiditis.
METHODS: We identified a cohort of 874, 507 parous women with self-reported information on smoking during pregnancy registered in the Swedish Medical Birth Registry from September 1983 through December 1997. Hospital diagnoses of thyroiditis (n = 286) and hypothyroidism (n = 690) following entry into the cohort were identified by record-linkage with the national Inpatient Registry. The hazard ratio (HR) of smokers compared to non-smokers and the corresponding 95% confidence limits (CL) were estimated by Cox regression.
RESULTS: Smoking was inversely associated with risk of overt thyroiditis (adjusted HR = 0.72; CL = 0.54-0.95), even when diagnoses of primary hypothyroidism were included. However, a diagnosis of thyroiditis within 6 months from a childbirth was positively associated with smoking (adjusted HR = 1.88; CL = 0.94-3.76). Being born in areas of endemic goiter was not associated to hospital admission for thyroiditis. Thyroiditis patients who were smokers had more often than non-smokers a co-morbidity with other autoimmune disorders.
CONCLUSIONS: Smoking may increase the risk of thyroiditis occurring in the post-partum period and influence the clinical expression of other thyroiditis, especially when occurring as part of a polymorphic autoimmune disease.
METHODS: We identified a cohort of 874, 507 parous women with self-reported information on smoking during pregnancy registered in the Swedish Medical Birth Registry from September 1983 through December 1997. Hospital diagnoses of thyroiditis (n = 286) and hypothyroidism (n = 690) following entry into the cohort were identified by record-linkage with the national Inpatient Registry. The hazard ratio (HR) of smokers compared to non-smokers and the corresponding 95% confidence limits (CL) were estimated by Cox regression.
RESULTS: Smoking was inversely associated with risk of overt thyroiditis (adjusted HR = 0.72; CL = 0.54-0.95), even when diagnoses of primary hypothyroidism were included. However, a diagnosis of thyroiditis within 6 months from a childbirth was positively associated with smoking (adjusted HR = 1.88; CL = 0.94-3.76). Being born in areas of endemic goiter was not associated to hospital admission for thyroiditis. Thyroiditis patients who were smokers had more often than non-smokers a co-morbidity with other autoimmune disorders.
CONCLUSIONS: Smoking may increase the risk of thyroiditis occurring in the post-partum period and influence the clinical expression of other thyroiditis, especially when occurring as part of a polymorphic autoimmune disease.