TOPIC: Excessive iodine intake and the risk of thyroid autoimmune disease
Title: Effect of iodine intake on thyroid diseases in China.
Authors: Teng W, Shan Z, Teng X, Guan H, et al.
Reference: New England Journal of Medicine 354: 2783-2793, 2006
Summary
Background
Normal thyroid function requires iodine to produce thyroid hormones. Both low (i.e. iodine deficiency) and high (i.e. iodine excess) iodine intake levels may lead to thyroid diseases. Worldwide, many people are still iodine-deficient, defined as a urinary iodine excretion (UIE) of less than 100 -g/L. Iodine excess (UIE >300 -g/L) may cause hypothyroidism in subjects with damaged thyroid gland, but may also induce hyperthyroidism in patients with multinodular goiter.
Purpose
The authors studied the prevalence of thyroid disease in China, in cohorts from three regions with different iodine intake levels: a) mildly deficient (median UIE: 84 -g/L); b) adequate (median UIE: 243 -g/L); and c) excessive (median UIE: 651 -g/L). Participants (N = 3.761) were unselected subjects (enrolled at baseline), but only 3.018 (80.2%) participated in the five-year follow-up (1999 - 2004). The authors examined the effect of regional differences in iodine intake on the incidence of thyroid disease.
Methods
Serum levels of thyroid hormones (free T4 and free T3), TSH, thyroglobulin, TPO-Ab, TG-Ab and TSH-Receptor antibody were measured using commercial kits. Urinary iodine excretion (UIE) was determined by the Sandell-Kolthoff reaction. Thyroid ultrasonography was performed by the same observers using the same equipment (model SA 600 with a 7.5 MHz linear transducer).
Results
The cumulative prevalence of autoimmune thyroiditis (defined as TPO-Ab >100 U/mL) was significantly higher in -Excessive- (2.8%) & -Adequate- (1.7%) iodine intake cohorts, compared with the low iodine intake cohort (0.5%; P < 0.001). Both overt hypothyroidism and subclinical hypothyroidism were more frequently detected in both -Excessive- (8.1%) & -Adequate- (3.8%) iodine intake cohorts, compared with the iodine deficient cohort (1.2%). There was no significant difference in cumulative incidence of overt hyperthyroidism between the 3 cohorts. Graves- disease was the main cause of hyperthyroidism (defined by TRAb > 2 IU/L and anti TPO >100 U/mL).
Conclusions
More than adequate or excessive iodine intake for a period of five years of follow-up may result in increased prevalence of hypothyroidism and autoimmune thyroiditis.
Commentary
Excessive iodine intake may be linked to increased prevalence of chronic autoimmune thyroiditis (AIT) and, consequently, to a higher prevalence of both clinical and subclinical hypothyroidism in the population. A change in the iodine intake level, from a documented iodine-deficient condition to iodine sufficiency via public health intervention (Universal Salt Iodisation) may also induce a higher prevalence of AIT. This has been well documented in Argentina, Greece, and more recently Brazil. In other regions, such as the African subcontinent, excessive iodine intake was associated with an increase in iodine-induced hyperthyroidism, that was first described in Tasmania and the Netherlands. Thus, it seems that the prevalence of thyroid disease under abnormal iodine intake is variable and dependent on various factors such as the ethnic composition of the population, the level of iodine intake, the severity of previous iodine deficiency, the presence of large multinodular goiter in the population, genetic background for autoimmune diseases, etc.
In present study conducted in China, hypothyroidism and AIT were observed in a relatively low percentage of the population with adequate/excessive iodine intake, during the five years of observation. In other population surveys with iodine replete subjects (UK, USA, Denmark, The Netherlands), the prevalence of AIT was close to 10%, and was higher in subjects over the age of 40 years.
The authors based their diagnosis of chronic AIT only on positive anti-TPO antibodies titers. More recently, several articles have shown that it was more reliable to associate the echographic pattern of the thyroid (hypoechogenicity) with the presence of anti-PTO antibodies for a more accurate diagnosis of Hashimoto-s thyroiditis. In this article by Teng et al., although all patients were presumably submitted to ultrasonography, no reference was made to hypoechoic changes in the patients with Hashimoto-s disease. Finally, it is difficult to accept that a large number of subjects (including school age children) were kept for five years in low or excessive iodine intake nutrition states without intervention of the public health authorities.
Summary and commentary prepared by Geraldo Medeiros-Neto (related to Chapter 20 of TDM)
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