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To compare thyroid-stimulating hormone (TSH) levels in neonatal cord blood between study sites in Bangladesh, Guatemala and the United States. Also, to compare neonatal TSH results with indicators of iodine deficiency in school children.
Consecutive births and, in school children, cross-sectional surveys.
Savar, Bangladesh; San Pedro Sacatepequez, Guatemala; and Atlanta, United States.
In each study site, cord blood was spotted on to filter paper and TSH levels determined using a sensitive monoclonal assay. In the USA, heel stick blood specimens from newborns spotted on to filter paper were also obtained as well as exposure to iodine-containing antiseptics during the birthing process. Urine specimens were collected from mothers of newborns and tested for iodine concentration. School children in the same areas were surveyed for thyroid size by palpation and ultrasonography, and urine specimens collected for iodine concentration.
Between 141 and 243 cord blood specimens were collected from each study site. The prevalence of elevated cord blood TSH levels (>5 mU l−1) was high in all study sites, from 58% to 84%. All sites would be categorised as having ‘severe’ iodine deficiency based on WHO/UNICEF/ICCIDD criteria. Iodine-containing antiseptics were used during 98% of the births in the USA but not in Bangladesh or Guatemala. The neonatal TSH classification indicated more severe iodine deficiency levels than classifications based on urinary iodine and goitre in school children.
In the USA, elevated TSH levels may be partially attributed to use of beta-iodine-containing antiseptics prior to birth. We recommend the cautious interpretation of TSH results in newborns for the assessment of iodine deficiency disorders when iodine-containing antiseptics are used during the birthing process.
The purpose of this trial was to compare three different iodine interventions.
School children aged 8–10 years were randomized into one of three groups: group A was provided with iodized salt by researchers with an iodine concentration of 25 ppm; group B purchased iodized salt from the market; and group C was similar to group B with the exception that they were given iodized oil capsules containing 400 mg iodine at the beginning of the study. Salt iodine content was measured bimonthly for 18 months and indicators of iodine deficiency were measured at baseline and 6, 9, 12 and 18 months after randomization.
The prevalence of abnormal thyroid volumes, based on the World Health Organization (WHO) body surface area reference > 97th percentile, was 18% at baseline and declined to less than 5% by 12 months in groups A and C, and to 9% after 18 months in group B. Results for goitre by palpation were similar. The median urinary iodine was 94 μgl−1 at baseline and increased in all groups to > 200 μgl−1 at the 6-month follow-up.
In this population of school children with initially a low to moderate level of iodine deficiency, the group receiving salt with 25 ppm (group A) was not iodine deficient on all indicators after 18 months of study. When the iodine content of the salt varied, such as in group B, by 18 months thyroid sizes had not yet achieved normal status.
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