According to the present study, the prevalence of goitre among school children in Isfahan has decreased from about 89% in 1989 (11
) and 62% in 1997 (12
) to 32.9% in 2005. This implies that iodine deficiency has been the most important cause of endemic goitre and also shows the effective role of the legislation for salt iodization in controlling goitre. However, goitre is still endemic in this area and is a severe public-health problem according to the WHO/UNICEF/ICCIDD-recommended criteria (1
). According to the criteria, the indicator of elimination of iodine deficiency is a median value for UIC of 100 μg/L, and UIC should not be below 50 μg/L in more than 20% of samples (1
). In the study population, the median UIC was 195.50 μg/L, and 3.7% of the population had UIC <50 μg/L, implying that there is no biochemical iodine deficiency in the overall population. More than 25% of the study children had iodine intake more than adequate, and 23.8% had excessive iodine intake. This indicates the risk of iodine-induced hyperthyroidism within 5–10 years after the introduction of iodized salt to susceptible groups (1
). It was reported that, after prophylaxis with iodine salt in Zaire, 14% of patients had undetectable serum TSH values (14
). In the present study, 1.2% of the children had subclinical hyperthyroidism, and there were no case of clinical hyperthyroidism. We suggest that the iodine content of salt in this region be monitored at regular intervals.
In areas with iodine-deficient people, multiple nutritional and environmental influences may contribute to the prevalence and severity of IDD. We showed that the school children with goitre in Isfahan had lower serum selenium levels than non-goitrous ones (15
). However, there was no significant difference in concentration of serum retinol as an indicator of vitamin A status between goitrous and non-goitrous school children in Isfahan (16
There are limited reports on interaction between the goitre rate and the iron status (17
). In the Philippines, there was no difference in goitre rate between anaemic and non-anaemic subjects (18
). In two studies in Iran and Ethiopia, no correlation was found between the iron status and the goitre rate or thyroid hormone levels (19
). In a clinical trial on goitrous children with and without iron deficiency, Zimmermann et al
. found that the therapeutic response to oral iodine was impaired in goitrous children with iron-deficiency anaemia, suggesting that the presence of iron-deficiency anaemia in children limits the effectiveness of iodine-intervention programmes (3
). In another trial, addition of encapsulated iron to iodized salt improved the efficacy of iodine in goitrous children with a high prevalence of anaemia (21
). In the present study, we investigated the role of iron deficiency as a contributor to endemic goitre in school children in Isfahan. Although the mean SF level in the goitrous and non-goitrous children did not differ significantly, the goitrous children had a higher iron-deficiency rate than the non-goitrous ones. A similar finding was reported from a recent study in Iran where iron deficiency was associated with an increased rate of goitre (22
). The mechanism by which the iron status influences thyroid and iodine metabolism is unclear (23
). Iron deficiency decreases plasma T4 and T3 concentrations, reduces peripheral conversion of T4 to T3, and may increase concentrations of TSH (7
). Subjects with lower iron stores may have higher reverse T3 concentration (27
). The two initial steps of thyroid hormone synthesis are catalyzed by thyroperoxidases that are dependent on iron (28
). In addition, iron deficiency may alter the control of thyroid physiology in the central nervous system and modify nuclear T3 binding (24
). In the present study, there was no significant difference in the mean TSH and T4 levels between the iron-deficient and the iron-sufficient subjects. This is in agreement with a previous study by Azizi et al
) and in contrast to another study by Dabbaghmanesh et al
. in which iron-deficient patients had a significantly higher TSH level and lower free T4 concentrations than those with a normal SF level (22
). However, in our study, children in the first distributional quartile of SF had lower UIC levels than children in the fourth distributional quartile of SF, and this may be a possible explanation for the higher rate of goitre in the iron-deficient subjects. The impairment of thyroid peroxidase (TPO) activity may also influence thyroid metabolism. Iron-deficient rats had sharply reduced TPO activity (23
). Although, in the present study, we did not determine the TPO activity, the iron-deficient children had higher anti-TPO Ab levels than iron-sufficient ones.
The main limitation of our study was that we categorized participants into goitrous and non-goitrous groups by inspection and palpation. It has been stated that, in areas of mild-to-moderate IDD, the sensitivity and specifity of palpation are poor (30
). Classification of children into different goitre groups would have been more accurate, had we used thyroid ultrasonography instead of inspection and palpation. The evaluation of body iron status in our study was based only on the SF level. It would have been better to use other iron status parameters, such as serum iron, total iron-binding capacity, serum-soluble transferrin receptor, or transferrin concentration besides SF level. Lack of any statistically significant difference between SF levels in goitrous and non-goitrous school children could be attributed to the small sample size which is another limitation of the present study. SF can be falsely elevated during an infection. This can be adjusted with serum C-reactive protein (CRP) levels, a marker of infection. Although we did not measure CRP, the study children were free of any clinical infection when blood sampling was done.
We have shown that goitre is still a public-health problem in Isfahan. Iron deficiency is associated with goitre only in a small proportion of goitrous children, and these children may benefit from iron supplementation. Other factors, such as goitrogens or autoimmunity, may have a role in the still high prevalence of goitre in school children of Isfahan.