Worldwide, iodine deficiency is the commonest cause of preventable mental retardation as well as goitrous hypothyroidism (endemic goitre), especially in developing countries. An insufficient supply of the essential micronutrient iodine, an integral part of thyroid hormones, results in impaired thyroxine production, producing a spectrum of iodine deficiency disorders including endemic goitre, cretinism, hypo- thyroidism, short stature and neuromuscular and neurosensorial deficit [1,2].

Most iodine absorbed in the body eventually appears in the urine, so urinary iodine concentration is a good marker for very recent dietary iodine intake [1]. Iodine concentrations can, however, vary con- siderably from day to day and over a single day in one individual [3]. Thus, a single urinary iodine measurement is not representative of individual nutritional iodine status. Urinary iodine concentrations are useful, however, when used in cross-sectional, epidemiological surveys in population samples of appropriate size [4].

Therefore, the assessment of other indicators of iodine deficiency disorder such as the presence of goitre, serum thyroid profile or serum thyroglobulin might be helpful at an individual level if used in conjunction with urinary iodine concentration to discover iodine deficiency, especially in moderate to severe cases, and would also help for follow-up after iodine supplementation to ensure its success and to prevent consequent morbidity [5].

It has been confirmed that urinary iodine excretion assesses iodine nutrition only at the time of measurement, whereas, thyroid size reflects iodine nutrition over months or years [1]. Serum thyroglobulin has been reported to change inversely with iodine intake in all age groups [6]. On the other hand, the pattern of circulating thyroid hormones in clinically euthyroid children in areas of severe iodine deficiency has been characterized by low serum tetra-iodothyronine (T4), elevated thyroid stimulating hormone (TSH) and normal or supernormal triiodothyronine (T3) [7].

In Egypt, endemic goitre and low urinary iodine concentration have been reported in several regions [8–11]. Most studies in Egypt, however, did not relate urinary iodine concentration with other laboratory indicators for iodine deficiency disorders.

The objective of this study was to relate the urinary iodine excretion in a sample of school-age children (5–13 years) to other indicators of iodine deficiency disorder such as thyroid profile, serum thyroglobulin and the presence of goitre. Children are at high risk of the consequences of iodine deficiency and hypothyroidism (growth and physical and mental development can be affected) and are the focus of school-based national surveys.

We interviewed 300 children as potential participants in this study. The inclusion criterion was age group (5–13 years) while the exclusion criteria were the presence of any systemic chronic or autoimmune disease. Informed consent was taken from all participants or their parents before entering the study. We excluded 74 of these children: 25 were outside the age range, 40 had chronic systemic disease and 9 had autoimmune disease. A total of 127 refused to participate, 55 because of fear of giving blood samples and 72 owing to lack of time.

In all, 99 school-age children 5–13 years old, 58 males and 41 females, were consecutively enrolled. These children were apparently healthy siblings and relatives of patients attending the clinic of Cairo University children’s hospital. People attending this hospital come from many regions of Egypt; most of them are of low or intermediate socioeconomic status.

History taking (which included questions on iodine supplementation and symptoms of hypothyroidism) and clinical examination were carried out, including neck examination by inspection and palpation for goitre according to World Health Organization (WHO) classification [1]. Blood samples (5 mL venous blood) were taken from each child. Sera were separated and divided into 2 aliquots for assay of thyroid hormones. One was used for serum free T3 and free T4 by solid phase radioimmunoassay [12], and serum TSH by solid-phase immunoradiometric assay (Allegro highly sensitive TSH kit, Nichols Institute Diagnostics, San Juan Capistrano, California). The second aliquot was used for assay of serum thyroglobulin by chemiluminescent immunoassay using the automated Immulite analyser [13]. All commercial kits were supplied by DPC (Diagnostic Products Corporation, Los Angeles).

A morning spot urine sample was obtained from each child in a clean cup and stored at –20 °C until assayed for urinary iodine. Urine was digested with ammonium persulfate to get rid of interfering substances, then iodide was measured by its catalytic action on the reduction of ceric ammonium sulfate (yellow) to the cerous form (colourless), coupled to the oxidation of arsenite to arsenate (Sandell–Kolthoff reaction) [14]. All chemicals were supplied by Sigma (Saint-Quentin, France).

We used SSPS, version 9 for data processing. Quantitative data were presented as mean and standard deviation for normally distributed variables and mean and percentiles for skewed distributions. For comparison of means, the Student t-test or Mann–Whitney test was used. For qualitative data chi-squared was used for comparison. Correlation between variables was done and Spearman’s rank correlation coefficient calculated. All tests were 2-tailed and considered statistically significant at P < 0.05.

There were 99 children in the study group, 59 male and 41 female. Mean age was 9.1 years (standard deviation 2.8), range 5–13 years.

By clinical examination, goitre was found in 25 of the children we studied. Urinary iodine concentration was decreased in all goitrous children (Table 2). Goitre was present in 64.5% of children who had moderate or severe iodine deficiency (mostly grade 2 goitre) compared to only 8.3% of children with mild deficiency (mostly grade 1 goitre). The difference was statistically significant (P < 0.01). Goitre was not present in the children who did not have iodine deficiency.

Mean serum free T3, serum TSH and serum thyroglobulin were significantly elevated in the children with moderate or severe iodine deficiency compared to those with optimal urinary iodine concentration or mild iodine deficiency (P < 0.001 for both). However, free T4 levels were not significantly different between groups (P = 0.9) (Table 3). Moreover, a negative correlation was observed between urinary iodine level and serum TSH (rs = –0.34; P < 0.001).

Our results showed a high prevalence of iodine deficiency in the children we studied; only 8.1% had optimal urinary iodine concentration according to the WHO cut-off points for urinary iodine levels [1]. One quarter of the children had clinical goitre. These results could signify that iodization of salt may not be adequate or they may be affected by consumption of goitrogens.

Previous studies reporting endemic goitre in Egypt are consistent with the results of this study. In Cairo, a prevalence of 13.5% has been reported in primary school children, with the highest prevalence (27.1%) in north Cairo [15]. In Upper Egypt, the overall prevalence of goitre was 34.6% in one study [16]. Other studies reported that the highest prevalence of goitre in Egypt (82.3%) was in the New Valley [8] followed by Minia (36.9%), Assuit (36.8%), Sohag (30.1%) in Upper Egypt [9] then Kafr El Sheikh (27.1%) [10] and Aswan (17.5%) [11].

The high prevalence observed among the children we studied as well as the previous studies is in contrast to the cut-off level recommended by WHO [1]. It is recommended that a total goitre rate of 5% or more in schoolchildren 6–12 years of age is used to signal the presence of a public health problem. This recommendation is based on the observation that in a normal, iodine-replete population, the prevalence of goitre should be quite low. The cut-off point of 5% allows both for some margin of error in goitre assessment and for goitre that may occur in iodine-replete populations due to other causes such as goitrogens and autoimmune thyroid disease [1].

Our results are also in agreement with the high prevalence encountered in countries such as in Turkey, where goitre prevalence ranged from 5% to 56%, indicating severe to moderate iodine deficiency in 14, and mild iodine deficiency in 6, of the cities surveyed [17]. In the Islamic Republic of Iran, goitre prevalence was 60%; after iodine supplementation, this dropped to 47% [18]. A lower prevalence rate was found in Indonesia: 12.5% in Bali, and 8.0% in Java and Sumatra [19]. Different prevalence rates were seen in India, ranging from 0.0% in some areas [20], to 30.2% in others [21]. Mild to severe iodine deficiency was also reported in 32 European countries in the late 1990s, and they still have not reached a state of iodine sufficiency [22].

Our study revealed increased free T3 in patients with moderate and severe iodine deficiency when compared with those with mild iodine deficiency. Increased serum TSH as well as elevated serum thyroglobulin levels were found only in patients with moderate and severe iodine deficiency.

Similar results were reported in 1993 in Indians of southern Venezuela by Cooper et al. who reported that 71% of children had a thyroid volume above normal and iodine deficiency was associated with predictable higher serum free T3 and TSH concentrations [23].

It has been mentioned that the pattern of circulating thyroid hormones in clinically euthyroid children in areas of severe iodine deficiency is characterized by low serum T4, elevated TSH, and normal or supernormal T3. The mechanisms responsible for this pattern are unclear but may include thyroidal secretion of T4 and T3 in the proportion in which they exist within the gland, preferential secretion of T3, or increased peripheral conversion of T4 to T3. The shift to increased T3 secretion and increased serum T3:T4 ratio may play an important role in the adaptation to iodine deficiency because T3 possesses about 4 times the metabolic potency of T4, but requires only 75% as much iodine for synthesis [5].

It has been reported that plasma thyroglobulin levels increase in iodine deficiency and in organification defects. Insufficient iodine intake induces proliferation of thyroid cells, which results in hyperplasia and hypertrophy. This leads to an enhanced turnover of thyroid cells, which release thyroglobulin into the circulation [6]. In this setting, serum thyroglobulin reflects iodine nutrition over a period of months or years, in contrast to urinary iodine concentration which assesses more immediate iodine intake. The results of our study match well with this hypothesis as 41.9% of participants with moderate and severe iodine deficiency had elevated serum TSH and 19.4% had elevated serum thyroglobulin and an inverse correlation was also found between urinary iodine and serum TSH. After iodine depletion, thyroglobulin rises before TSH shifts to higher values and long before goitre develops. Following iodine supplementation, thyroglobulin normalizes before thyroid volume has decreased. Therefore, an increase in TSH and/or thyroglobulin could be considered the first sign of a fall in effectiveness of iodized oil injection [7].

It has to be stressed, however, that the sample size in this study was not large enough to comment adequately on the iodine status of the population. The sample size was constrained by the limited financial resources available, therefore, conclusions should be limited to the relation of urinary iodine excretion to other indicators of iodine deficiency. Urinary iodine excretion was highly variable in our sample as has been documented before [3]. Other indicators for iodine deficiency disorder (free T3, free T4 serum TSH, serum thyroglobulin and presence of goitre) are interrelated with urinary iodine excretion and can be used as monitors for the screening of iodine deficiency at an individual level, especially in people with moderate to severe deficiency.

These indicators could be also used for monitoring the success of an iodine supplementation programme. More studies need to be done on a larger scale for assessment of the current status of iodine deficiency in Egypt and for supervision of proper iodine supplementation, which is required to prevent iodine deficiency disorder with all its consequent morbidities.