Iodine deficiency
	Costante et al., Catanzaro, Italy, used the results of screening programs for congenital hypothyroidism to detect populations at risk for endemic goiter in Calabria, a southern region in Italy. They analyzed 21.674 samples from infants taken at the 5th day after birth and found that TSH levels >10-< 20 mU/ml identified areas of mild to moderate iodine deficiency (ranging from 47-74 mg I/g creat.). Also Sorcini et al., Rome and Parma, Italy, found that the congenital hypothyroidism screening program in Italy could be used to identify areas with mild iodine deficiency, since in those areas the frequency of congenital hypothyroidism was higher (>1: 2000) than in iodine sufficient areas (1:3200). They found that in the iodine deficient areas transient neonatal hypothyroidism or hyperthyrotropinemia could exist. Grueters et al., Berlin and Leipzig, Germany, did a similar study with regard to the former eastern and western part of Berlin, because until the re-unification an adequate iodine prophylaxis program existed in the eastern part, while no prophylaxis program existed in West Berlin. Although the incidence of congenital hypo thyroidism was the same in the eastern and the western part (1:2790 and 1:3200 respectively), the percentage of transiently elevated TSH levels (TSH >15 mU/L) was different, being 0.74% in the western part as compared to 0.1% in the former eastern part. After the re-unification higher iodine excretion was still found in 1991 and 1993 in the former eastern part and TSH levels were significantly lower in both years in newborns from the former eastern part as compared to the former western part. No differences were seen in serum T4 levels. Sviridenko et al., Moscow, Russia, treated 385 village and 452 town children in areas near Moscow, living in areas with mild to moderate iodine deficiency (2.5-4.9 llg/dl and 5.7-8.8 mg/dl respectively) with a single dose of iodized oil, containing 0.2 g iodine. Goiter prevalence decreased from 43-61% to 29-42% in village children and 31-47% to 18-22% in town children. Serum TSH decreased into the normal range 9 months after iodine administration. Iodine urinary excretion increased after 1 week to a maximum of 39 pg/dl and averaged 11 ug/dl after 9 months. Aghini-Lombardi et al., Pisa, Italy, studied thyroid volume in children between 7 and 14 years of whom mean urinary iodine excretion in 1985 was 39 mg/L and after iodine prophylaxis 98 ug/L in 1993. They found that between the age of 7 and 11 years there was no difference in thyroid volume as compared to controls, however beyond this age there was a persisting increase in thyroi d volume of maximally 3 ml (9.15 ml versus 6.4 ml in controls) in 14 year olds. The authors conclude that in assessing endemic goiter in this age group it is important to know the previous history of the iodine status because adequate iodine prophylaxis does not decrease thyroid volume to the normal level in these subjects. Liesenkötter et al., Leipzig, Germany, studied the effect of 300 ug iodine supplementation per day to 38 pregnant women and compared the results with 70 pregnants without iodine supplementation. During 10-12 weeks of gestation, urinary iodine excretion increased from 53 µg/g creatinine at the beginning of gestation to 106 ug/g creatinine postpartum. Iodine excretion in the newborns of treated mothers was 77.0 vs. 56 mg/g creatinine in newborns from untreated mothers. No abnormalities in thyroid function or production of anti-TPO antibodies was seen in either group of mothers or neonates. The newborns of iodine supplemented mothers had lower thyroid volumes i.e. 0.7 ml versus 1.5 ml. Even after 3 years, while iodine prophylaxis was not continued after birth, a difference in thyroid volume was seen 1.4 ml vs. 2.3 ml. Smith et al., Dublin, Ireland, and Cardiff, Wales, UK studied the possible genetic influence of HLA phenotypes, class II (DR/DQ) on goiter prevalence in a province in Senegal, West-Africa, because not all subjects in that region develop endemic goiter, although iodine deficiency (41 ug/g creatinine in urine) is present in the whole area. They found no significant associaton with thyroid enlargement or presence of thyroid auto-antibodies with results of HLA typing. Gerasimov et al., Moscow, Russia, showed again that, using iodized salt for bread production (60 mg of KI per 100 kg of flour) increased iodine excretion in schoolchildren from 4.8 to 12.6ug/dl, 3 months after introduction of iodized bread. Within this short period there was no decrease in thyroid volume. Tiwari et al., Gorakhpur and New Delhi, India, assessed learning potential and achievement motivation in 100 male children of different ages from an iodine deficient area and compared results with children from an iodine sufficient area. Mean iodine urinary excretion was 2.79 vs.5.70 ug/dl, T4 90 vs. 124 nmol/L, TSH 6.32 vs. 4.85 uU/L. They found that both aspects were less well developed in children from the iodine deficient area. Mirmiran et al., Tehran, Iran, tested thyroid function parameters, pschymotorfunction, and IQ levels in 69 children from an iodine deficient area who were injected with 480 mg iodide in oil, and compared results in children (n = 70) who were given saline injections. Thyroid function parameters were tested at 0.1, 2, 3, and 4 years after intervention and psychomotor performance and IG levels were tested 5 years after intervention. In iodine treated children iodine urinary excretion increased from 21 to 98 mg/g creatinine. Goiter rate and severity decreased progressively and T4 increased from 8.3 to maximally 10.0 ug/dl at year 3, while TSH decreased from 3.0 to minimally 1.0 uU/L at year 3. No changes were seen in the control group. IQ was 97 + 9 and 97 + 6 before and 111 + 8 and 98 + 11 at 5 years in the iodized and controle group respectively. Psychomotor function was better in the iodized group. (Comment: It has now been well-established that in iodine deficient areas psychomotor function and cognitive ability may be also impaired in children without obvious creatinism. These abnormalities may be even present in children exposed to only mild or moderate iodine deficiency. Iodine deficiency disorders are a global problem because 1 billion people are living in iodine deficient areas.) Antonelli et al., Pisa, Italy, and Westmead, Australia, studied pathophysiological abnormalities in four cretins of the hypothyroid type and 7 cretins of the neurological type. They found that neurological damage was also present in the hypothyroid type and conclude that neurological damage is a general phenomenon caused by maternal and fetal hypothyroidism during pregnancy, whereas the presence of hypothyroidism may be explained by the extent and duration of postnatal thyroid insufficiency. Medeiros-Neto et al., Sao Paulo, Brasil, studied the presence of anti-oc galactosyl antibody (anti-GAL) in endemic goiter patients. Anti-GAL is a natural antibody comprising approximately 1 % of circulating IgG in normals. Anti-GAL can mimic TSH effects in vitro and if these antibodies may be prevalent in goiter, they may play a role in its formation. In this studie anti-GAL antibodies were found in elevated concentration in patients with goiters, both with small goiters (n = 20) and with large goites (n = 36). The patients studied were from an endemic goiter area but iodine excretion in the urine was normal because of recent iodine prophylaxis. Bourdoux et al., Brussels, Belgium and Bangui, Africa, report on the iodization of drinking water for correction of iodine deficiency. They use NaI incorporated in silicone matrices immersed in water that constantly releases iodide. Iodine urinary excretion increased from 2.1 to 28.9 ug/mL 6 months after iodization of drinking water, and was 17.4 ug/mL after one year. The prevalence of goiter rate dropped from 61 % to 44%. The authors conclude that this type of iodization may be efficient when drinking supply systems are suitable for this type of prophylaxis.