Abstract Assessment of the status of iodine prophylaxis was studied in 5,523 schoolchildren randomly selected in all cantons in Bosnia and Herzegovina Federation (BHF). According to the iodine content of household salt samples, all cantons of BHF were divided into two groups: Group A: 95.5% of the salt used is produced in the Tuzla plant, in which the salt is iodized at 5-15 mg Kl/kg salt, and 4.5% of the salt used is produced in the Pag plant, in which the salt is iodized at 20-30 mg Kl/kg of salt, and Group B: 19.9% of the salt used is produced in the Tuzla plant and 80.1% in the Pag plant. In Group A the amount of iodine in salt was significantly lower than in Group B (11.4 mg/kg vs 18.9 mg/kg, P <0.001). In Group A the prevalence of goiter was significantly higher than in Group B (32.6% vs 19.7%, P <0.001). The highest prevalence of goiter was in Bosnian Podrinje Canton (51.2%) and Central Bosnian Canton (42.6%) while the lowest was in West Herzegovina Canton (12.9%). Significantly higher concentrations of urinary iodine were found in Group B than in Group A (82.6 μg/1 vs 75.2 μg/1, P <0.001). In Group A the percentage of urine samples below 50 μg/1 iodine was significantly higher than in Group B (35.6% vs 26.9%, P <0.001), but there was no difference in the percentage of urine samples with iodine values less than 100 μg/1 (70.7 μg/1 vs 68.25 μg/1, P >0.05). We conclude that FBH is an iodine deficient area and that the improvement of iodine prophylaxis is urgently required, primarily by increasing salt iodine content to 20-30 mg/kg, in order to eradicate endemic goiter.

Iodine deficiency which causes the wide spectrum of disorders for all ages, is one of the significant public health problem worldwide. From the ancient times different iodine deficiency disorders were noticed in Bosnia and Herzegovina and in its some areas the goiter existed in endemic form. These facts confirm that its soil bas been iodine deficient and that necessity for iodine prophylaxis is obvious on its territory. The study was based on 5,523 children, of both sex boys and girls school age from 7 to 14 years, randomly selected with the equal participate subjects in relation to the age. The sample is representative and it has been assessed based on: total number of school children aged from 7 to 14 years, anticipated prevalence of goiter 5% level of probability 95%, relative punctuality 30% and the factor called "design effect" which is 3. The study was carried out in whole ten cantons in the schools with equal representation among cities and villages. In examining of prevalence of giter we used inspection and palpation. Determination of iodine concentration in urine was carried out by the method is based on Sandel-kolthof's reaction. The technique used for determination of concentration of iodine in salt was iodinemetric titration. The prevalence of goiter was 27.6% in Federation of Bosnia and Heryegovina. The highest prevalence of goiter was in Bosnia Podrinje Canton (51.20%) while the lowest was in West Herzegovina Canton (12.90%). The urinary iodine excretion in investigated children varied from 1 to 208 *mg/L with median of 77.6 *mg/L. Iodine contetn in household salt samples was from 3 to 29.8 mg/kg, range 14.4 + 5.9 mg/kg. The results of our study show the persistence of mild to moderate iodine deficiency in Bosnia and Herzegovine Federation. Therefore according to the recommendations of the World Health Organisation, UNICEF and International Council for Control of Iodine Deficiency Disorders, the salt for human, and animal consumption as well as for food industry which is consuming on its teritory, has to be iodinated on the place of its production without looking back whether or not it is produced or imported in Bosnia and Herzegovina Federation, lodination has to be performed with 20 to 30 mg KI per one kg of salt, thereby an average the iodine content has to be 25 mg per kg. In this way it will be prevented the wide spectrum of disorders, which we often are not aware for that its are caused by iodine deficiency. In addition it will be prevented many very important socioeconomical consequences of iodine deficiency.

The aim of this study was to evaluate the effects of prenatal asphyxia on perinatal thyroid function by measuring the levels of serum T4, FT4, T3, rT3, TSH and TBG in twenty-seven asphyxiated full-term infants delivered by emergency cesarean section, at birth and on the 5th day of age. All the babies had a one-minute Apgar score of less than 6 and body weight from 3 to 4.6 kg. The control group consisted of 30 healthy neonates which were delivered by elective cesarean section. The mean values of T4 and FT4 observed in the cord blood of the asphyxiated neonates were significantly lower compared to the matched controls, while there were no differences in concentrations of T3, rT3, TSH and TBG. At five days of life, serum concentrations of T4 and FT4 became normal. These results demonstrate the existence of transient hypothyroxinemia at birth in hypoxic babies delivered by emergency cesarean section.

According to the clinical findings, the activity of serum asparate aminotransferase (EC 2.6.1.1), alanine aminotransferase (EC 2.6.1.2) and the level of total bilirubin, 45 children with acute viral hepatitis A were divided into two groups: with mild and moderately severe degree of disease. By determining the products of the peripheral thyroxine metabolism-T3 and rT3, as well as the other thyroid parameters (T4, FT4, TSH and TBG) we have found significantly lower T3 level and significantly higher T4 and TBG levels in both groups of patients in comparison with control group. At the same time, the level of biologically less active rT3 was increased in patients with moderately severe form of disease, while no differences were found in the values of TSH between the ill and control patients. TRH induced TSH release was normal in all patients. The results of this study point to the development of euthyroid sick syndrome or low T3 syndrome in children with viral hepatitis A.

The influence of acidosis on peripheral metabolism of T. was studied in infants with 4 diarrhea and metabolic acidosis. The serum concentrations of T4, T3, rT3, TSH and TBG were compared to those of healthy control subjects. Significantly lower T3 and T4 and significantly higher rT3 serum concentrations were found in the patients in contrast to the control group. No significant differences were found in TSH and TBG values between infants with metabolic acidosis and control subjects. Initial pH showed a significant correlation with T3 but not with T4 and rT3. Despite the reduced serum T3 and T4 concentrations, TSH values were within the normal range. Our data show that the metabolic acidosis with normal anion gap could result in the abnormal peripheral conversion of T4 to T3 and the significant reduction of T3 serum levels, all of which are characterized by the low T3 syndrome.

We studied concentrations of thyroid hormones (T3, T4, FT4, rT3, TBG and TSH) in 62 type I diabetic children and adolescents. The patients were classified into group A (n = 27, good control, HbA1c less than 10%), group B (n = 19, poor control, HbA1c greater than 10%) and group C (n = 16, diabetic ketoacidosis, pH less than 7.1 and HCO3 less than 15 mmol/L. All patients were treated with two daily injections of purified monocomponent insulins. Thirty healthy subjects of the same age served as control group. Patients in group B and C had significantly lower T3 and higher rT3 levels (p less than 0.001) compared to the matched controls (1.5 vs 2.2; 0.9 vs 2.2; 0.58 vs 0.3 and 0.6 vs 0.3 nmol/L). Serum TBG levels were significantly lower (p less than 0.01) in the group A (19.5 +/- 4.3 mg/L), group B (20.3 +/- 3.3) and group C (18.0 +/- 3.4) compared with control group (24.2 +/- 3.1). There was significantly negative correlation between T3 and HbA1c in group B (r = 0.546; p less than 0.02). The results of this study confirm that euthyroid sick syndrome does exist in type I diabetic children and adolescents with poor metabolic control and ketoacidosis. The inverse relationship between T3 and HbA1c percentage (low T3 and high HbA1c) points to the poor diabetic control.