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In the mountainous areas of Azerbaijan the schoolchildren suffer from severe Iodine Deficiency (ID) with median Urinary iodine excretion (UIE) 36 mcg/l and prevalence of goiter 99% (estimated by US). In a population of 293,000 schoolchildren aged 8-14 y.o. we administered capsules containing 190 mg of iodized oil (Lipiodol-Guerbet, Cedex, France) twice yearly in 6 months apart (total 380 mg). The aim of the present study was to evaluate the efficacy, the benefits, as well as the possible side-effects in a follow-up period of 6 and 12 months after the initial administration of iodized oil.Six and 12 months after the initial administration of iodide, two representative samples of 391 and 326 children respectively were examined. The evaluation included: estimation of goiter by US, determination of UIE and serum measurements of T3, T4, TSH, Tg, autoantibodies against thyroid peroxidase (anti-TPO) and thyroglobulin (anti-Tg).There was an improvement in median UIE which increased from 36 mcg/l to 68 and 81 mcg/l after 6 and 12 months of treatment respectively. The prevalence of goiter decreased from 99% to 54% and 26% respectively. Tg was decreased at 6 and 12 months from the first administration, whereas TSH remained unchanged at 6 months and decreased at 12 months when compared to the latter value. Hypothyroidism was detected in 7% of children after iodide administration both at 6 and 12 months, but overt hypothyroidism was observed only in 0.5% at 12 months. Subclinical hyperthyroidism was detected in 2% and 6% after iodide administration both at 6 and 12 months. There was a significant increase in the title of thyroid auto antibodies in 6 months which was retained and increased in 12 months. There was no relation between the appearance of thyroid dysfunction and the positive thyroid auto antibodies.The dose of 190 mg iodide administered twice yearly, improved iodine deficiency and endemic goiter in schoolchildren. The increase of UIE resulted from iodide administration, was accompanied by an increased title of thyroid auto-antibodies and an increased prevalence of hyper- and hypothyrotropinemia apparently of no autoimmune etiology.

Hypothalamic amenorrhea is a treatable cause of infertility. Our patient was presented with secondary amenorrhea and diabetes insipidus. Cortisol and prolactin responded normally to a combined insulin tolerance test (ITT) and thyrotropin-releasing hormone (TRH) challenge, while thyroid-stimulating hormone (TSH) response to TRH was diminished, and no response of growth hormone to ITT was detected. Both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels increased following gonadotropin-releasing hormone (GnRH) challenge. No response of LH to clomiphene citrate challenge was detected. Magnetic resonance imaging findings demonstrated a midline mass occupying the inferior hypothalamus, with posterior lobe not visible and thickened pituitary stalk. Ovulation induction was carried out first with combined human menopausal gonadotropins (hMG/LH/FSH) (150 IU/day) and afterwards with pulsatile GnRH (150 ng/kg/pulse). Ovulation was achieved with both pulsatile GnRH and combine gonadotropin therapy. Slightly better results were achieved with the pulsatile GnRH treatment.