The prevalence of iodine deficiency disorders and the thyroid status of the population were studied in an endemic goitre area in Algeria. After oral administration of lipiodol (0.5 ml), three treated groups of mother-newborn couples were compared to an untreated group: group A, mothers treated 1-3 months before conception; group B, mothers treated during the first month of pregnancy; group C, mothers treated during the third month of pregnancy. Untreated mothers were used as a control (group D). After lipiodol treatment, all newborn babies and mothers were clinically euthyroid. All tested newborn babies were full term and no goitre was observed in the four groups. In the mothers, goitre prevalence and thyrotrophin levels decreased significantly, whereas maternal milk and urinary iodine and serum-free thyroxine levels were significantly higher after treatment. The rate of prematurity, stillbirths and abortions in the treated groups was reduced when compared to the untreated group, whereas placental and birth weights were significantly higher. In group D two cases of neonatal hypothyroidism were detected. Their re-evaluation confirmed that hypothyroidism was transient. Groups A, B and C were statistically different from group D with regard to neonatal thyrotrophin and thyroxine. Positive correlations were found between neonatal thyroxine and birth weights and placental weights on the one hand, and maternal urinary iodine and free thyroxine on the other. Consequently, these data indicate that oral administration of lipiodol before or during the first trimester of pregnancy normalizes thyroid function in newborn babies and mothers, increases placental and birth weight and reduces the frequency of iodine deficiency disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Oral iodized oil is the major alternative to iodized salt for correcting endemic iodine deficiency. This study responds to a need for better guidelines in its use. Schoolchildren, aged 6-11 yr, from a severely iodine-deficient area of Algeria received iodized poppy seed oil (Lipiodol) in a single oral dose containing 120, 240, 480, or 960 mg iodine (groups A-D) or in an im injection of 480 mg iodine (group E). Thyroid volume by ultrasonography had not changed 395 days after treatment in groups A, B, and C, had decreased in groups D and E. Urinary iodine concentration rose rapidly from an initial median of 0.21 mumol/L, but fell below 0.79 mumol/L (the currently accepted level for indicating iodine deficiency) by 150 days for groups A and B, and by 395 days for groups C and D. Median serum TSH and T4 levels were normal before and after treatment, whereas high initial serum thyroglobulin values decreased in all groups after iodized oil treatment. For correcting iodine deficiency in children, we recommend single oral doses of Lipiodol containing 240 mg iodine for 6-month coverage or 480 mg for 12 months. These doses may not completely sustain iodine sufficiency, but will prevent the worst of the iodine deficiency disorders. Additionally, we conclude that the urinary iodine concentration is the most useful epidemiological indicator for assessing current iodine status, and thyroid volume and serum thyroglobulin levels are the best markers for assessing chronic effects.

The echo patterns of diffuse thyroid lesions in children are not yet well known. We present here the ultrasound findings of 32 children aged 5 to 15 years with a newly diagnosed diffuse thyroid disease. 23 patients had thyromegaly by palpation, 9 had hypothyroidism but no goiter. Of the 23 goitrous patients 9 were hypo-, 3 hyper-and 11 euthyroid. The 9 with hypothyroidism had all autoimmune thyroiditis as judged by antithyroid antibodies, and confirmed cytologically in 5. They had all 9 a hypoechogenic patchy, partly nodular thyroid by ultrasound.2 of the 3 with Graves disease had initially a similar pattern than in thyroiditis, the 3rd showed hypoechogenity later. Of the 11 euthyroid patients 8 had antithyroid antibodies and the ultrasound suggested thyroiditis in 5 of them, 3 were judged normal (2 and 1 became later hypothyroid). Of the 3 patients with euthyroid goiter but without antithyroid antibodies the ultrasound finding was normal in 1, showed multicystic thyroid in 1 and suggested thyroiditis in 1 who later had antithyroid antibodies. Of the 9 hypothyroid patients without thyromegaly one had an unusually small hit otherwise normal thyroid by ultrasound. The others had an echopoor thyroid, but the patchy and nodular pattern was often less marked than in goitrous hypothyroidism. We conclude that autoimmune thyroiditis gives a typical ultrasound pattern, and ultrasonography gives useful information especially of euthyroid goiter and nongoitrous hypothyroidism. PERICARDIAL EFFUSION IN CONGENITAL HYPOTHYROID/ ; A 1NFANTS:AN AETIOLOGICAL CORRELATION. Gianfili~po -" ...~e h children positive at the newborn screen'ing program for congenital hypothyroidism were studied. Confirmlng diagnosis was made in 8/10 infants,while 2/10 were false positive. Moreover we have considered in the study a patient clinically diagnosed at 19 months (he did not undergo the screening prograrn),in which was demonstrated an ectopic g1and.A complete thyroid function evaluation (FT3,FT4,T3,T4,TBG,TRH test),scintlgraphy (TC99),echocardiography (B-mode)were carried out in all the babies (scintigraphy was not performed in the 2 false positive children). Pericardial effusion was demonstrated in 4/9 patients (44%); complete resolution occurred after a variable period of L-T4 therapy (15 days to 5 months).None of the patients showed clinical symptoms nor electrocardiographrc signs of cardiac failure. Data collected in Zaire suggested that severe iodine deficiency resulted in neonatal hypothyroidism and its longterm consequence, endemic cretinism. In order to further evaluate this possibility, we initiated neonatal thyroid screening in an endemic goiter area in Algeria (area A) with a high prevalence of goiter (51.3 %) and cretinism (1.1 %) and a low dietary supply of iodine (I)(Mean urinary I : 16.2 uglg creatinine) and in a non goitrous area (B) with no cretinism and a normal iodine supply (urinary 1:73.9 ug/g creat.). Serum TSH levels in 3135 newborn infants of area A were shifted towards high values as compared to the results obtained in a...

Background/Aims: True gigantism is an exceptional and fascinating pediatric disease. Our aim in this study was to describe the different etiologies of a large group of children with gigantism and the natural history of their growth. Methods: In this multicenter study, we considered as giant children, adolescents and adults whose heights were ≥3 SD compared to their target stature or to our population average lengths. Isolated hypogonadism and Klinefelter syndrome were excluded from this series. All underwent clinical exam, and hormonal and neurological investigations. Results: From 1980 to 2010, we observed 30 giants: 26 males (86.6%) and 4 females (mean age 19.8 ± 11 years). Among the 13 patients (40.3%) who consulted before the age of 16 years, 9 had acromegaly and 6 had mental retardation and body malformations. Based on growth hormone (GH) secretion evaluation, 2 groups were observed: pituitary gigantism (n = 16): GH = 150 ± 252 ng/ml (n ≤ 5), and other causes with normal GH (0.7 ± 0.6 ng/ml): 6 Sotos syndrome and 8 idiopathic cases. Only the first group had neurological, ophthalmological, metabolic and cardiovascular complications and received treatment. The result was not optimal as GH normalization was not observed. Reduction of tumor size and decreased GH plasma values were not observed. Conclusion: Gigantism predominates in males. The main cause is GH excess. The diagnosis was very late except for cerebral gigantism. Complications were observed in pituitary gigantism only.

The clinical and biochemical features of myxoedematous and neurological cretinism were studied in an endemic goitre area in Algeria (goitre prevalence 51.3%; endemic cretinism 1.1%; mean urinary iodine level 127.6 nmol/l). When comparing the data collected in six different villages of the area, significant negative correlations were found between the decrease in urinary iodide and iodide/thiocyanate ratio (I/SCN) and the increase in prevalences of visible goitres, endemic cretinism and transient neonatal hypothyroidism. The cretins were divided on clinical signs into two groups: myxoedematous (MC) and neurological (NC) cretinism. Differences were noted in the neurological signs and the type of deafness encountered in both types. Although some overlap did exist, proximal spasticity and rigidity were characteristic of NC. The hormonal profiles of the two groups, including TRH tests, were clearly different. The two groups were similar with regard to the percentage of palpable thyroids, the absence of antimicrosomal and anti-thyroglobulin antibodies, seropositive viral antibodies and thiocyanate concentrations in serum and urine. Thus it is unlikely that these factors have any significant aetiological role in NC. The data collected in the general population in this area and those obtained in the mothers of the myxoedematous and neurological cretins support the hypothesis that the neurological signs are the result of hypothyroxinaemia in the mothers and the fetus at different periods of pregnancy. They could be aggravated by neonatal hypothyroidism, which may be transient in NC and permanent in MC.