In 1990, iodine deficiency affected almost one-third of the world population and was the greatest single cause of preventable brain damage and mental retardation. Following a resolution adopted by the World Summit for Children in 1990. major programmes of iodine supplementation were implemented by the governments of the affected countries with the support of major donors. Iodisation of salt was recognised as the method of choice. Nine years later, by April 1999, 75% of the affected countries had legislation on salt iodisation and 68% of the affected populations had access to iodised salt. The prevalence of iodine deficiency disorders decreased drastically in most countries and the deficiency disappeared completely in some such as Peru. This result constitutes a public heath success unprecedented with a non-infectious disease. However, occasional adverse effects occurred. The principle effect is iodine-induced hyperthyroidism which occurs essentially in older people with autonomous nodular goitres, especially following iodine intake that is too rapid and of too massive an increment. The incidence of the disorder is usually low and reverts spontaneously to the background rate of hyperthyroidism or even below this rate after 1 to 10 years of iodine supplementation. The possible occurrence of iodine-induced thyroiditis in susceptible individuals has not been clearly demonstrated by large epidemiological surveys. Iodine supplementation is followed by an increased prevalence of occult papillary carcinoma of the thyroid discovered at autopsy but the prognosis of thyroid cancer is improved due to a shift towards differentiated forms of thyroid cancer that are diagnosed at earlier stages. Iodine-induced hyperthyroidism and other adverse effects can be almost entirely avoided by adequate and sustained quality control and monitoring of iodine supplementation which should also confirm adequate iodine intake. Available evidence clearly confirms that the benefits of correcting iodine deficiency far outweigh the risks of iodine supplementation.
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...
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