Iodine intake and the thyroid
	Caron, Toulouse, France, measured thyroid function parameters during normal pregnancy in women, living in the southwest of France and correlated these parameters as well as thyroid volume, measured with echography, with iodine intake. During the first trimester and the 9th month of pregnancy 347 women were tested, and mean urinary iodine concentration was < 10µ/dl in both instances. Goiter formation (echographic thyroid volume > 18 ml) was present in 37% of women with an iodine excretion < 10µ/dl and in 14% when iodine excretion was > 10 µ/dl. It is concluded that a marginally low iodine intake is associated with goiter formation and it is advised that pregnant women, living in areas of low iodine intake, should receive iodine supply. Szabolcs et al., Budapest, Hungary, and Düsseldorf, Germany studied thyroid function, the presence of thyroid antibodies and thyroid echography in nursing home residents from three regions with different iodine intake. A: mean iodine excretion 70 µg/g creatinin (n = 119), B: 108 mg/g creatinin (n = 119), C: 512 µg/g creatinin (n = 92). Clinical hypothyroidism was present in 0.8, 1.7, and 7.5% respectively. Subclinical hypothyroidism occurred in 4.2, 11.8, and 23.9%. Antibody prevalence was not significantly different (19.3, 22.7, and 22.8%). Goiter rate was 38.5, 17.9, and 12.2% respectively. Eighty-three percent of patients with poor echography texture in region C were antibody positive or had elevated TSH, whereas this was 52% in region A. It is concluded that a high iodine intake is correlated with development of hypothyroidism, and that in these patients echography of the thyroid is predictive for development of hypothyroidism. Salvi et al., Parma, Italy, and Worcester, MA, USA, evaluated thyroid function in 60 euthyroid subjects, previously treated with recombinant interferon-a (rIFNa) for hepatitis C, of which 8 subjects did not develop any thyroid dysfunction (group A), and 8 patients did (group B). rIFNa therapy was withdrawn 12 and 14 months previously respectively. Before and after administration of 10 drops of saturated solution of KI (SSKI) for 60 days, thyroid function was measured. No patient from group A, but 4 of group B developed abnormal thyroid function, mainly iodine-induced subclinical hypothyroidism. It is concluded that subjects with previous thyroid dysfunction induced by rIFNa are at risk to develop iodine induced thyroid dysfunction. Ares et al., Madrid, Spain, measured iodine excretion in 69 preterm (P) and 28 fullterm (N) newborns up to 6-8 postnatal weeks. The amount of iodine ingested was also determined as well as serum levels of T4, FT4, T3, TSH, and thyroglobulin (Tg). In the very premature infants as well as in the very sick ones there was negative iodine balance in the first week after birth, but then it became positive in this group as well as in the other P infants and in the N infants. Apparently iodine was accumulated by the thyroid. From these data and measurements of thyroid function the authors concluded that urinary iodine excretion is not equivalent to iodine intake in newborns in the first week of birth, whether P or N. Care should be taken that in P infants iodine supplementation is given, because the lower intake affects serum parameters of thyroid function negatively. However, they also calculated that, even when iodine intake is adequate, P newborns remain hypothyroxinemic as compared to N babies. It is suggested that temporary treatment with T4 may be necessary during this important period of brain development (see also below, section miscellaneous, the report of Van Wassenaer et al.). Loviselli et al., Cagliari and Pisa, Italy, report thyroid antibody (TA) prevalence and islet cell antibody (ICA) in relation to endemic goiter and urinary iodine excretion in 8088 school children (age 6-14 years), living in 29 communities from areas with mild to moderate iodine deficiency in Italy. Highly variable TA and ICA prevalences with individual geographical "hot spots" were detected without apparent correlation. Both antibodies were also unrelated to goiter and to iodine excretion. The results suggest the involvement of genetic and/or environmental factors independent from iodine deficiency in triggering thyroid and/or islet autoimmunity.