Pathogenesis of Iodine-Induced Thyrotoxicosis: Studies in Northern Tasmania

The availability of iodinated salt containing 20 mg of iodine as iodate/kg salt consumed on a voluntary basis enabled us to investigate its effect on goitre prevalence and iodine excretion in urine in a longitudinal, prospective, randomized study over 4 years. With this salt, under the assumption of a consumption of 5 g salt per day and person, an additional intake of 100 \ g=m\ g of iodine can be achieved. The study was performed on initially 334 children (168 boys, 166 girls) at the age of 10 years living in an area of iodine deficiency. After 4 years, 286 children still participated in the study. Initially, goitre prevalence as assessed by palpation was found to be 30.5% (37.4% in girls and 23.8% in boys). Neck circumference was found to be significantly higher in children with goitre compared with those without (30.2 \m=+-\1.4 vs 29.4 \m=+-\1.4 cm; P < 0.001). Iodine excretion in the urine was significantly lower in children with goitre compared with those without (40.4 \ m=+-\ 16.7 \ creatinine vs 46.1 \ m=+-\ 24.9 \ creatinine; x \ m=+-\ sd; P < 0.05). The children were randomly assigned to two different groups: group A

Section: Discussionmentioning

confidence: 99%

Effect of voluntary intake of iodinated salt on prevalence of goitre in children

Hintze

Emrich²,

Richter³

et al. 1988

“…This unresponsiveness is more often seen in elderly patients (Emrich & Bahre 1978;Smeuler et al 1977). Furthermore, development of thyrotoxicosis as a complication of iodine prophylaxis in endemic goitre is mostly seen in the elderly (Clements 1960;Ermans 1969;Vidor et al 1973). This observation has led to restriction of prop¬ hylaxis in this age group.…”

Section: Discussionmentioning

confidence: 99%

TSH-regulation and goitrogenesis in severe iodine deficiency

Bachtarzi

Benmiloud

1983

Since goitre prevalence increases sharply during the first two decades of life, age-related changes in the adaptation of the thyroid to iodine deficiency may occur. In order to study this, we have measured serum levels of TSH, T4 and T3 in 247 subjects (age range 5 to 60 years) living in an endemic goitre area of North Algeria (group A) and in 64 control subjects living in the non-iodine deficient city of Algiers (group B). TRH tests were also performed in 88 subjects from the goitrous area and in 30 controls.Patients from group A had significantly higher serum TSH and T3 and lower serum T4 than those from group B. Analysis of group A by age groups revealed significantly higher TSH concentrations in the 2\p=n-\9 years group and a moderate but significant decrease in the group from 50\p=n-\59 years. No significant changes were demonstrated for T4 and T3.In the goitrous area, the response of TSH to TRH was exaggerated and prolonged. \g=D\TSH20 was inversely correlated with age. The different age groups showed a significantly progressive and continuous decrease of \g=D\TSH20, \g=D\TSH60, \g=D\TSH120 from age 10\p=n-\19 to age 50\p=n-\59 years.Our findings thus show a sharp increase of TSH during the first decades of life, which coincides with the phase of maximal growth of the thyroid gland. These results suggest that TSH plays a definite role in the genesis of endemic goitre. The subsequent progressive decrease of TSH secretion and reserve, with unchanged T4 and T3, imply a gradual development of autonomous activity in longstanding multinodular goitre.With adequate iodine supply, minor age-related differences in the levels of T4, T3 and TSH have been observed in man. Except for a characteristic

“…Because of the relatively slow intrathyroidal iodine turnover in the human gland, its responses to fluctuations on iodide supply are likely to be slower than those of the rat thyroid, but no qualitative difference has as yet been demonstrated with regard to the mechanisms discussed in this paper. Moreover, the occur¬ rence of hyperthyroidism following increased iodide supply in some goitrous subjects (Vagenakis et al 1972;Vidor et al 1973) could well be due to the failure of one or several of the intrathyroidal control mechanisms which enable the normal thyroid gland to maintain its hormone secretion within narrow limits in the face of a widely varying iodide supply.…”

Section: Discussionmentioning

confidence: 99%

“…Little is known about the mechanisms by which the thyroid handles this suddenly increased hormone content. However, it is common knowledge that normal man as well as normal animals exposed intermittently to small iodide loads will remain euthyroid, whereas some patients with nodular goitre may develop hyperthyroidism (Vidor et al 1973;Vagenakis et al 1972).…”

mentioning

confidence: 99%

A Transient Rise of Hormone Secretion: A Response of the Stimulated Rat Thyroid Gland to Small Increments of Iodide Supply

Studer¹,

Bürgi²,

Köhler³

et al. 1976

Small doses of iodide (2 times 3.2 \g=m\g at 12 h interval), below those capable of inducing Wolff-Chaikoff effect, were injected into rats kept on a moderately low iodine diet. By means of a 125I equilibration technique as well as by direct measurement of cold T4, it was demonstrated that the level of circulating PB125I (representing iodothyronines as confirmed by column chromatography) increased by a mean of 40 % within 24 h following the first iodide injection. The serum TSH concentration (measured by radioimmunoassay) was simultaneously depressed. Thus, in stimulated thyroid glands, a biologically significant fraction of an iodide load escapes autoregulatory control of iodothyronine synthesis. A small, transient increase of hormone release is likely to represent the physiological response of a normal gland to a sudden supplement of iodide supply. The ensuing depression of TSH secretion may be necessary for final adjustment of thyroid function. It is considered to be the last step in a cascade of mechanisms whose interaction keeps the thyroidal hormone output within narrow limits in the face of a fluctuating iodide supply. Failure of one or several of these mechanisms in the goitrous human gland could conceivable explain the phenomenon of "Jod Basedow".If the iodide supply to the thyroid gland is suddenly increased by an amount below the critical dose causing a Wolff-Chaikoff effect, an important fraction