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At least 37 records · Page 2Linked to original sources

Endemic goiter with iodine sufficiency: a possible role for the consumption of pearl millet in the etiology of endemic goiter.

BACKGROUND: Deficiencies of iodine, iron, and vitamin A are the 3 most common micronutrient deficiencies in developing countries, although control programs, when properly implemented, can be effective. OBJECTIVE: We investigated these deficiencies and their possible interaction in preschool children in the southern Blue Nile area of Sudan. DESIGN: Goiter, signs of vitamin A deficiency, and biochemical markers of thyroid, vitamin A, and iron status were assessed in 984 children aged 1-6 y. RESULTS: The goiter rate was 22. 3%. The median urinary iodine concentration was 0.79 micromol/L and 19.3% of the children had a concentration >1.57 micromol/L. Although serum thyroxine and triiodothyronine concentrations were within reference ranges, the median thyrotropin concentration was 3.78 mIU/L and 44% of the children had thyrotropin concentrations above normal. The mean urinary thiocyanate concentration was high (259 +/- 121 micromol/L). The prevalences of Bitot spots and night blindness were 2.94% and 2.64%, respectively, and 32% of the subjects had serum retinol binding protein concentrations <15 mg/L. A significant positive correlation was observed between thyrotropin and retinol binding protein. Whereas 88% of the children had hemoglobin concentrations <1.86 mmol/L, only 13.5% had serum ferritin concentrations below the cutoff of 12 microg/L and 95% had serum transferrin concentrations above the cutoff of 2.50 g/L. CONCLUSIONS: Our results indicate that goiter is endemic in this region of Sudan despite iodine sufficiency and that both anemia and vitamin A deficiency are health problems in the area. Moreover, consumption of millet, vitamin A deficiency, and protein-energy malnutrition are possible etiologic factors in this endemic area.

Child↗

[Thyroid hormones in the treatment of iodine deficiency goiter. Superfluous like goiter?].

In recent years, the widespread use of iodized salt in households and industrially produced foods has considerably improved the shortage of iodine in the German diet. Recent epidemiologic studies have shown that we are now at the threshold of adequacy. Over the last decade, views on the pathogenesis of iodine deficiency goiter have changed: while TSH was previously assumed to be the major factor underlying this form of goiter, experimental data now finger the activation of local growth factors, in particular IGF1. Iodinated organic compounds, in particular iodolacton produced by iodination of unsaturated fatty acids in the thyrocyte, are the key regulators of IGF1 activity by inhibitory action, and iodine is now the therapeutic agent of first choice for iodine deficiency goiter; long-term thyroxine treatment in TSH suppressive doses has been abandoned. The recommended daily dose of iodine is 200 micrograms; higher doses may induce or aggravate autoimmune thyroiditis, and should not be used for a length of time. In pregnant women, an adequate supply of iodine is of critical importance for optimal neurophysiological development, and the general use of iodine supplementation in pregnancy therefore remains mandatory in Germany.

Adolescent↗

[Physiological basis of goiter transformation of the thyroid gland and the pathogenesis of euthyroid goiter].

Endemic goiter disease develops as a result of iodine insufficiency in the environment, that induces advancing reproduction of thyrocytes realized by endomitosis. Eventually goiter-transformed gland ceases responding to the lack of iodine in the environment, that is due to the destruction of thyrocyte ++thyroreceptors. It should be taken into account that goiter disease depends upon the female sexual hormones.

Cell Division↗

[Endemic goiter in Austria. Is iodine deficiency the primary cause of goiter?].

In spite of government-regulated iodide admixture to table salt, the incidence of goiter is still high in Austria. Iodine excretion and thyroid function were therefore investigated in 80 patients suffering from ordinary goiter in whom thyroid size and resulting symptoms had increased lately. 25 euthyroid non-goitrous subjects served as controls. 48% of the goitrous patients investigated presented with iodine excretion of less than 70 micrograms/24 h, suggesting an insufficient iodine supply. Thyroid I131 uptake, basal and TRH-stimulated plasma TSH concentrations, and serum T3 levels were higher, whereas serum T4 levels were lower in these patients than in goitrous patients with higher iodine excretion and non-goitrous controls. Iodine deficiency thus appears to be of pathogenetic relevance in about half of the goitrous Austrian population. Other factors enhancing goiter development seem to assume particular importance in goitrous patients with a sufficient iodine supply.

Adolescent↗

[Single weekly doses of 1 mg 1-thyroxine for the treatment of mild goiter and for the prevention of recurrence after goiter surgery].

The possibility of using weekly single doses of 1 mg l-thyroxine for treatment of euthyroid goiters and for prophylaxis against recurrence after thyroidectomies was studied in a series of 37 patients. The treatment was continued over a period of about 3 months. Before therapy and during therapy T 4, T 3 und ETR values were determined, and TSH in plasma was assayed under TRH stimulation. 131I-24 hour-uptakes and thyroid weight were followed, together with scintigraphic studies. X-ray films of the trachea were done prior to and after therapy, and eventual side effects of the prescribed therapy were noted. Results show a significant rise in T 4 and ETR values, which however, remained in the normal range. T 3 levels did not change. 131I uptake figures were kept as low as 18 per cent of the given dose and the TSH response to TRH was markedly decreased. Non toxic goiters showed a slight decrease in weight, while thyroid remnants after thyroidectomy did not increase in size. In some patients subjective symptoms improved considerably under the given therapy. 4 of our patients showed transient signs of thyrotoxicosis factitia during the first 1 to 2 days after taking 1 mg of l-thyroxine, so that a modification of the treatment--2X500 mcg/week--might be advisable. The overall effect of this form of treatment is considered as about equivalent to others forms of thyroid hormone therapy.

Goiter↗

Toxic nodular goiter. Toxic adenoma and toxic multinodular goiter.

Solitary toxic adenoma and toxic multinodular goiter are very common forms of thyrotoxicosis around the world. Advances in molecular biology and genetics have led to new insights into the pathogenesis of these disorders. Current theories on autonomy in the thyroid are discussed in this article. The therapeutic roles of surgery, radioiodine ablation, and percutaneous ethanol administration also are reviewed.

Adenoma↗

Thyroid hormone profile in children with goiter in an endemic goiter area.

The thyroid hormone profile was investigated in goitrous schoolchildren aged 6-11 years living in Antalya, an area with mild/ moderate iodine deficiency. With few exceptions, the serum levels of T4 and TSH were in the normal range in children with different grades of goiter. Compensatory elevated T3 levels were detected in 24% of the subjects. Thyroid hormones did not differ significantly with respect to the urinary iodine (UI) level. No correlations were found between thyroid volume, UI excretion level and thyroid hormones. It was concluded that thyroid hormones, except compensatory T3 elevation in some subjects, were not affected significantly in a mild/moderate iodine deficient area.

Child↗

[Secretion of TSH and stimulation-ability of the hypophysis after long-term suppression therapy in euthyroid nodular goiter and residual thyroid gland after subtotal resection of goiter].

In 51 patients, 33 with euthyroid goiter and 18 after subtotal thyroidectomy, plasma concentrations of T4, T3, and TSH before and after stimulation with TRF were determined under long term suppression with thyroid hormone and 1,2, and 4 weeks after stopping it. Even after complete suppression (delta TSH less than 0, 5 muU/ml) resumption of TSH secretion occurred within 4 weeks in all but two. A significantly higher increase of TSH and somewhat lower thyroid-hormone concentrations turned out in operated patients. An excessive decrease of T3 (and T4) concentrations within the 1st (and 2nd) week after therapy, dependent on the degree of previous TSH suppression, could be due to transitory thyrotropic insufficiency.

Goiter, Nodular↗