Endemic Goiter in Western New Guinea: Iodine Metabolism in Goitrous and Nongoitrous Subjects

Choufoer, J. C.; Rhijn, M. Van; Kassenaar, A. A. H.; Querido, A

doi:10.1210/jcem-23-12-1203

Cited by 51 publications

(18 citation statements)

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“…The loss of iodine through extra-renal routes is reportedly minor. Thus, the concentration of iodine in sweat has been estimated at 0.29 AE 0.04 mmol/L (Mao et al, 1990), and about 5% of the body's iodine loss occurs in the stools (Choufoer et al, 1963). We therefore consider it likely that the Sudanese women had a lower iodine intake than the Swedish women.…”

Section: Discussionmentioning

confidence: 99%

Iodine status, thyroid function and pregnancy: study of Swedish and Sudanese women

et al. 1998

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Objective: To examine and compare the effects of pregnancy on the thyroid hormone homeostasis in two different populations with variable iodine supply. Design: A longitudinal prospective cohort study throughout pregnancy involving Swedish and Sudanese pregnant women. Setting: The subjects were enrolled consecutively during their antenatal follow-up at health centres at Nyby in Uppsala, Sweden and Omdurman in Sudan. Subjects: Fifty-one apparently healthy women from Uppsala, Sweden and twenty-eight pregnant women from Omdurman, Sudan were recruited during pregnancy. The mean age and weight of the Swedish women at the beginning of pregnancy were 29.9 AE 5.4 y and 66.3 AE 12.9 kg respectively. The corresponding ®gures for the Sudanese women were 28.0 AE 4.9 y and 64.8 AE 9.4 kg respectively. Methods: Blood samples were drawn on four occasions from the Swedish group at 11±13, 24, 32, and 38 weeks of pregnancy, and on three occasions from the Sudanese group at 10±12, 20±24, and 36±39 weeks. Twenty-four hour urine samples were collected from the same subjects and on the same occasions as blood sampling. The urine samples were kept in a refrigerator until the volumes were measured, after which 20 mL aliquots were taken and kept frozen until analysed. No signi®cant changes in daily urinary iodine loss were observed in the two groups with progression of pregnancy. However, in the Swedish women the mean free T4 concentration fell from 11.81 pmol/l at the beginning of pregnancy to 8.82 pmol/l and the mean TSH rose from 1.11±1.95 mU/l between the beginning and end of pregnancy. Such changes were not detected among the Sudanese women, who had signi®cantly lower mean TSH values than the Swedish women in weeks 36±39 of pregnancy (P`0.02), and signi®cantly higher FT4 values than the Swedish women both in weeks 20±24 and in weeks 36±39 (P`0.005 and P`0.001) respectively. Conclusions: The study suggests that determination of urinary iodine alone gives inadequate information about the capacity of an individual to utilize an available iodine supply and it also shows the existence of different patterns of thyroid response during pregnancy. The history of iodine availability prior to and during pregnancy seems to be an important determinant of the mechanism of thyroid gland response to ensure the extra iodine needed by the growing fetus. Sponsorship: Financial support for this work was provided by the Swedish Medical Research Council and InDevelop AB, Uppsala University.

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Section: Discussionmentioning

confidence: 99%

Iodine status, thyroid function and pregnancy: study of Swedish and Sudanese women

et al. 1998

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“…Although the importance of iodine deficiency for the development of the disease is generally recognized (25), low iodine intake does not necessarily result in goitrogenesis, and NTG may occur in spite of a sufficient iodine supply (17,26). Iodine deficiency is thus permissive for the development of NTG, but the initiating pathogenetic factor is still unknown (25).…”

Section: Discussionmentioning

confidence: 99%

Transforming growth factor beta regulates thyroid growth. Role in the pathogenesis of nontoxic goiter.

Grubeck‐Loebenstein¹,

Buchan²,

Sadeghi³

et al. 1989

J. Clin. Invest.

135

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The production and growth regulatory activity of transforming growth factor f were studied in human thyroid tissue. As estimated by its mRNA expression in fresh tissue samples, transforming growth factor , was produced in normal and in diseased thyroid glands. Transforming growth factor , mRNA was mainly produced by thyroid follicular cells and in lesser quantities by thyroid infiltrating mononuclear cells. The concentrations of transforming growth factor #t mRNA were lower in iodine-deficient nontoxic goiter than in Graves' disease and normal thyroid tissue. Transforming growth factor ft protein secretion by cultured thyroid follicular cells was also low in nontoxic goiter, but could be increased by addition of sodium iodide (10 ,uM) to the culture medium. Recombinant transforming growth factor # did not affect basal tritiated thymidine incorporation in cultured thyroid follicular cells, but inhibited, at a concentration of 10 ng/ml, the growth stimulatory influence of insulin-like growth factor I, epidermal growth factor, transforming growth factor a, TSH, and partly that of normal human serum on cultured thyroid follicular cells. This inhibition was greater in Graves' disease than in nontoxic goiter. These results suggest that transforming growth factor ,B may act as an autocrine growth inhibitor on thyroid follicular cells.

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“…The fact that in the New Guinea endemic iodine deficiency TSH increased only in goitrous patients also suggested a failure of adaptation (Buttfield et al, 1966) Efficlent adaptation to iodine deficiency Is possible in the absence of goltre but with thyroid hyperplasia Efficient adaptation to iodine deficiency is possible without the development of a large goitre but not without a high iodide trapping capacity and some thyroid enlargement. This has been demonstrated by several studies: the well adapted non-goitrous patients in endemic goitre areas such as New Guinea (Choufoer et al, 1963), the Uele or Southern Idjwi (Delange et al, 1971), probably including all the pygmies (Delange et al, 1968), the Venezuelan Indians (Roche, 1959;Roche et al, 1961) in endemic iodine deficiency areas with no goitre, and experimental animals such as rats (Denef et al, 1989). The morphological characteristics of the thyroids of iodine deficient rats include hypertrophy of the gland with a great increase in vascularity and in the small follicles with much decreased luminal spaces.…”

Section: Defectlve Hormonogenerlr In Large Goltrer Adapted To Iodlne mentioning

confidence: 91%

Large goitre as a maladaptation to iodine deficiency

Dumont¹,

Ermans²,

Maenhaut³

et al. 1995

Clinical Endocrinology

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Endemic Goiter in Western New Guinea: Iodine Metabolism in Goitrous and Nongoitrous Subjects

Cited by 51 publications

References 0 publications

Iodine status, thyroid function and pregnancy: study of Swedish and Sudanese women

Iodine status, thyroid function and pregnancy: study of Swedish and Sudanese women

Transforming growth factor beta regulates thyroid growth. Role in the pathogenesis of nontoxic goiter.

Large goitre as a maladaptation to iodine deficiency

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