8 Endemic goitre and cretinism

Ibbertson, H. K.

doi:10.1016/s0300-595x(79)80012-2

Cited by 21 publications

(12 citation statements)

References 72 publications

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“…Since abnormally high levels of MsAb can be detected by radioassay in patients with autoimmune thyroid diseases and low MsAb titres by haemagglutination technique (Mariotti et al 1978), it is possible that the lower rate of MsAb than TgAb positive patients may at least in part depend on the different sensitivity of the two assay methods. Furthermore, many hyper¬ prolactinaemic women with either positive (high titre or low titre) or negative antibodies had diffuse or nodular goitre, with a 20% prevalence even if the patient with Graves' disease and the one with acromegaly are excluded, a figure which is in the range found in areas of mild endemic goitre and may exceed that found in the general population in non-iodine deficient areas (see Ibbertson 1979, andHennemann 1979 for review). None of the hyper¬ prolactinaemic men studied had any evidence of primary thyroid disorders, a fact which, beside the low number of subjects under investigation, may be explained by the well known lower prevalence of autoimmune thyroid disease and goitre in males than in females (Tunbridge et al 1977;Hall & Evered 1979).…”

Section: Discussionmentioning

confidence: 99%

Thyroid autoimmunity in hyperprolactinaemic disorders

Ferrari¹,

Boghen²,

Paracchi³

et al. 1983

Acta Endocrinologica

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Circulating thyroglobulin antibodies (TgAb) and microsomal antibodies (MsAb) and thyroid function (total and free T4 and T3, TSH basal and after TRH) have been evaluated in 92 hyperprolactinaemic patients (82 females and 10 males; 9 with macroprolactinoma, 22 with microprolactinoma, 4 with acromegaly, 5 with organic lesions of the hypothalamus, 2 with empty sella, 2 with idiopathic hypopituitarism, 2 with primary hypothyroidism, and 46 with idiopathic hyperprolactinaemia). Thyroid function was normal in all cases except 3 with hypothalamic disease and central hypothyroidism, the 2 patients with primary hypothyroidism and 2 with thyrotoxicosis (one due to Graves' disease and one to autonomous thyroid adenoma). High titres of TgAb (\m=ge\1/1250) and/or MsAb (\ m=ge\ 1/1600) were found in the subject with Graves' disease, in one acromegalic, in the 2 primary hypothyroids, and in 12 women with either adenomatous or idiopathic hyperprolactinaemia; low titres of one or both antibodies were found in 9 other euthyroid women and in the one with toxic adenoma. In a control population of 185 subjects studied with the same methods, the prevalence of TgAb and/or MsAb positive (low titres) was 3.3% in females and 2.5% in males. Diffuse thyroid hyperplasia was clinically detectable in 12 euthyroid women and in the one with Graves' disease; 3 others had been previously operated for nodular goitre with histological evidence of Hashimoto's thyroiditis (2 cases) or for a cold nodule; a single thyroid nodule was present in the woman with toxic adenoma and in one euthyroid woman. Most of these subjects also had circulating TgAb and/or MsAb, and a few had increased TSH secretion. No significant differences were found in mean thyroid hormone and TSH levels between euthyroid hyperprolactinaemic subjects and healthy controls, but TRH-stimulated TSH levels were significantly higher in thyroid antibodies positive than negative subjects. These data, in agreement with a few previous reports, suggest that autoimmune thyroid disorders (especially asymptomatic autoimmune thyroiditis) occur in hyperprolactinaemic women with a prevalence far exceeding that observed in many surveys in the general population.The association of autoimmune thyroiditis with prolactinoma has been known for some years (Thorner 1977), but thyroid antibodies were found in that study in only 2 of 38 women, corresponding to the general incidence of circulating thyroid antibodies in the population studied (Tunbridge et al. 1977). Recently, Pelkonen et al. (1982) observed autoimmune thyroiditis in combination with pro¬ lactinoma in 3 of 36 women. The diagnosis of autoimmune thyroiditis was based on the criteria of Gordin et al. (1972), i.e. the presence of circulating microsomal and thyroglobulin antibodies in high titres (> 1/100000 and > 1/25000, respectively). Moreover, the same investigators found exagge¬ rated TSH response to TRH in 4 prolactinoma patients without autoimmune thyroiditis (Pelkonen et al. 1982). It seemed therefore of interest to report our data on thyroi...

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Section: Discussionmentioning

confidence: 99%

Thyroid autoimmunity in hyperprolactinaemic disorders

Ferrari¹,

Boghen²,

Paracchi³

et al. 1983

Acta Endocrinologica

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“…Goitre and hypothyroidism due to iodine defici¬ ency are major world health problems (Ibbertson 1979). During programmes of iodine supplemen¬ tation in areas with dietary iodine deficiency, hyperthyroidism is occasionally precipitated (Jod Basedow phenomenon) and this is thought to be due to exacerbation of pre-existing Graves' disease or autonomously functioning nodular goitre in subjects whose previous iodine intake was insuffi¬ cient to permit excessive hormone production (DeGroot & Stanbury 1975).…”

mentioning

confidence: 99%

Iodide enhances IgG synthesis by human peripheral blood lymphocytes in vitro

Weetman¹,

McGregor²,

Campbell³

et al. 1983

Acta Endocrinologica

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Several studies have suggested that iodide may increase thyroiditis and autoantibody synthesis. We have investigated the effect of iodide in vitro at physiologically relevant concentrations on immunoglobulin synthesis by normal human peripheral blood lymphocytes stimulated with pokeweed mitogen. Both the number of cells which synthesised IgG and the amount of IgG released into the culture supernatant increased significantly after culture in a medium with added iodide compared to a medium with added chloride. No effect of increasing concentrations of the added iodide from 10-3 mM to 10 mM was observed.

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“…Whatever the method of treatment and prophylaxis ofenderme iodine deficiency, and whatever its costs, these are certain to be far less than the costs of that group of iodine deficiency disorders in terms of health care delivery, loss of productivity, and human suffering. Mankind owes a debt of gratitude to Sid Ingbar for his seminal role in so many studies No» 1979 Augl9>0 that have benefited millions of people with these disorders throughout the world.…”

Section: Prophylaxis Of Iodine Deficiency Disordersmentioning

confidence: 99%

Iodine Deficiency Disorders

Medeiros‐Neto¹

1990

Thyroid

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FOR MANY YEARS, IT HAS been recognized that there is usually, if not always, a close and inverse relationship between the concentration of iodine in the soil and water and the prevalence of goiter. Nutritional, constitutional, genetic, environmental, or immunologie factors may be additive to the sum total of causes that lead to the appearance of the condition.More recently, the impact of iodine deficiency on brain function in the fetus, the newborn, and the child has been emphasized and recognized as a major threat to the population at risk. Environmental goitrogens that prevent thyroidal utilization of trapped iodine may induce several changes in the thyroid metabolism, both in iodine deficiency areas and in localities where iodine intake is abundant. Finally, prophylaxis of iodine deficiency disorders by the addition of supplements of iodine to the daily diet has been accepted and widely employed since the beginning of the twentieth century, using salt or flour iodination, iodized oil injections, or adding iodine to the local water supply.In this review, I will attempt to summarize our current knowledge of the altered thyroid metabolism in the iodinedeficient thyroid gland, thyroid function, and the pituitary-thyroid relationship in untreated endemic cretinism and the role of environmental goitrogens and prevention of iodine deficiency disorders by iodination of the water supply. Sidney H. Ingbar was very interested in all these aspects of iodine deficiency disorders, and collaborative studies were conducted with local teams of distinguished investigators from Greece, Colombia, Italy (Sicily), Thailand, and Brazil, among others. MECHANISMS INVOLVED IN ADAPTATIONTO IODIDE DEFICIENCY Adaptation to iodine deficiency involves a number of biochemical and physiologic adjustments that ultimately result in maintenance of the intracellular concentration of T3 within normal limits. These mechanisms are listed in Table 1.Morphologic abnormalities and synthesis of iodoalbumin One of the early works of Ingbar et al/1' was related to the presence of abnormal iodoproteins in the blood of goitrous individuals. These halogenated proteins were not thyroglobulin and migrated in the albumin zone during electrophoresis. The abnormal iodinated moiety was present in these goitrous subjects in large amounts, and it was speculated that constant sequestration of iodine from the enlarged gland could play an important role in genesis of the goiter. A few years later, Stanbury's group'2~4' recognized that the presence of iodinated albumin commonly is associated with hyperplastic changes in the goitrous tissues, such as rupture of follicles, formation of colloid lakes, and areas of necrosis, calcification, and fibrosis within a multinodular goiter. These morphologic abnormalities created special conditions that would increase the iodination of serum albumin by the apical villi of the disrupted follicles/5' It occurs in practically every large diffuse goiter, in some nodular tissues, in goiter associated with defective expression of the Tg g...

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8 Endemic goitre and cretinism

Cited by 21 publications

References 72 publications

Thyroid autoimmunity in hyperprolactinaemic disorders

Thyroid autoimmunity in hyperprolactinaemic disorders

Iodide enhances IgG synthesis by human peripheral blood lymphocytes in vitro

Iodine Deficiency Disorders

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