Hypothyroidism pathogenesis

The etiology and pathogenesis of hypothyroidism are outlined in Table 38-5. Hypothyroidism can occur with or without thyroid enlargement (goiter). The laboratory diagnosis of hypothyroidism in the adult is easily made by the combination of a low free thyroxine and elevated serum TSH (Table 38-2). 

Behavioral disorders, including hyperactivity and impaited concentration, are known to be associated with hyperthyroidism and hypothyroidism, respectively. This evidence validated the hypothesis that ADHD might be similarly related to thyroid disease. Nonetheless, the vast majority of the studies carried out to address this issue failed to demonstrate a definite association between ADHD and thyroid function abnormalities, and therefore the effective role of thyroid hormones in the pathogenesis of the disorder became a candidate for reassessment. It must be pointed out however, that most of these studies evaluated thyroid function in schoolchildren or adults, without taking into account any previous thyroid dysfunction suffered either by them or their mothers during gestation. 

Urinary iodine concentrations in Tibet are very similar to those observed in Sudan (Moreno-Reyes et ai, 1993), but the frequency of goiter or hypothyroidism is lower. The lack of goitrogens in Tibet probably explains the lower frequency of hypothyroidism and goiter despite similar urinary iodine concentrations to those in Central Africa. Experimentally, the involvement of thiocyanate in the pathogenesis of myxedematous cretinism has recently been corroborated (Contempre et al, 2004). 

Iodine-induced thyrotoxicosis in apparently normal thyroid glands has been reported in two patients after exposure to 2—10 mg iodine daily for 2—12 months before thyrotoxicosis was diagnosed. Although the pathogenesis of this kind of IIH remains obscure, the positive family history for thyroid disease in both patients may indicate a latent abnormality of their thyroid glands (Skare and Frey, 1980). Moreover, 10 further cases of iodine-induced thyrotoxicosis in apparently normal thyroid glands have been reported (Savoie et al, 1975). In contrast, a more-than-adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis, as shown in China in areas with more than adequate and excessive iodine consumption (Teng et al., 2006). 

The thyroid gland may be damaged in many ways. A comprehensive description of the anatomical pathology of the thyroid will not be attempted, but since the pathogenesis of hyper- and hypothyroidism cannot be properly understood without an adequate morphological description of the lesion, the major forms of thyroid injuries are outlined (see Table 8-5). The reader is referred to specialized books for further information on the anatomical pathology of the thyroid. 

The pathogenesis of primary myxedema is not always easy to trace except when hypothyroidism follows thyroidectomy or massive necrosis of the thyroid. Autoimmune reactions probably are at least in some cases responsible for thyroid destruction. In myxedema, the thyroid is usually small and hard. Histologically, the typical follicular pattern has disappeared and is replaced by fibrosis. The thyroid is goitrous in a few cases, and presents the histological characteristics of hyperplasia. 

Hypothyroidism induced by iodine is well documented and it has been postulated that is is the iodide ion that is responsible, a phenomenon classically known in the Wolff-Chaikoff effect (37) This blocking effect has been shown to be enhanced by antithyroid antibodies (38,39), antipyrine (40) and lithium (41) The pathogenesis of the clinical entity known as "iodide goiter (37) in which goiter and/or hypothyroidism appears and subsides concomittantly with iodide intake and withdrawal, has been related to the Wolff-Chaikoff effect that had been demonstrated in animal In our laboratory a few cases of iodide goiters were discovered by means of XRF (see example in Fig 3) A correlation could be established between the clinical state of the patient and its TITI, demonstrating the validity of the pathogenic hypothesis Because an important part of iodine ean be washed out by perchlorate in these cases, it has been... 

The pathogenesis of amiodarone induced dysthyroidism is discussed defective intrathyroidal autoregulation due to the high iodine level does not seem sufficient to explain hypothyroidism and h5q)erthyroidism in the same patient. Alternative explanations could be autoimmune phenomenas and genetic predisposition. 

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