Goiter and hyperthyroidism

Treatment Regimens in Toxic and Diffuse Goiters in Iodine Deficiency Goiter and Hyperthyroidism in Iodine Deficiency... 

Mild-to-moderate ID in a well-nourished population leads to a frequent occurrence of goiter and hyperthyroidism in the elderly. 

It is nsed for hyperthyroid forms of endemic and sporadic goiters, diffnse, toxic goiters, and other illnesses accompanied by thyrotoxicity. Synonyms of this drug are ditirin, iodoglobin, and others. 

Because of its adverse effects, it is logical to omit iodine from all pharmaceutical formulations whenever possible, and at least clearly label its presence when it is necessary. The adverse effects of iodine include goiter and hypothyroidism (20,22), hyperthyroidism (SEDA-18,176), neutropenia (23), metabolic acidosis (24), and generalized iododerma (17). 

Extensive iodine absorption from povidone-iodine can cause transient hypothyroidism or in patients with latent hypothyroidism the risk of destabilization and thyrotoxic crisis (SEDA-20, 226 SEDA-22, 263). Especially at risk are patients with an autonomous adenoma, localized diffuse autonomy of the thyroid gland, nodular goiter, latent hyperthyroidism of autoimmune origin, or endemic iodine deficiency (51). 

The many effects of lithium on thyroid physiology and on the hypothalamic-pituitary axis and their clinical impact (goiter, hypothyroidism, and hyperthyroidism) have been reviewed (620). Lithium has a variety of effects on the hypothalamic-pituitary-thyroid axis, but it predominantly inhibits the release of thyroid hormone. It can also block the action of thyroid stimulating hormone (TSH) and enhance the peripheral degradation of thyroxine (620). Most patients have enough thyroid reserve to remain euthyroid during treatment, although some initially have modest rises in serum TSH that normalize over time. 

Thyroid disorders. Disturbances in thyroid metabolism can occur at any level of the hypothalams-pituitary-thyroid-peripheral tissue axis. Several of these disorders have been discussed previously. Hyperthyroidism is more prevalent in women than men. The three most common causes of hyperthyroidism are Graves hyperthyroidism, toxic multinodular goiter, and toxic adenoma. The clinical features of hyperthyroidism include hyperkinesis, weight loss, cardiac anomalies (e.g., atrial fibrillation), fatigue, weakness, sweating, palpitations, and nervousness. The typical biochemical laboratory parameters are increased serum free T4 and decreased serum TSH. 

The incidence of iodine-induced hyperthyroidism is dependent on the iodine dose and the prevalence of goiter and, in connection with this, the occurrence of autonomies. 

The beneficial effects of iodine supplementation in the prevention and control of developed thyroid abnormalities due to iodine deficiency have been discussed so far in this chapter. However, supplementation with excess iodine, including the improvement of a previous iodine-deficient state, may cause thyroid dysfunctions, viz., iodine-induced hypothyroidism/iodide goiter in susceptible subjects (Roti and Vagenakis, 2000) and iodine-induced hyperthyroidism (IIH) especially in individuals over 40 years of age and who have been iodine deficient for a long period in the past (Vidor et ai, 1973). It may also increase the ratio of papillary/follicular carcinomas (Slowinska-Klencka et ai, 2002). In other words, both low and excess intake of iodine is related to further risk of thyroid disease. Although a daily intake of up to 1000 pg/day by a normal adult individual is quite safe (WHO, 1994), the upper limit is much lower in a population that has been exposed to iodine deficiency in the past. Therefore, to prevent IDD, the recommended iodine requirement in an adult individual is fixed within a narrow range of 150 rg/day (Knudsen et ai, 2000). Iodine supplementation under certain conditions in certain populations causes adverse effects, e.g., iodide goiter and iodine-induced hypothyroidism, IIH, iodine-induced thyroiditis and thyroid cancer. 

From a functional point of view, euthyroid diffuse goiter and hypofunctional thyroid nodules have to be discerned from hyperthyroid conditions, mainly toxic adenoma and toxic multinodular goiter. 

Another important group, the National IDD Advisory Committee (NIDDAC) chaired by Professor Chen Zupei, has played a crucial role in the national program. Under the leadership of the MOH, NIDDAC provides scientific and technical guidefines, standards and recommendations. It also provides evidence for poficy development (IDD Newsletter, 1998). Since 1993 NIDDAC has re-evaluated and standardized the measmement of thyroid gland size by palpation and ultrasound standardized urinary iodine testing methods. It has also evaluated the technical aspects and the application of neonatal TSH in IDD monitoring, iodine excess and excessive dietary iodine-induced goiter, and the role of iodized oil in the prevention and control of IDD and iodine-induced hyperthyroidism (Chen, 2002). 

Abnormalities in thyroid function were common in both areas, but they developed in opposite directions in Jutland, there was a high prevalence of goiters and undiagnosed hyperthyroidism. The incidence of diagnosed... 

Normal TSH excludes the diagnosis of hyperthyroidism. However, it does not necessarily exclude small autonomous areas in a (nodular) goiter. Larger autonomous areas may be detectable by scintigraphy in patients with palpatory thyroid nodules or goiter and thus at increase risk for IIH in formerly iodine-deficient areas. 

The assessment of iodine intake and status is important in elderly subjects. Mild-to-moderate iodine deficiency is associated with a high incidence and prevalence of goiter and nodular hyperthyroidism in middle-aged and elderly subjects (Laurberg et ai, 1991 Pedersen et ai, 2002). In populations with high iodine intake, there is an increased risk of hypothyroidism, especially among... 

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