Thyroid gland direct effects

Calcitonin. This hormone, which is also secreted from the thyroid gland, is synthesized by the parafollicular cells (C cells) located between the follicles. The primary effect of calcitonin is to decrease the blood levels of calcium and phosphate. The mechanism of action involves the direct inhibition of osteoclast activity, which decreases bone resorption. This results in less demineralization of the bone and therefore a decrease in the release of calcium and phosphate from the bone into the blood. Calcitonin has no direct effect on bone formation by osteoblasts. 

Calcitonin is a peptide hormone produced in the thyroid gland that serves to lower serum calcium and phosphate levels by inhibiting bone resorption. Calcitonin has been used in the treatment of a variety of diseases, such as primary hyperparathyroidism, Paget s disease, and postmenopausal osteoporosis [99,100]. Salmon calcitonin has a longer half-life than human calcitonin. Salmon calcitonin, 3.6 kDa, is available as a nasal formulation that contains only benzalkonium chloride as a preservative, without an absorption enhancer, and as a parenteral product for injection. The direct effect of benzalkonium chloride on the nasal mucosa is under... 

Both central and peripheral defects in thyroid secretion are noted in patients with cirrhosis. Alcohol plays a major role with direct toxic effects on the thyroid gland. Management includes thyroid hormone... 

Concurrent administration of thyroxine with thionamide therapy for thyrotoxicosis and subchnical hyperthyroidism may reduce autoantibodies directed toward the thyroid gland and improve the remission rate however, these effects have not been consistently observed in aU studies. " In a Japanese study, adjunctive treatment with thyroxine was associated with a 20-fold reduction in the recurrence rate of Graves disease compared with the recurrence rate seen in patients treated with antithyroid drugs alone. Attempts to reproduce these results in American and European patients with Graves disease have failed to show any delay or reduction in the recurrence of Graves disease with thyroxine administration. ... 

CN intoxication may result in morphological and functional adverse effects in specific organ systems or tissues as a consequence of acute or repeated exposure to CN. These include both direct adverse reactions to and lesions of the respiratory, cardiovascular and central nervous systems. Secondary toxic effects, from SCN, may occur with the thyroid gland. These organ and tissue effects are summarized below. 

Under most circumstances, there are no health hazards associated with potassium iodide. Taking an excess of the compound may have harmful effects on the thyroid gland, however. For that reason, people with an overactive thyroid should not take potassium iodide unless so directed by their doctors. Also, a person should not take potassium iodide as a preventative treatment against radiation. It provides no protection in advance of radiation exposure and, in excessive amounts, can create problems of its own for the thyroid. 

In conclusion, it appears that most effects caused by dioxins and PCBs on circulating TH concentrations are mainly due to mechanisms not related to direct effects on iodine uptake by the thyroid gland, although the latter cannot be excluded. 

Therefore, based on the above Hmited evidence, we conclude that excess iodine exposure may influence maternal-fetal TH metabohsm by three mechanisms (1) excess iodine affects the maternal hormone thyroid level by inhibition of thyroid function and/or Dl activity (2) excess iodine has an effect on maternal—fetal TH transfer by affecting placental D2 and D3 activity and (3) excess iodine transferred by the placenta has a direct inhibition on the development and function of the fetal thyroid gland (Figure 88.2). 

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