Thyroid pathology

Kologlu S, Baskal N, Kologlu LB, Laleli Y, Tuccar E. Hirsutism due to the treatment with L-thyroxine in patients with thyroid pathology. Endocrinologie 1988 26(3) 179-85. 

Schmid KW, Bocker W. Thyroid pathology. Current topics in pathology. Vol 91. New York Springer-Verlag, 1996. 

CBA mouse model of Grave s disease synergism with cyclosporine A, lower incidence of thyroid pathology, milder [146]... 

Previous studies demonstrated an improvement in the general iodine supply in different areas and different age groups in Europe. The underlying reasons for this improvement, and its consequences for thyroid pathologies, are not always obvious. 

Previous studies (as mentioned above) demonstrated an improvement in the general iodine supply in different areas and different age groups. The underlying reasons for this improvement (e.g., altered nutrition, use of iodinated salt) and its consequences for thyroid pathologies are not always obvious. To clearly assess a populations iodine status, the WHO recommended monitoring the iodine content in salt at the production level, measurement of urinary iodine concentration and carrying out surveys in large cohorts under local circumstances as the most suitable method for iodine status assessment (WHO, 2001). 

Gy Whole body Single brief exposure Linear dose relation to thyroid cancer, and pathology in adjacent parathyroid and salivary glands 16... 

T4 and T3 in plasma are reversibly bound to protein, primarily thyroxine-binding globulin (TBG). Only about 0.04% of total T4 and 0.4% of T3 exist in the free form. Many physiologic and pathologic states and drugs affect T4, T3, and thyroid transport. However, the actual levels of free hormone generally remain normal, reflecting feedback control. 

The function of the target molecule may be critical or mncritical. Thus, if the target molecule is an enzyme, this could be involved in a crucial metabolic pathway, such as mitochondrial oxidative phosphorylation. In this case, an adverse interaction with the ultimate toxicant is likely to lead to cell dysfunction and possibly death (e.g., as with cyanide or salicylate). Chemicals such as methimazole and resorcinol, which are activated to free radical intermediates by thyroperoxidase, cause destruction of the enzyme. This then disturbs thyroid hormone synthesis and thyroid function with pathological consequences such as thyroid tumors. 

Antimony spots are temporary pustular skin eruptions that afflict workers exposed to antimony compounds. Prolonged or acute exposure results in the build up of antimony in the tissues, especially in liver, kidney, adrenals and thyroid. Antimony(III) is considered to be more toxic than antimony(V) because it is relatively slowly excreted. Long term exposures (up to 28 years) have resulted in pneumoconiosis and emphysema, but even after a few months exposure (5-10 mg m-3) to fumes from antimony smelting pathological symptoms were observed, e.g. rhinitis, pharyngitis and tracheitis.174... 

Even a single dose of corticotropin briefly inhibits the secretion of thyrotrophic hormone. The uptake of radioactive iodine is also suppressed by corticotropin and by glucocorticoids, but this has no clinical relevance. Pathological changes in thyroid function induced by glucocorticoid treatment are reportedly rare. 

Horie, S., Maeta, H., Endo, K., Ueta, T., Takashima, K., and Terada, T. 2001. Overexpression of p53 protein and MDM2 in papillary carcinomas of the thyroid correlations with clinico-pathologic features. Pathol. International 57 11-15. 

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