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Clinical and subclinical thyroid disease is usually used to describe patients with mild symptoms correlated to hyperthyroid or hypothyroid state. Therapeutic decision for clinical and subclinical thyroid dysfunction should be considered individually. But long term outcome for treatment of such functional and structural thyroid diseases had not been recorded delicately in Taiwan. Further investigations should be observed in the future.The purpose of this study is aiming for early prevention and detection the potential risk factors for thyroid diseases in Taiwan.
Clinical and subclinical thyroid disease is usually used to describe patients with mild symptoms correlated to hyperthyroid or hypothyroid state. Thyroid ultrasonography could differentiate benign or malignant nodular lesion, together with fine needle aspiration cytology and surgical pathology. Thyrotropin (TSH, thyroid stimulating hormone) is the pivotal investigation in laboratory diagnosis to define subclinical thyroid diseases. An elevated TSH with normal free thyroxine and triiodothyronine levels in serum is defined to be subclinical hypothyroidism, and a subnormal TSH with normal thyroid hormone concentrations to be subclinical hyperthyroidism. Generally, the prevalence of subclinical hypothyroidism and hyperthyroidism were reported as 4% -10% & 1%-2% in general population, respectively. Although subclinical thyroid disease is prevalent, there is still no consensus for screening clinical and subclinical thyroid disease, including hyperthyroidism, hypothyroidism, nodular goiter and thyroid cancer. Under consideration of age, gender or familial history of autoimmune thyroid disease. However, screening for thyroid dysfunction should be considered in some high risk patients, including 1) elderly; 2) history of atrial fibrillation; 3) previous thyroid disease history; 4) other confirmed autoimmune diseases; 5) neck exposure of radiation (for example, nasopharyngeal cancer, post-radiation); 6) family history of probable autoimmune thyroid disease, and 7) pregnant state with prior thyroid disease history. Therapeutic decision for clinical and subclinical thyroid dysfunction should be considered individually. Therapeutic options will be anti-thyroid medications and/or radioactive iodine, and thyroidectomy could be considered with larger goiters for hyperthyroidism. For clinical and subclinical hypothyroidism, the therapeutic consideration should be aimed on reduction of progression to overt hypothyroidism, improving heart function, correction of dyslipidemia, and relieving senescence depressive mood. Thyroid ultrasonography will help us to keep long term observation of thyroid structural change. But long term outcome for treatment of such functional and structural thyroid diseases had not been recorded delicately in Taiwan. Further investigations should be observed in the future. We hope to check the relationship between various thyroid diseases and biochemical survey/ultrasonography. The purpose of this study is aiming for early prevention and detection the potential risk factors for thyroid diseases in Taiwan.
Observational Model: Cohort, Time Perspective: Prospective
Not yet recruiting
National Taiwan University Hospital
Published on BioPortfolio: 2016-08-17T10:53:22-0400
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Pathological processes involving the THYROID GLAND.
An aggressive THYROID GLAND malignancy which generally occurs in IODINE-deficient areas in people with previous thyroid pathology such as GOITER. It is associated with CELL DEDIFFERENTIATION of THYROID CARCINOMA (e.g., FOLLICULAR THYROID CARCINOMA; PAPILLARY THYROID CANCER). Typical initial presentation is a rapidly growing neck mass which upon metastasis is associated with DYSPHAGIA; NECK PAIN; bone pain; DYSPNEA; and NEUROLOGIC DEFICITS.
Cell surface proteins that bind pituitary THYROTROPIN (also named thyroid stimulating hormone or TSH) and trigger intracellular changes of the target cells. TSH receptors are present in the nervous system and on target cells in the thyroid gland. Autoantibodies to TSH receptors are implicated in thyroid diseases such as GRAVES DISEASE and Hashimoto disease (THYROIDITIS, AUTOIMMUNE).
Conditions of abnormal THYROID HORMONES release in patients with apparently normal THYROID GLAND during severe systemic illness, physical TRAUMA, and psychiatric disturbances. It can be caused by the loss of endogenous hypothalamic input or by exogenous drug effects. The most common abnormality results in low T3 THYROID HORMONE with progressive decrease in THYROXINE; (T4) and TSH. Elevated T4 with normal T3 may be seen in diseases in which THYROXINE-BINDING GLOBULIN synthesis and release are increased.
Autoantibodies that bind to the thyroid-stimulating hormone (TSH) receptor (RECEPTORS, THYROTROPIN) on thyroid epithelial cells. The autoantibodies mimic TSH causing an unregulated production of thyroid hormones characteristic of GRAVES DISEASE.
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