Thyroid-stimulating hormone . where

Types of autoimmune diseases vary widely, from organ-specific diseases such as thyroiditis where there may be stimulation (thyrotoxicosis) by antibody against the receptor for pituitary thyroid-stimulating hormone (TSH) or inhibition (myxoedema) by cell destruction probably mediated by NK cells and autoantibody, through to non-... 

This holds also for thyroid-stimulating hormone (TSH), where, as demonstrated in Figure 15, at least three different areas of acceptance have to be used depending on the test kits applied. 

Simultaneous injection of premixed antigen and enzyme-labeled antibody into the column has also been employed in studies where HPLC microcolumns (1 mm ID) were packed with perfusible packing materials. This approach provided short diffusion distances and a high surface area/volume ratio in the immobilized antibody bed. Using a horseradish peroxidase label and absorbance detection at 450 nm, the detection limits for thyroid-stimulating hormone (TSH) and human chorionic gonadotropin (hCG) in the sandwich format were 4.3 X lO" - and 5 x 10 M, respectively [38],... 

As a rule, a hypothalamic hormone should always control a hormone in the anterior pituitary. The pituitary hormones (e.g. follicle-stimulating hormone, prolactin, or thyrotropin) are then transported through the bloodstream to the secondary target organs, where, for example, they stimulate the production of corticosteroids in the adrenals or the formation of thyroxine in the thyroid. 

FIGURE 41-1. Hypothalamic-pituitary-thyroid axis. Thyrotropinreleasing hormone (TRH) is synthesized in the neurons within the paraventricular nucleus of the hypothalamus. TRH is released into the hypothalamic-pituitary portal circulation and carried to the pituitary, where it activates the pituitary to synthesize and release thyrotropin (TSH). TSH activates the thyroid to stimulate the synthesis and secretion of thyroxine (T4) and triiodothyronine (T3). T4 and T3 inhibit TRH and TSH secretion, closing the feedback loop. 

When the thyroid gland is stimulated to secrete thyroxine, a small piece of iodinated Tgb is taken from the lumen into a follicular cell, where the hormones are released from the protein. Both T3 and T4 are secreted from the vesicle directly into the bloodstream but the plasma concentration of T4 is substantially higher than that of T3. In contrast, T3 has a higher biological activity than T4 and conversion of T4 to T3 occurs at the target site. 

Primary goitrous hypothyroidism results when the synthesis of T4 and T3 is impaired, either because of some extrinsic factor or because of an intrinsic, inherited defect in thyroid hormone biosynthesis. As a result, the positive feedback loop causes compensatory thyroid enlargement (goiter) through the hypersecretion of TRH and TSH. Primary nongoitrous hypothyroidism is characterized by loss or atrophy of thyroid tissue, resulting in decreased production of thyroid hormones despite maximum stimulation by TSH. Hashimotos thyroiditis is the most frequent cause of primary hypothyroidism in developed countries where iodine intake is sufficient. Worldwide, iodine deficiency is the most common cause of goitrous hypothyroidism. The... 

Thyroxine is one of the few hormones for which unequivocal effects on isolated biochemical systems can be observed in particular, it has been shown that thyroxine at high concentrations has a direct effect on mitochondrial oxidation. Tissues from animals which have been injected with thyroid extracts or purified thyroxine show a raised oxygen consumption, particularly in liver and muscle. Similarly the addition of thyroxine to tissue slices of the same organs results in increased oxidation. Thyroxine seems to be especially trapped by the mitochondria, where it stimulates the... 

Primary hypothyroidism where the thyroid gland is unable to make sufficient thyroid hormone despite continued stimulation by TSH... 

Thyroid hormone production is governed by the actions of the hypothalamic-pituitary-thyroid axis (HPT axis). Thyrotropin releasing hormone (TRH) synthesized by the hypothalamus is transported to the anterior pituitary, where TRF stimulates thyrotrophic cells to produce thyrotrophin (TSH). TSH is a glycoprotein with a short half-life of less than 20 min it is one of three pituitary glycoprotein hormones with alpha- and beta-subunits. These three pituitary glycoproteins (luteotrophin, fol-liotrophin, and TSH) share the same alpha-subunit. 

Thyroid Hypofunction Hypothyroidism is the most common disorder of thyroid function. It can be divided into patients who have a failure of the thyroid gland to produce sufficient thyroid hormone (primary hypothyroidism) and patients in which pituitary or hypothalamic disease is associated with impaired TSH stimulation (central or secondary hypothyroidism). Worldwide, primary hypothyroidism is caused most often by iodine deficiency. In areas where iodine is sufficient, chronic autoimmune thyroiditis (Hashimoto s thyroiditis) accounts for most cases. Other causes include postpartum thyroiditis, surgical removal, or radioactive iodine ablation of the gland. Hypothyroidism present at birth (cretinism) is the most common preventable cause of mental retardation in the world. 

The expression of the sodium iodide symporter is perhaps nowhere more important than in the thyroid gland. A complete review of the physiological importance of the thyroid is beyond the scope of this chapter. It is sufficient to say that the symporter provides the iodine needed for normal thyroid function. Once the symporter has been trafficked to the basolateral surface of the thyrocyte, it can transport iodine from the blood into the cell. Once inside the cells, iodine is transported to the apical membrane where it is organified through attachment to a tyrosine residue and incorporated into the thyroid hormone thyroglobulin. The thyroglobu-lin is then stored inside thyroid follicles as colloid, to be released into the bloodstream as thyroid hormones (thyroxine and triiodothyronine) via TSH stimulation. 

About 5-10 years ago thyroid uptake measurements were becoming more frequently used because of the development of functional type tests such as Ta suppression (W17) and TSH stimulation (H25), which required the measurements of both thyroid uptake as well as of serum thyroid hormone levels before an after treatment with Ts or TSH, respectively. This type of test was of great value at the time, particularly for investigation of patients whose thyroid function was either borderline high or borderline low, and where the existing chemical assays on blood were of limited value. Improved procedures were devised for the Ta... 

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