Thyrotropin-releasing hormone pituitary level

Thyroid hormone production is regulated by TSH secreted by the anterior pituitary, which in turn is under negative feedback control by the circulating level of free thyroid hormone and the positive influence of hypothalamic thyrotropin-releasing hormone. Thyroid hormone production is also regulated by extrathyroidal deiodination of T4 to T3, which can be affected by nutrition, nonthyroidal hormones, drugs, and illness. 

TSH-secreting pituitary adenomas are diagnosed by demonstrating lack of TSH response to thyrotropin-releasing hormone stimulation, inappropriate TSH levels, elevated TSH a-subunit levels, and radiologic imaging. 

Secondary hypothyroidism, or pituitary hypothyroidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less common than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tumor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In secondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to synthesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration. 

The thyroid-pituitary-hypothalamus axis controls thyroid hormone homeostasis. Thyrotropin-releasing hormone (TRH), released from the hypothalamus, stimulates the synthesis and release of thyroid-stimulating hormone (thyrotropin, TSH) from the anterior pituitary. TSH increases the release of thyroid hormones by several mechanisms, including stimulation of the I pump. While lower than normal levels of T3 and T4 cause an exaggerated response of the pituitary to TRH, released thyroid hormones, in feedback control, blunt the stimulating action of TRH on the pituitary. For further discussion of TSH and TRH biochemistry, see, for example, the review by Kannan48. 

The pituitary gland is involved in feedback regulation of thyroid activity High levels of T4 in the bloodstream result in inhibition of TSH secretion. Low levels of T4 result in an increase in TSH secretion. These effects are dependent on the conversion of T4 to T3 within the pituitary, fhe activity of the pituitary is controlled by thyrotropin-releasing hormone (TRH), a hormone synthesized in the hypothalamus. TRH is a tripeptide with the structure pyroglutamate-histidine-proline-NH . Note the C-terminal amide group, which is required for the activity of many peptide hormones. TRH stimulates the synthesis and secretion of TSH. Apparently TRH is involved in regulating the sensitivity of the pituitary to the inhibitory feedback control mechanism mentioned earlier. 

Thyroid hormones also accelerate fetal lung maturation. Fetal thyroid hormone levels may be increased by antenatal administration of thyrotropin-releasing hormone (TRH), a tripeptide that crosses the placental barrier, stimulates fetal pituitary production of thyroid stimulating hormone (TSH), and which, in turn, increases fetal thyroid hormone production (Chapter 33). This indirect method of enhancement of fetal thyroid hormone production is utilized because thyroid hormones do not readily cross the placental barrier. Insulin delays surfactant synthesis and so fetal hyperinsulinemia in diabetic mothers may increase the incidence of RDS even in the full-term infant. Androgen synthesized in the fetal testis is the probable cause of a slower onset of surfactant production in male fetuses. Prophylactic, or after onset of RDS, administration of synthetic or natural pulmonary surfactants intratracheally to preterm infants improves oxygenation and decreases pulmonary morbidity. 

FIGURE 56-5 Regulation of thyroid hormone secretion. Myriad neural inputs influence hypothalamic secretion of thyrotropin-releasing hormone (TRH). TRH stimulates release of thyrotropin (TSH, thyroid-stimulating hormone) from the anterior pituitary TSH stimulates the synthesis and release of the thyroid hormones and T,. and T, feed back to inhibit the synthesis and release of TRH and TSH. Somatostatin (SST) can inhibit TRH action, as can dopamine and high concentrations of glucocorticoids. Low levels of L are required for thyroxine synthesis, but high levels inhibit thyroxine synthesis and release. 

Prolactin secretion by pituitary cell cultures is inhibited by GH-RIH, but to a lesser extent than GH (VI). GH-RIH does not appear to affect basal PRL levels in normal subjects, but it has been reported to lower PRL release by otherwise normal pituitary cells when its secretion has been elevated by hypothyroidism or by chronic administration of estrogens. It does not affect the fall in PRL produced by i-dopa (S8) nor the rise in PRL resulting from insulin-induced hypoglycemia (H3) or thyrotropin-releasing hormone (Cl). Further critical studies of the effect of GH-RIH on basal circulating PRL levels are required. 

Thyrotropin-releasing factor (TRF) is produced in the hypothalamus and arrives at the pituitary via the hypophyseal portal blood system. TRF mediates the release of thyrotropin from the anterior hypophysis. The thyrotropin release is inhibited by thyroxine, presumably free thyroxine, and the inhibition is dose dependent. Thus excessive levels of thyroxine depress thyrotropin release, and lower thyroxine levels result in increased thyrotropin release from the anterior pituitary. TSH, in turn, stimulates thyroid hormone synthesis and secretion by the thyroid gland. Thyroxine and triiodothyronine are bound to specific binding proteins in the blood. The amounts and binding constants of the specific thyroid-binding proteins, together with the rate of thyroid hormone release from the thyroid, determine the amount of free thyroxine in the blood. Free thyroxine levels are determined not only by the rate of... 

TSH Thyroid-stimulating hormone or thyrotropin a glycoprotein hormone released from the anterior pituitary in response to increased levels of TRH. TSH binds to TSH receptors on the basal membrane of epithelial cells of the thyroid gland to stimulate the release of the thyroid hormones, Tj and T. ... 

Administration of synthetic TRH to humans causes a dose-related release of thyrotropin (TSH) by the pituitary (BIO, HI) between the intravenous doses of 15 and 500 /ig. Oral, subcutaneous, or intramuscular administration requires bigger doses. The TSH response to intravenous TRH is significant within 2-5 minutes, peaking at 20-30 minutes with a return to basal levels by 2-3 hours. An elevation in thyroid hormone levels in response to TRH is seen, with triiodothyronine (Ta) peaking at 3 hours and thyroxine (T ) at 8 hours (LI). TRH stimulates the synthesis as well as the release of TSH (M5). 

The formation of thyroglobulin and the release of thyroxine (T4) and tri-iodothyronine (T3) is controlled by the thyroid-stimulating hormone (TSH or thyrotropin) of the anterior pituitary, which is secreted on a feedback basis when the level of circulating T4 and T3 falls, or as a result of neural stimulation of the hypothalamus. 

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