Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Thyroid hormones concentrations

The treatment goals for hypothyroidism are to normalize thyroid hormone concentrations in tissue, provide symptomatic relief, prevent neurologic deficits in newborns and children, and reverse the biochemical abnormalities of hypothyroidism. [Pg.248]

The lARC has determined that there is sufficient evidence for the carcinogenicity of amitrole to experimental animals and inadequate evidence for carcinogenicity to humans. It was noted that amitrole produces thyroid tumors in rodents by a nongenotoxic mechanism that involves interference with the functioning of the thyroid peroxidase, resulting in a reduction in circulating thyroid hormone concentration and an increase secretion of thyroid-stimulating hormone. Amitrole would not be expected to produce thyroid cancer in humans exposed to concentrations that do not alter thyroid hormone homeostasis. [Pg.44]

Dorn, L.D., Burgess, E.S., Dichek, H.L., Putnam, F.W., Chrousos, G.P., and Gold, P.W. (1996) Thyroid hormone concentrations in depressed and nondepressed adolescents group differences and behavioral relations [see comments]. / Am Acad Child Adolesc Psychiatry 35 299-306. [Pg.134]

The iodine-containing cream was withdrawn and she was given a beta-blocker. The palpitation resolved within 2 weeks and her plasma thyroid hormone concentrations normalized within 1 month. [Pg.320]

A 48-year-old woman developed palpitation and insomnia. The clinical history, physical examination, and laboratory tests supported hyperthyroidism. Since July 1994 she had been combating constipation by improper use of an iodine-containing antiseptic cream for external use only. She had inserted povidone-iodine into her rectum by means of a cannula. The iodine-containing cream was withdrawn and she was given a beta-blocker. The palpitation resolved within 2 weeks and her plasma thyroid hormone concentrations normalized within 1 month. [Pg.329]

In a retrospective review of 497 patients taking propylthiouracil for hyperthyroidism, clinically overt hepatitis developed in six patients at 12-49 days after starting the drug (50). Jaundice and itching were present in five, fever in two, rash in two, and arthralgia in one. Serum bilirubin, alanine transaminase, and alkaline phosphatase were increased in five, four, and six patients respectively. The type of hepatic injury was cholestatic in three, hepatocellular in one, and mixed in two. There were no differences in age, sex, drug dose, or serum thyroid hormone concentrations at time of diagnosis in those with hepatic injury compared with those without. Liver function normalized in all patients at 16-145 days after withdrawal of propylthiouracil. In addition to these cases of overt liver injury, 14% of the cohort had mild asymptomatic liver enzyme rises at a mean of 75 days after the start of treatment. [Pg.338]

In a small randomized controlled study the combination of propylthiouracil 100 mg bd with colestyramine 4 g bd for 4 weeks led to a more rapid and complete fall in thyroid hormone concentrations in 30 patients with Graves disease (113). The authors proposed that colestyramine reduced the total body pool of thyroid hormone by enhanced fecal loss, thus inducing a more rapid response to propylthiouracil. [Pg.342]

In 50 women taking levothyroxine either for primary thyroid failure or for hypothyroidism secondary to radioiodine treatment for hyperthyroidism, there was no difference between the two groups in terms of bone density at the hip or spine and no difference from the reference population (31). In addition, there was no correlation between bone density and circulating thyroid hormone concentrations or duration of levothyroxine replacement. These findings are reassuring, although large studies of fracture risk are required, in view of previous evidence of an adverse effect of levothyroxine on bone mineral density, especially in post-menopausal women (32). [Pg.348]

While this pattern of biochemistry does not exclude transient relapse of Graves hyperthyroidism (despite the finding of negative TSH receptor antibodies), or a transient thyroiditis, the authors speculated that indinavir (prescribed in this patient together with stavudine and lamivudine) had inhibited the glucuronidation of thyroxine and hence caused a rise in serum thyroid hormone concentrations. [Pg.352]

The spectrum of interferon alfa-induced thyroid disorders ranges from asymptomatic appearance or increase in antithyroid autoantibody titers to moderate or severe clinical features of hypothyroidism, hyperthyroidism, and acute biphasic thyroiditis. Antithyroid hormone antibodies have also been found in one patient, and this could have been the cause of erroneously raised thyroid hormone concentrations (504). [Pg.607]

Interleukin-6 reduced serum thyrotropin and thyroid hormone concentrations and increased LH concentrations (SEDA-20, 336). [Pg.612]

Lithium blocks the release of iodine and thyroid hormones from the thyroid and has been used to treat hyperthyroidism, as an adjunct to radioiodine therapy (602-605) and in metastatic thyroid carcinoma (606). However, it can also cause hyperthyroidism. Lithium enhanced the efficacy of radioiodine in 23 patients (607), but was ineffective in a larger comparison of lithium (n = 175) or radioiodine alone (n = 175) (608). In 24 patients with Graves disease, lithium attenuated or prevented increases in thyroid hormone concentration after methimazole withdrawal and radioiodine treatment (602,609). [Pg.615]

Hypothyroidism developed within 2 weeks of rifampicin therapy in these patients and resolved when it was withdrawn. Rifampicin increases thyroxine clearance, possibly by enhancing hepatic thyroxine metabolism and the biliary excretion of iodothyronine conjugates. In healthy volunteers rifampicin reduces circulating thyroid hormone concentrations without affecting thyrotropin, suggesting that rifampicin directly reduces thyroid hormone concentrations. [Pg.644]

Herlihy JT, Stacy C, Bertrand HA. Long-term food restriction depresses serum thyroid hormone concentrations in the rat. Mech Ageing Dev 1990 53 9-16. [Pg.234]

TCDD on blood thyroid hormone concentrations, hepatic UDPGT activity, and the consequent increase of serum TSH. This was consistent with the observation that induction of UDPGT results in increased glucuronidation and biliary excretion of T4. The results of Kohn et al. (1996) provided further support to the hypothesis that induction of UDPGT is an early event in the generation of thyroid tumors by 2,3,7,8-TCDD in the rat. [Pg.267]

Pluim HJ, deVijlder JJM, Olie K, et al. 1993c. Effects of pre and postnatal exposure to chlorinated dioxins and furans on human neonatal thyroid hormone concentrations. Environ Health Perspect 101 504-508. [Pg.672]

Seo B-W, Li M-H, Hansen LG et al. 1995. Effects of gestational and lactational exposure to coplanar polychlorinated biphenyl (PCB) congeners or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on thyroid hormone concentrations in weanling rats. Toxicol Lett 78 253-262. [Pg.687]

Measurement of thyroid hormone concentrations in the serum has become an important final step in the endocrine safety pharmacology procedures (Capen 1992, O Connor et al. 2002). Basal concentrations are measured in serum samples in the morning before treatment (to avoid artefacts by the in diurnal fluctuation of thyroid hormone concentrations). In contrast to the rise in TSH after a test injection of TRH (dynamic function test), there is no pronounced rise after TRH stimulation. However, in specific situations, the secretion of thyroid hormones may be stimulated by the injection of a biosynthetic TSH preparation. [Pg.361]

Q9 Secretion of T3 and T4 is normally stimulated by TSH, released from the anterior pituitary. A rise in circulating thyroid hormone concentration reduces the production of TSH by negative feedback. If the gland fails to produce adequate thyroid hormone, production of TSH is not inhibited and its secretion continues to increase. Patients with hypothyroidism generally have reduced T3 and T4 production and raised plasma TSH, which is seen in Zadie s case. [Pg.147]

Q10 Many endocrine secretions are controlled by negative feedback systems. When the thyroid is stimulated and thyroid hormone concentration increases, it inhibits production of TSH to reduce further stimulation of the gland. As thyroid hormone secretion then diminishes, the negative feedback on the anterior pituitary is reduced and TSH secretion increases again. Basically, in... [Pg.147]

Anon. 2002 Bromocriptine mesylate. In Mosby s drug consult. Mosby, St Louis, MO pp. III356-III358 Bayly W, Andrea R. Smith J et al 1996 Thyroid hormone concentrations in racing thoroughbreds. Pferdeheikunde 12 534-538... [Pg.82]

Hypothyroidism and hyperthyroidism are the two primary pathological conditions that involve the thyroid glands. Laboratory testing of thyroid hormones is used to diagnose and document the presence of thyroid disease, a condition that often presents with vague and subtle symptoms. Accurate measurement of thyroid hormone concentrations is key to the proper diagnosis of thyroid gland dysfunction. [Pg.2057]

Reduced concentrations and availability of T, andTs lead to hypersecretion of pituitary TSH and marked elevations in serum TSH concentrations. The elevated concentration of TSH is an important laboratory finding, particularly in the early detection of thyroid failure. In mild or subclinical hypothyroidism, thyroid hormone concentrations can remain within the normal reference interval, but the TSH concentration is elevated. The etiology of primary hypothyroidism is usually determined on the basis of a good history, a physical examination, and the tests for circulating thyroid autoaiitibodies. [Pg.2058]

Laboratory tests most commonly used to evaluate patients for thyroid gland dysfunction are listed in Table 52-1. Familiarity with normal physiology and with pathophysiology is important if these tests are to be properly used and selected. However, it is important to note that normal serum thyroid hormone concentrations do not exclude thyroid disease, and abnormal thyroid tests do not always indicate thyroid disease. Diffuse or nodular thyroid enlargement, for example, maybe seen in euthyroid patients. ... [Pg.2063]

The THBR is derived from a version of the T3 or T4 uptake test. Uptake tests are used to estimate the number of unoccupied (unsaturated) thyroid hormone bindhig sites on serum proteins. This information is important because variations in total thyroid hormone concentrations in blood, as discussed previously, have resulted from changes in binding protein concentrations. Values obtained by uptake methods are expressed as a THBR, which is directly proportional to the free hormone fraction (within limits). Measurement of THBR, in conjunction with a total hormone concentration, is a clinically useful indirect method for calculating the FT4 (or FT3) index. The index approach is particularly useful in patients with nonthyroidal illness in whom FT4 immunoassay methodologies are unreliable. Specifically, TT4 measurement is more diagnostically useful in such patients provided that values are interpreted in accord with the severity of illness in the patient that is indirectly reflected by abnormalities in THBR. [Pg.2076]

De Jesus, E.G., T. Hirano and Y. Inui. Changes in cortisol and thyroid hormone concentrations during early development and metamorphosis in the Japanese flounder, Paralichthys olivaceus. Gen. Comp. Endocrinol. 82 369-376, 1991. [Pg.359]


See other pages where Thyroid hormones concentrations is mentioned: [Pg.71]    [Pg.581]    [Pg.126]    [Pg.582]    [Pg.700]    [Pg.280]    [Pg.1802]    [Pg.2901]    [Pg.76]    [Pg.82]    [Pg.82]    [Pg.2538]    [Pg.2056]    [Pg.2062]    [Pg.2064]    [Pg.1369]   


SEARCH



Thyroid hormones

Thyroidal hormone

© 2024 chempedia.info