Disease relevance of D-Thyroxine

• We tested this assumption by examining long-term growth in 18 girls (mean [+/- SD] age, 11.4 +/- 2.7 years; bone age, 6.2 +/- 3.1 years) and 6 boys (age, 10.6 +/- 4.7 years; bone age, 6.4 +/- 2.7 years) with severe primary hypothyroidism (serum thyroxine level 1.1 +/- 0.3 micrograms per deciliter [13 +/- 4 nmol per liter]) [1].
• Lack of effect of thyroxine in patients with Graves' hyperthyroidism who are treated with an antithyroid drug [2].
• The patients were treated with levothyroxine (3.4 +/- 0.3 micrograms per kilogram of body weight per day) to maintain normal thyroid function [1].
• Maternal thyroxine and congenital hypothyroidism [3].
• Among the 21 patients studied serially while receiving levothyroxine, thyrotropin-blocking antibodies disappeared in 15 (group 1), 7 of whom had goiter initially, and persisted in 6 (group 2), none of whom had goiter initially [4].

Psychiatry related information on D-Thyroxine

• Peroxidase-catalyzed halogenation reactions have been established as being important in the biosynthesis of the hormone thyroxine and in biological defense mechanisms [5].
• OBJECTIVE.--The issue of patient compliance with pharmacological therapy vs malabsorption of medication was explored in the context of persistent hypothyroidism despite the administration of large doses of levothyroxine sodium [6].
• MAIN OUTCOME MEASURES: Prenatal and postnatal MeHg exposure and 6 age-appropriate neurodevelopmental tests: the McCarthy Scales of Children's Abilities, the Preschool Language Scale, the Woodcock-Johnson Applied Problems and Letter and Word Recognition Tests of Achievement, the Bender Gestalt test, and the Child Behavior Checklist [7].
• Dietary modification of thyroxine deiodination in rat liver is not mediated by hepatic sulfhydryls [8].
• Application of thyroxin did not interrupt the cyclic fasting motor activity [9].

High impact information on D-Thyroxine

• METHODS: In 11 postmenopausal women with normal thyroid function and 25 postmenopausal women with hypothyroidism treated with thyroxine, I assessed thyroid function before they started estrogen therapy and every 6 weeks for 48 weeks thereafter [10].
• Increased need for thyroxine in women with hypothyroidism during estrogen therapy [10].
• Similarly, among 15 visual-analogue scales used to indicate mood and physical status, the results for 10 were significantly better after treatment with thyroxine plus triiodothyronine [11].
• The pulse rate and serum sex hormone-binding globulin concentrations were slightly higher after treatment with thyroxine plus triiodothyronine, but blood pressure, serum lipid concentrations, and the results of neurophysiologic tests were similar after the two treatments [11].
• The symptoms improved after the initiation of thyroxine therapy, and all patients became euthyroid after treatment with bexarotene was stopped [12].

Chemical compound and disease context of D-Thyroxine

• Because of increased serum thyroid hormone binding in these patients total thyroxine and tri-iodothyronine concentration can be normal despite hypothyroidism [13].
• One patient in the thyroxine-treated group (1.7 percent) and 17 patients in the placebo group (34.7 percent) had recurrences of hyperthyroidism within three years after the discontinuation of methimazole [14].
• All the patients received thyroxine to avert hypothyroidism, except those treated with iodine-131, who received thyroxine only if hypothyroidism developed [15].
• The mutants are characterized by retarded growth, infertility, mild anemia, elevated serum cholesterol, very low to undetectable serum thyroxine, and elevated serum thyroid-stimulating hormone [16].
• To examine this action in vivo, A/J mice were immunized with human thyroglobulin (hTg) (0.5 mg intraperitoneal injections for 5 d) beginning on days 6, 24, and 43 with or without methimazole (M) (0.05%) and l-thyroxine (T4) (0.1 micrograms/ml to prevent thyroid hypertrophy) in their water supply [17].

Biological context of D-Thyroxine

• Bone mineral density was not affected by whether or not thyroxine replacement therapy was given [18].
• METHODS: We carried out a randomized, placebo-controlled, double-blind trial of thyroxine supplementation in 200 infants born at less than 30 weeks' gestation [19].
• This albumin has an abnormal binding site with a much greater affinity for thyroxine (relative to its affinity for triiodothyronine) than that of the hormone-binding site on thyroxine-binding globulin [20].
• The mean postpartum thyroxine dose was decreased to 0.117 +/- 0.011 mg per day (P less than 0.01 as compared with the dose during pregnancy) [21].
• The effects of severe hypothyroxinemia, defined as a blood thyroxine value more than 2.6 SD below the mean for New Jersey newborns, were assessed before and after adjustment for gestational age and potentially confounding variables [22].

Anatomical context of D-Thyroxine

• Maternal free thyroxine levels were closely correlated with cord levels in both groups, being essentially identical in Group 2 but slightly lower in fetuses than in mothers in Group 1 [23].
• The mean thyroxine and 3,3',5-tri-iodothyronine levels in amniotic fluid were much lower and the mean 3,3'5'-tri-iodothyronine much higher than the corresponding values in maternal serum at both 15 to 19 and 36 to 42 weeks of pregnancy [24].
• In 19 patients thyroxine declined sharply after bone-marrow transplantation and was associated with a reduction of the serum thyrotropin in the 17 patients tested, often to levels below the normal range [25].
• We present evidence that Pax8 is necessary for providing cues for the differentiation of competent endoderm primordia into thyroxin-producing follicular cells [26].
• The thyroid gland develops from two distinct embryonic lineages: follicular cells (which produce thyroxine) and parafollicular C-cells (which produce calcitonin) are of endodermal and neural crest origin, respectively [26].

Associations of D-Thyroxine with other chemical compounds

• Thyroid function was evaluated by measurements of serum thyrotropin, free thyroxine, and triiodothyronine [27].
• Measurement of the serum thyroxine response to intramuscular thyrotropin-releasing hormone will usually suffice to determine the integrity of the hypothalamic-pituitary-thyroid complex [28].
• Cimetidine did not affect the responses of thyroid-stimulating hormone, prolactin, growth hormone and thyroxine to thyrotropin releasing factor [29].
• Drug interaction between thyroxine and lovastatin [30].
• The effects of thyroxine and propylthiouracil on nerve growth factor concentrations in cerebral cortex, cerebellum, and brainstem of adult male mice were assessed by using a sensitive radioimmunoassay for the beta-subunit of mouse nerve growth factor [31].

Gene context of D-Thyroxine

• Serum thyroxine, T3, and thyroid-stimulating hormone (TSH) levels and pituitary Tshb mRNA levels were inappropriately elevated compared with those of WT animals, and L-T3 treatment failed to suppress serum TSH and pituitary Tshb mRNA levels [32].
• Serum thyroxine (T4) levels were only marginally elevated in transgenic mice and thyrotropin-releasing hormone (TRH) gene expression in the paraventricular hypothalamus was downregulated [33].
• Erythrocytes are hemolyzed by myeloperoxidase, an H2O2-generating system (glucose + glucose oxidase; hypoxanthine + xanthine oxidase) and an oxidizable cofactor (chloride, iodide, thyroxine, triiodothyronine) [34].
• However, bone marrow cellularity in thyroxine-treated dw/dw mice was comparable to that in control animals, and both the frequency and absolute number of B lineage cells had increased to normal or even above normal [35].
• The Dio2 gene encodes the type 2 deiodinase (D2) that activates thyroxine (T4) to 3,3',5-triiodothyronine (T3), the disruption of which (Dio2(-/-)) results in brown adipose tissue (BAT)-specific hypothyroidism in an otherwise euthyroid animal [36].

Analytical, diagnostic and therapeutic context of D-Thyroxine

• Five months after treatment, the levels of thyrotropin had decreased and those of thyroxine had increased in all children, but greater changes occurred in the 13 younger patients than in the 14 older patients [37].
• Three standard management plans were considered: immediate subtotal thyroidectomy; a six month trial of thyroid suppression with L-thyroxine, with non-suppressible lesions being removed surgically; and aspiration cytology followed by surgery or thyroid suppression based on the cytologic examination [38].
• Physicians should be aware of possible product changes being made by manufacturers of levothyroxine products over the next year or so as more companies switch to the HPLC method [39].
• Two indices of free thyroxine (T4) and four methods of free T4 measurement were compared in 85 patients with acute illness, hospitalized in intensive care units [40].
• DESIGN: Prospective cohort study conducted from November 1998 to June 1999, supplemented with an in vitro study of thyroxine (T(4)) binding to calcium carbonate [41].

References