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Failure of D-thyroxine to increase fetal hemoglobin levels in normal and anemic baboons.

The synthesis of Hb F in baboons after erythropoietic stress is markedly increased. The mechanism of this "reverse switch" is unknown, but erythropoietin is not directly responsible for it. Since D-thyroxine has been reported to cause Hb F increases in marmosets, we determined its effect in normal and anemic baboons whose erythropoiesis, hemoglobin fractions and regulation of hemoglobin synthesis are similar to those of man. No effect was demonstrated in the normal baboons. In the anemic animal the Hb F level did not increase beyond the elevation attributable to the erythropoietic stress itself. It is therefore, unlikely that D-thyroxine will increase Hb F levels in man.

Anemia↗

Hypolipidemic drugs.

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Cholestyramine Resin↗

Reactions of hypothalamic ascorbic acid, serum ceruloplasmin and the adenohypophysis to oestradiol: inhibition by L-thyroxine.

Four weeks' administration of oestradiol benzoate to male and female rats in doses of 1 mg twice a week leads to adenohypophyseal hyperplasia and to an increase in the thyroxine-binding capacity of the adenohypophyseal proteins in vitro. At the same time, serum polyphenol oxidase (ceruloplasmin) activity rises and the hypothalamic ascorbic acid concentration falls. The simultaneous administration of L-thyroxine (0.1 mg/rat/per day) or dried thyroid (but not D-thyroxine) significantly inhibits these changes (adenohypophysis, ceruloplasmin) or completely suppresses them (hypothalamic ascorbic acid). L-thyroxine evidently blocks the action of oestradiol in the adenohypophysis, the liver and the hypothalamus; the significance of this inhibition is discussed in relation to dopaminergic modulation of the adenohypophyseal reaction to oestradiol.

Adrenal Glands↗

[Thyroid hormones].

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Biological Transport↗

[Influence of a highly purified D-thyroxine medication on thyroid iodine uptake and in vitro tests of thyroid function (author's transl)].

25 euthyroidal patients with elevated serum cholesterol levels were treated with 4 mg of D-thyroxine daily for 4 weeks; controls were made after this period and after a withdrawal period of another 4 weeks. At the end of the treatment period there was a significant decrease of the serum cholesterol level, of the basal and TRH-stimulated serum TSH and of the thyroidal radioiodine uptake. The radioimmunologically determined values of total T 3 and Free Thyroxine index and of the serum iodine level rose significantly without being accompanied by clinical hyperthyroid symptoms. These changes can be explained on one hand by the well known cholesterol lowering effect of D T-4 and by the inclusion of D-isomeres of thyroid hormones in the radioimmunoassay, and, on the other hand, by the fact that the above-mentioned medication causes an uptake of iodine, and, possibly, by a direct inhibitory effect of D T-4 on the pituitary gland.

Adult↗

[Drug therapy of hypercholesterinemias (author's transl)].

Every permanent substantiated primary hypercholesterolemia which does not respond adequately to diet must be treated with drugs. For monotherapy first of all fenofibrate, bezafibrate and nicotinic acid derivatives are suitable for the treatment of adult patients. For supportive therapy colestyramine and colestipol come into consideration as well as beta-sitosterol. D-thyroxine and etiroxate should be reserved for refractory cases. Drug therapy is only given for secondary hypercholesterolemias in justifiable exceptions.

Adult↗

[Treatment of glycogenosis type III with total parenteral nutrition, continuous intragastric infusion and D-thyroxine].

A 4-year-old patient with glycogenosis type III suffered from hypoglycemic attacks during the night and from an enormous hepatomegaly. The latter was the cause of a life-threatening respiratory insufficiency. Shrinkage of the liver size was an urgent necessity. The beneficial influences of total parenteral nutrition, continuous intragastric infusion during the night, and of D-tyhroxin are described.

Blood Glucose↗

Effect of theophylline on binding of triiodothyronine, thyroxine, thyroxamine, tetraiodothyroacetic acid and cortisol in the cytosol of human leukocytes.

Inhibition constants describing competitive potency of thyroactive analogues and cortisol against labelled triiodothyronine (T3) in cytosol in human leukocytes were determined in the presence and the absence of theophylline by means of charcoal-dextran assay. L-triiodothyronine, L-thyroxine,L-thyroxamine,L-tetraiodothyroacetic acid, D-thyroxine and cortisol competed with T3 in binding sites of cytosolic proteins without theophylline addition. While theophylline addition increased the competitive potency (decreased the values of inhibition constants) of all thyroactive analogues, no such equivocal effect has been found in the case of cortisol.

Binding Sites↗