Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Dextrothyroxine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

THE EFFECTS OF DEXTROTHYROXINE IN DIABETES.

Eighteen diabetic patients were treated with dextrothyroxine (from 2 mg to 8 mg daily) for varying periods up to six months. This produced a decided reduction of serum cholesterol levels. Statistically valid comparisons were made of their fasting blood sugar levels before and after two weeks of dextrothyroxine treatment. Administration of this drug was associated with a significant elevation of fasting blood sugar levels. Good diabetic control did not preclude this adverse effect. After more prolonged treatment with the drug, 8 of the 18 patients experienced progressive deterioration of their diabetic control, necessitating increased amounts of insulin or oral drugs. Despite close observation, one patient developed acidosis. When dextrothyroxine was discontinued, there was a significant drop in blood sugar levels in these patients. Two patients had hypoglycemic reaction. When the fasting blood sugar values of the 18 patients, studied while they were receiving significant doses of dextrothyroxine, are compared with a control series of blood sugar determinations obtained on these same patients before dextrothyroxine administration was begun, the diabetogenic effect of this drug is confirmed by the highly significant difference demonstrated. Four patients were given dextrothyroxine a second time, and again experienced deterioration of diabetic control.

Acidosis↗

Comparative effectiveness of dextrothyroxine and levothyroxine in correcting hypothyroidism and lowering blood lipid levels in hypothyroid patients.

Data reported here establish that treatment regimens of 4 mg dextrothyroxine and 0.15 mg levothyroxine in hypothyroid subjects produce similar degrees of lowering of serum TSH, cholesterol, triglycerides, and phospholipid levels and equal stimulation of metabolic rate. The Murphy-Pattee total T4 determination applied to blood samples drawn 24 h after the last dose of dextrothyroxine can be used to assess adequacy of treatment. Correction of hypothyroidism requires high serum levels of dextrothyroxine than of levothyroxine. Serum T3 levels increase in patients treated with dextrothyroxine. In the treatment of hypothyroidism, the cholesterol-lowering and metabolic rate-stimulating effects of dextrothyroxine do not appear to be dissociated. Further studies are needed to determine whether such an effect can be demonstrated in euthyroid hypercholesterolemic subjects with doses established herein as equivalent in terms of the stimulating effect on metabolic rate.

Basal Metabolism↗

[Drug treatment of hypercholesterolemia. Experience with a combination of dextrothyroxine and betapyridylcarbinol (author's transel)].

22 patients of our lipid ambulance with hypercholesterolemia received 6 mg highly purified dextrothyroxine (group 1, n = 10) or 900 mg beta-pyridylcarbinol (group 2, n = 12) for 12 weeks and both groups for another 8 weeks a combination of 4 mg dextrothyroxine and 600 mg beta-pyridylcarbinol daily. Most of the patients with an age from 8 to 57 years showed a family history of hypercholesterolemia, some of them suffered from coronary insufficiency. 20 patients completed the therapeutic progrand of 20 weeks. Total cholesterol decreases in both groups during monotherapy significantly, and still more during the combination, singificant in group 1. LDL cholesterol showed greater decrease during mono- and combination therqpy. The frequency of side effects was higher in the monotherqpy periods: increase of preexisting angina pectoris in one case during dextrothyroxine, severe flush in two cases during beta-pyridylcarbinol, gastrointestinal disturbances three times in both groups together. During the combined treatment minimal gastrointestinal symptoms were reported from one patient. The lower incidence and severity of side effects in spite of similar or better effects recommend the combination of dextrothyroxin and beta-pyridylcarbinol for longterm therapy of moderate hypercholesterolemia.

Adolescent↗

Elevated triiodothyronine and dextrothyroxine levels: a potential cause of iatrogenic hyperthyroidism.

A woman in whom the use of dextrothyroxine was associated with clinical hyperthyroidism is described. She had a markedly elevated T3 level while receiving the drug, apparently resulting from conversion of the dextrothyroxine to triiodothyronine. The T3 levels fell to normal after withdrawal. Patients receiving dextrothyroxine should be examined for possible elevation of T4 and T3 thyrotoxicosis.

Aged↗

Dextrothyroxine treatment of phosphorylase-kinase deficiency glycogenosis in four boys.

Four boys, aged 2 years 5 months to 3 years 7 months, with large hepatomegaly due to phosphorylase-kinase deficiency glycogenosis, were given a trial of sodium dextrothyroxine (D-T4) at a mean dose of 0.165 mg/kg/day for an average period of 6 months. Phosphorylase-kinase was undetectable in the haemolysates of erythrocytes (3 patients) or in the liver (one patient) before, and still undetectable in the haemolysates of the four patients during treatment, thus pointing to X-linked phosphorylase-kinase deficiency glycogen storage disease (GSD IXb). D-T4 administration resulted in complete normalization of liver size, decrease of serum GOT (p less than 0.02), GPT (p less than 0.05) and triglycerides (p less than 0.01) to normal values, as well as correction of mild asymptomatic hypoglycemia (p less than 0.01). As long as the outcome of type IXb glycogenosis in adult life remains undefined, dextrothyroxine therapy seems an effective means of reducing liver size and correcting part of the biochemical abnormalities of the disease.

Alanine Transaminase↗

Effects of dextrothyroxine on hyperlipidemia and experimental atherosclerosis in beagle dogs.

Beagle dogs, 24 +/- 6 months old, fed a thiouracil-free semi-synthetic diet containing hydrogenated coconut oil and cholesterol (SS diet) for 12 months, developed marked hyperlipidemia and severe atherosclerosis. SS diet produced a marked elevation of serum cholesterol, triglyceride, phospholipid, and beta-lipoprotein and severe atherosclerosis in large and small arteries. Intimal fatty lesions were always present in the abdominal aorta and many of its branches. Large and small coronary arteries showed similar lesions. The degree of atherosclerosis was directly related to circulating lipid levels. Dextrothyroxine, at dose levels of 0.1 (equivalent to normal human dose) and 0.5 mg/kg body weight, produced a significant dose related lowering of serum lipids and was associated with a markedly decreased severity of aortic and coronary artery lesions. Untreated control dogs that were maintained on purina dog meal developed neither hyperlipidemia nor atherosclerosis.

Animals↗

10 years of successful treatment with dextrothyroxine in a girl with TSH-induced hyperthyroidism.

14 years ago, a 5.7-year-old healthy girl was treated with desiccated thyroid for a goiter and elevated TSH levels. The goiter disappeared and TSH levels were normalized. However, hyperthyroidism appeared. Without therapy, the goiter reappeared and hyperthyroidism aggravated. Based on hormone values, TSH-induced hyperthyroidism was diagnosed. After exclusion of neoplastic TSH secretion, treatment with dextrothyroxine (DT4) was initiated at age of 10 years and continued during the last 10 years (except for short periods). The girl became euthyroid, has no goiter and normal TSH values. Since thyrotrophs and peripheral tissues are probably normally sensitive to T4, we postulate that her hypothalamopituitary-thyroid control is operating on a higher set point level for T4.

Adolescent↗

Effects of dextrothyroxine on the pituitary-thyroid axis in hypercholesterolemic children and goitrous adults.

To evaluate the effects of dextrothyroxine (D-T4) on the pituitary-thyroid axis, we have measured the secretion of TSH in response to TRH in six goitrous adults and six euthyroid children with familial hypercholesterolemia. Since the effects of thyroid hormones appear to be mediated by specific nuclear receptors, the binding affinity of D-T4 was also studied. In both groups of subjects, D-T4 completely abolished the expected TRH stimulation of TSH and T3 secretion. The in vitro binding of D-T4 to rat pituitary nuclear receptors is only 3% that of L-T3, but the binding of D-T3 was similar to that of L-T4 (13% and 11%, respectively). The high circulating levels of D-T4 and possibly of D-T3 after chronic administration of D-T4 may be responsible for the saturation of pituitary nuclear T3 receptors, resulting in the suppression of the TRH-induced TSH response. During the treatment period, total cholesterol, low density lipoprotein cholesterol, and high density lipoprotein cholesterol were significantly decreased by 18%, 18%, and 19%, respectively. Plasma triglyceride levels and the ratio of total to high density lipoprotein cholesterol were not affected. Although D-T4 lowers cholesterol levels, in view of its suppressive effect on the pituitary-thyroid axis, caution must be exercised with regard to its long term use in children.

Adult↗

[Comparative studies of the lipid-lowering activity of etiroxate hydrochloride and dextrothyroxine (author's transl)].

The effect of etiroxate and dextrothyroxine (CT4) on lipoproteins was determined in a long-term study comprising 40 patients with Type IIa hyperlipoproteinaemia and 19 patients with Type IIb. 40 mg etiroxate daily lowered the total lipids, phosphatides, cholesterol, and beta-lipoproteins more significantly than 6 mg DT4/day. After the administration of etiroxate and DT4, cholesterol decreased by 17.9% and 14.5% respectively in Type IIa and 16.6% and 12.6% respectively in Type IIb. The mean decrease in the beta-lipoproteins after etiroxate was 134 plus or minus 75 mg/100 ml in Type IIa and 96 plus or minus 101 mg/100 ml in Type IIb, and after DT495 plus or minus 69 mg/100 ml in Type IIa and 79 plus or minus 58 mg/100 ml in Type IIb. Transient gastric intolerance occurred after both drugs. In susceptible patients cardiac side effects were more frequently observed after DT4 than after etiroxate, but there was no statistical difference between the two drugs or the placebo phase.

Adult↗