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At least 19 recordsLinked to original sources
PubMed1979

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↗
PubMed1978

[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↗
PubMed1977

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↗
PubMed1978

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↗
PubMedDate not supplied

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↗
PubMed1991

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↗
PubMed1975

[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↗
PubMed1992

Dextrothyroxine in the treatment of generalized thyroid hormone resistance in a boy homozygous for a defect in the T3 receptor.

The dextroisomer of thyroxine (D-T4) has been shown to have suppressive effects on pituitary TSH secretion in euthyroid individuals and patients with mild thyroid hormone resistance. We treated a 3-year-old boy with D-T4 who was homozygous for a T3 receptor defect, resulting in a complex clinical picture of tissue-specific hyperthyroidism and hypothyroidism. There was no evidence of significant alteration in thyroid physiology, including serum concentrations of basal and TRH stimulated TSH or echocardiographic parameters measuring systolic time interval. We conclude that D-T4 at a daily dose of 6 mg (0.65 mg/kg) was ineffective in this boy with homozygous dominant negative thyroid hormone resistance.

Child, Preschool↗
PubMed1978

Treatment of established atherosclerosis during cholesterol feeding in monkeys.

A semipurified diet containing 43% of the calories as fat and 1.2 mg of cholesterol/cal was fed to cynomolgus monkeys (Macaca fascicularis) for 6 months; the cholesterol content was reduced to 0.34 mg/cal for the next 18 months. During the latter period, the monkeys were assigned to 4 groups of 18 animals each and received the following dietary additions: A, none (controls); B, cholestyramine (5%, w/w); C, dextrothyroxine (0.003%); and D, Wy-14,643 (0.45%). Cholestyramine normalized plasma lipid levels and reduced the size of aortic and coronary atherosclerotic lesions in spite of the high-fat, high-cholesterol intake. Dextrothyroxine reduced cholesterolemia but did not modify the extent of arterial lesions. Wy-14,643 changed neither plasma cholesterol levels nor the extent of atherosclerosis.

Acetates↗
PubMed1976

Drug treatment of hyperlipidemia.

The most frequent indication for treatment of hyperlipidemia is for prevention of arteriosclerosis, a suspected but unproved benefit. The cornerstone of treatment of primary hyperlipidemia is diet; drugs may be added to, but do not replace, diet. When a drug is used with any patient, its potential benefits and hazards must be carefully weighed for the given subject. The subjects should be carefully followed and observed for side effects. Plasma lipids should be monitored during the course of treatment. Five drugs have been approved by the U.S. Food and Drug Administration for the treatment of hyperlipidemia: cholestyramine, clofibrate, nicotinic acid, sodium dextrothyroxine and beta-sitosterol. The use, the actions and the side effects of each and of several nonapproved agents are discussed.

Aminosalicylic Acids↗
PubMed1975

Treatment of generalized scleroderma with inhibitors of connective tissue formation.

103 patients suffering from generalized scleroderma were studied in order to assess the effect of treatment with inhibitors of connective tissue formation. 93 patients with generalized scleroderma were given D-penicillamine, benzyl-penicillin-diethylamino-ethyl-ester hydroiodide, adrenal glucocorticoids, dextro-thyroxine, hydralazine, and "mixed treatment" (one or several of the drugs in consecutive courses, or concurrently). The effect of dextrothyroxine could not be evaluated in this study. No improvement could be seen after adrenocortical steroid therapy. Hydralazine seemed to be effective. D-penicillamine improved 25 of 34 treated patients; penicillin hydroiodide 12 out of 16. The dermal sclerosis of 6 patients regressed completely; in 16, sclerosis regressed with the exception of finger sclerosis; in 32, partial regression was registered; 20 had their progression arrested, but there was no regression; in 19 cases, there was no effect whatsoever. The prognosis seemed to be better for young than for old people. The age at onset was lower in the better groups. The higher the total dose, the better the results. The length of the treatment course is probably of some significance. The short-lasting cases had better prospects than the longer lasting. Ten untreated patients of this material and 11 patients seen earlier showed continued progression. Side effects leading to discontinuation of the drugs were seen in a substantial number of patients, especially after D-penicillamine. Twelve deaths could not be related to the treatments.

Adult↗
PubMed1991

Hyperthyroidism due to familial pituitary resistance to thyroid hormone: successful control with 3, 5, 3' triiodothyroacetic associated to propranolol.

We herein describe a family with thyroid hormone resistance. Thyroid hormones and basal TSH were elevated. Pituitary tumor or abnormality in thyroid hormone binding proteins were ruled out by appropriate tests. Mother and sister of the propositus presented similar abnormal hormonal features but no hyperthyroidism. Initially the patient was treated with carbimazole (30 mg/day): three months later a dramatic increase in the size of the thyroid gland and in TSH levels (12.5 to 28 mU/l) were noted. Thereafter, dextrothyroxine (D-T4) and 3, 5, 3'-triiodothyroacetic acid (TRIAC) were given consecutively and treatment was accompanied by a decrease of TSH levels (2 mU/l) but thyroid hormone remained elevated. The symptoms and signs of hyperthyroidism improved with the addition of propranolol (30-60 mg/day). In conclusion, the present report describes a new family with the syndrome of THR and variable degrees of involvement among relatives. We suggest the usefulness of TRIAC therapy to decrease TSH levels and propranolol to improve thyrotoxicosis due to pituitary resistance to thyroid hormone.

Adolescent↗
PubMed1990

Review of clinical trials: proving the lipid hypothesis.

The Lipid Hypothesis, which states that lowering blood cholesterol levels should significantly reduce the incidence of coronary heart disease (CHD), has been repeatedly tested in primary and secondary intervention trials. Viewed as a whole, it is apparent that the incidence of CHD in treated groups decreased in proportion to the degree of plasma cholesterol reduction. An early study at the Wadsworth Hospital in Los Angeles showed that a diet high in polyunsaturated fat and low in cholesterol reduced the incidence of CHD. The Oslo study of diet and smoking intervention demonstrated a significant decrease in CHD concomitant with a 13% reduction in serum cholesterol achieved through a low saturated-fat diet and cessation of smoking. In the World Health Organization primary prevention trial, clofibrate reduced serum cholesterol by 9% and first clinical episodes of myocardial infarction by 20%. There was a 37% rise in total mortality, but no causal link with clofibrate has been found, and this was not significant when corrected for age at death. A secondary trial, the Coronary Drug Project, demonstrated that oestrogen and dextrothyroxine were clearly toxic. In this trial, niacin produced a 10% fall in serum cholesterol and mortality was 11% lower than in the placebo group after long-term follow-up. The Lipid Research Clinics-Coronary Primary Prevention Trial (LRC-CPPT) found an 8% reduction in plasma cholesterol and a 19% reduction in the incidence of CHD in the group treated with cholestyramine compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Coronary drug project: experience with niacin. Coronary Drug Project Research Group.

Niacin was one of the treatments compared in the Coronary Drug Project, a placebo-controlled, multicenter trial of lipid-lowering drugs in the secondary prevention of coronary heart disease. A total of 1119 men, aged 30-64 at entry, were randomized to niacin and 2789 to placebo by the end of recruitment in March 1969. Although side-effects interfered with adherence to the niacin regimen, it was the most effective agent in achieving cholesterol-lowering (10% overall); other agents in the trial were clofibrate, dextrothyroxine, and conjugated equine estrogens. At the scheduled conclusion of the trial in February 1975, the niacin-treated group exhibited a statistically significantly lower incidence of definite, non-fatal myocardial infarction (MI) than the placebo group. There was a trend toward improvement in the life-table mortality curve, but this was not statistically significant. In 1981 an extended follow-up was carried out concerning vital status for the 6008 men who were still alive at the end of treatment and active follow-up in the trial in 1975 (827 in the niacin group and 2008 in placebo groups). Vital status was determined for 99.1% of these men after a mean of 9 years from conclusion of the trial. In the group previously randomized to niacin, there were 69 (11%) fewer deaths than were expected on the basis of mortality in the placebo group. This difference was significant (z = -3.52; P = 0.0004). The data also suggested that patients with a higher baseline cholesterol experienced greater benefit from niacin therapy, as did those with the best response to the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Prescribed use of cholesterol-lowering drugs in the United States, 1978 through 1988.

Data from two pharmaceutical marketing research databases, the National Prescription Audit and the National Disease and Therapeutic Index, were used to study trends in outpatient use of cholesterol-lowering drugs in the United States from 1978 through 1988. Retail pharmacies dispensed an estimated 4.4 million prescriptions for cholesterol-lowering drugs in 1978. This declined to 2.6 million in 1983 and increased dramatically to nearly 13 million in 1988. This fivefold increase between 1983 and 1988 was accounted for primarily by the introduction and use of two new drugs, gemfibrozil and lovastatin, and, to a lesser extent, by the increasing use of some older drugs. In 1988, after 1 full year of marketing, lovastatin was the leading cholesterol-lowering drug, followed closely by gemfibrozil; both drugs are currently considered second-line agents. Clofibrate and dextrothyroxine, drugs that ranked first and second in 1978, declined to ranks of sixth and eighth out of eight in 1988. Cholestyramine, gemfibrozil, and lovastatin accounted for about 75% of all lipid-lowering prescriptions in 1988. From 1978 through 1988, an average 54% of individuals using cholesterol-lowering drugs were 60 years of age or older. The 13 million prescriptions for cholesterol-lowering drugs in 1988 represent a maximum estimate of 13 million treated individuals. This number compares with the 60 million Americans with high cholesterol levels who are candidates for dietary advice, and, if cholesterol levels do not improve, for combined diet and drug intervention.

Anticholesteremic Agents↗