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At least 163 records · Page 9Linked to original sources
PubMed1990

Thyrotoxicosis due to pituitary resistance to thyroid hormones. Successful control with D thyroxine: a study in three patients.

Selective pituitary resistance to thyroid hormone (PRTH) is responsible for thyrotoxicosis due to inappropriate secretion of TSH. The TSH suppressive action of D-thyroxine (DT4) has been previously documented in euthyroid and hypothyroid subjects. This prompted us to treat with DT4 three patients with PRTH uncontrolled by anti-thyroid drugs (ATD) alone or supplemented with bromocriptine, and whose follow-up had been complicated by atrial fibrillation in two patients. Because of 100% cross-reactivity between the D and L isomers of T4 and T3 in our RIAs, thyroglobulin (Tg) was used as an index of thyroid secretion. Under ATD, TSH and Tg levels were respectively: 35 mIU/l and 670.5 pmol/l (patient 1), 87 mIU/l and 453 pmol/l (patient 2) and 110 mIU/l and 906 pmol/l (patient 3). When DT4 was added (patient 1, 3 mg daily; patients 2 and 3, 2 mg daily) to the same dose of ATD, plasma TSH and Tg levels fell but were still over the upper limit of normal and thyrotoxicosis persisted as illustrated by a recurrence of atrial fibrillation in one patient. When ATD were withdrawn and DT4 given alone (2 mg daily) all symptoms subsided within 1 month while TSH and Tg levels fell within the normal range. TSH normalization was documented within 1 week in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Treatment of generalized scleroderma with inhibitors of collagen synthesis.

Clinical evaluation of scleroderma and the urinary excretion of collagen specific amino acids and uronic acid indicate disease activity and have become a guide for treatment. During an experimental search for inhibitors of the synthesis of collagen and ground substance glycosaminoglycans, a few connective-tissue active agents were selected for therapy of scleroderma: D-penicillamine, benzyl-penicillin-diethylamino-ethylester-hydroiodide, L-glutamine, hydralazine, glucocorticoids, dextro-thyroxine, L-dopa, diphenylhydantion, chlorpromazine, and (+) catechine. Treatment for several years was required to bring about an arrest of progression in 89% of the patients, a regression in three-quarters, and subtotal or total recovery in more than 40%. Indications of favorable prognosis are youth, short disease history, a high total dose of agent, and long duration of the treatment.

Catechin↗
PubMed1996

Treatment of pituitary resistance to thyroid hormone (PRTH) in an 8-year-old boy.

We report on an 8-year-old boy with pituitary resistance to thyroid hormone (PRTH) having a cysteine for arginine substitution at codon 320 in the TR-beta gene who was presented because of thyrotoxicosis. Due to its suppressive effect on the pituitary thyrotropin secretion, treatment with D-thyroxine (D-T4) was started. After a few days, clinical euthyroidism was achieved but thyroid stimulating hormone secretion was not suppressed. Symptoms of thyrotoxicosis relapsed when therapy was interrupted so that therapy with D-T4 was reinstituted and continued to date. Symptoms did not recur, and the psychomotor development proceeded normally. D-T4 should therefore be considered in the treatment of thyrotoxicosis in PRTH.

Amino Acid Sequence↗
PubMed1977

Thyroid hormone action: the mitochondrial pathway.

The subcellular compartments have been investigated to compare proteins capable of binding triiodothyronine and thyroxine; specific binders have been found in cytosol, nuclei, and mitochondria from rat liver and kidney. The binding protein from the inner mitochondrial membrane had the highest association constant (greater than 10(11) liters per mole), suggesting possible direct hormone action on the mitochondria. Binding of hormone analogs was found to be related to known physiological potency, and stereospecific discrimination between L- and D-thyroxine was observed. The saturable receptor was found in the mitochondrial membranes of rat liver, kidney, myocardium, and skeletal muscle but not in mitochondria from the unresponsive tissues: brain, spleen, and testis. Oxidative phosphorylation by mitochondrial vesicles from hypothyroid rats increased after the addition of physiological concentrations of triiodothyronine, which corroborated direct hormone action on mitochondria.

Animals↗
PubMed1985

Clinical trials on the efficacy of pharmacologic intervention reducing mortality from cardiovascular diseases.

Results of recent clinical trials on secondary prevention of ischemic heart disease indicate that judicious, long-term administration of adrenergic beta blockers and platelet-active drugs such as aspirin and Persantine (dipyridamole) would seem to yield protection against mortality associated with acute myocardial infarction, including sudden death. These drugs are beneficial also in prevention of recurrent myocardial infarction, especially among patients with unstable angina. These drugs should be considered as soon as the diagnosis of myocardial infarction or unstable angina is confirmed clinically. In terms of primary prevention of ischemic heart disease and cerebrovascular disease (stroke), the results of the Hypertension Detection and Follow-Up Program provide an excellent set of data on the efficacy of rigorous treatment of hypertension, especially those with mild hypertension. To be effective, treatment must start before there is evidence of target end organ damage, such as left ventricular hypertrophy. Recent data from the Australian Therapeutic Trial in Mild Hypertension also confirms these findings.

Adrenergic beta-Antagonists↗