Topic
Propylthiouracil
About: Propylthiouracil is a research topic. Over the lifetime, 2181 publications have been published within this topic receiving 46996 citations. The topic is also known as: Thyreostat® & 2,3-dihydro-6-propyl-2-thioxo-4(1H)-pyrimidinone.
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TL;DR: It is concluded that the postnatal increase in sodium pump activity can be accounted for by coordinate increases in the pool sizes of α1 and β1 subunits and that, like in brain, this increased Na,K-ATPase expression is dependent on normal thyroid status.
Abstract: Renal Na,K-ATPase drives active reabsorption of sodium and cotransported solutes along the nephron. There is a large increase in net Na+ reabsorption in the postnatal rat kidney. It has previously been established that the postnatal increase in expression of sodium pump isoforms in the brain, but not the heart, is blunted in the hypothyroid neonate. The aims of this study were to establish whether the developmental increase in renal sodium transport is associated with coordinate increases in the abundance of the sodium pump α1 catalytic and β1 glycoprotein subunits and Na,K-ATPase activity, and to determine whether thyroid status influences the postnatal increase in renal Na,K-ATPase expression. Pregnant rats were made hypothyroid with low iodine diet, propylthiouracil and perchlorate. Offspring were hypothyroid assessed by triiodothyronine/thyroxine RIA. Renal cortical membranes were prepared from euthyroid and hypothyroid rats from 6 to 24 days of age. There was no change in Na,K-ATPase activity or expression between 6 and 15 days. Between 15 and 24 days, Na,K-ATPase activity increased 1.35-fold while sodium pump α1 and β1 subunit abundance increased coordinately to 1.7- and 2-fold over the previous period, respectively. In hypothyroid neonates, kidney weight was less than in euthyroids, and Na,K-ATPase activity, α1 and β1 subunit pool sizes did not significantly increase as a function of age between 6 and 24 days. We conclude that the postnatal increase in sodium pump activity can be accounted for by coordinate increases in the pool sizes of α1 and β1 subunits and that, like in brain, this increased Na,K-ATPase expression is dependent on normal thyroid status.
22 citations
TL;DR: In 5 patients the serum decay curve during treatment was slightly elevated above the extrapolated control decay curve, but the slope was unchanged, and in 2 of 3 patients, counting over the liver indicated increased concentration of iodine.
Abstract: The effect of 5-propylthiouracil (5-PTU) and 6-propylthiouracil (6-PTU) on the metabolism of thyroxine was studied in 10 euthyroid patients. After a single dose of I131-labeled L-thyroxine given intravenously, radioactivity in the serum, urine and stool was measured daily. Potassium perchlorate was given throughout the study to block recycling of iodide by the thyroid. After an 8- to 9-day control period, either 5-PTU (400 mg daily) or 6-PTU (400–800 mg daily) was given for 8 days. 5-PTU reduced urinary I131 30–44 % and increased fecal I131 in all patients. 6-PTU reduced urinary I131 only 0–11 % and increased fecal I131 in only 1 patient. Decay in serum was slowed significantly in 2 patients given 5-PTU. In 5 patients the serum decay curve during treatment was slightly elevated above the extrapolated control decay curve, but the slope was unchanged. Serum protein-bound iodine (PBI) was increased 1.2±0.4 μg/100 ml in 7 patients. In 2 of 3 patients, counting over the liver indicated increased concentration ...
21 citations
TL;DR: A case of severe mania due to thyrotoxicosis responded to propranolol and propylthiouracil.
Abstract: A case of severe mania due to thyrotoxicosis responded to propranolol and propylthiouracil.
21 citations
Journal Article•
TL;DR: Hypothyroidism produces significant decreases in GH mRNA and also decreases PRL mRNA and that mammosomatotropic cells can be detected in pituitaries from normal and hypothyroid rats.
21 citations
TL;DR: The following represents the first report of bone marrow aplasia and pancytopenia following therapy with propylthiouracil.
Abstract: Although ALTHOUGH agranulocytosis occurs in approximately 1% of patients treated with some antithyroid drugs, notably methylthiouracil, propylthiouracil, and methimazol, the association of bone marrow aplasia with their use appears to be extremely rare. 1 An occasional case of aplastic anemia has been reported following methylthiouracil 2 and methimazol (Tapazole) therapy. 3 The following represents the first report of bone marrow aplasia and pancytopenia following therapy with propylthiouracil. Report of a Case A 53-year-old white housewife was first admitted to Jackson Memorial Hospital on March 17, 1966, with complaints of tiredness, weakness, nervousness, palpitation, and weight loss of 15 months' duration. Physical examination revealed blood pressure, 130/70 mm Hg; pulse rate, 100 beats per minute and irregular; respiration, 16/min; and temperature 98.6 F (37 C). The patient had a questionable lid lag, moderate diffuse thyroid enlargement, an irregular cardiac rhythm, and mild ankle edema. Laboratory data included hemoglobin level, 15 gm
21 citations