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.

Propylthiouracil-Induced Liver Injury in Mice and the Protective Role

Abstract: A B S T R A C T Background: Propylthiouracil (PTU) is a thionamide drug used in the management of hyperthyroidism in human. On the other hands, several cases of hepatotoxicity, hepatic failure and even death have been reported after PTU administration. No specific protective agent has been developed against this complication yet. Taurine is a sulfur containing amino acid which its beneficial effects in liver tissue has been reported in previous studies. This study was designed to investigate the effect of taurine on PTU-induced liver injury. Methods: Mice received PTU (100 mg/kg, oral) and different doses of taurine (250, 500 and 1000 mg/kg, i.p, administered 2 hours after PTU) and markers of liver injury were monitored. Results: Acute exposure to PTU caused hepatotoxicity in mice as evidenced by increase in plasmatic alanine aminotransferase (ALT), occurrence of significant lipid peroxidation, and hepatic glutathione depletion. The mentioned changes were endorsed by histopathological lesions of liver which were mainly manifested as pre-portal inflammation. Taurine administration (500 and 1000 mg/kg, i.p) resulted in reduction of lipid peroxidation, showed rebalancing effect on liver GSH level, and normalized plasma ALT. Taurine administration didn't affect PTU-induced inflammatory cell aggregation in liver. Conclusion: In view of these results, taurine seems to exert some beneficial effects against PTU-induced liver injury. A r t i c l e i n f o

The Effect of Graded Doses of Thyroxine on Plasma Thyrotropin Concentration in Rats Made Hypothyroid by Thyroidectomy or Propylthiouracil

Abstract: Adult male rats were made chronically hypothyroid by surgical thyroparathyroidectomy or by feeding propylthiouracil. In one set of experiments, each rat was injected ip daily with doses of T4 ranging from 0.01–3.0 μg/100 g BW, which were progressively increased every 3 days. Compared to the saline-treated controls, there was no statistically significant depression of plasma TSH until doses of 0.3 μg T4/100 g BW daily had been exceeded; there was no significant rise in plasma TSH with any dose of T4. No difference was detected in the quantitative suppression of plasma TSH concentration in the thyroidectomized or propylthiouracil-treated rats, even though a given dose of T4 caused a greater rise in plasma T4 concentration in the latter. In a separate experiment, chronically thyroidectomized rats injected for 3 days with saline or with 0.01, 0.1, or 1 μg T4 for 3 days were given 100 ng TRH/100 g BW iv. There was no effect on the rise in plasma TSH produced by TRH in any group, except in the group receiving t...

The onset of antineutrophil cytoplasmic antibody-associated vasculitis immediately after methimazole was switched to propylthiouracil in a woman with Graves’ disease who wished to become pregnant

Abstract: Propylthiouracil (PTU) is recommended as a first-line antithyroid drug (ATD) during first trimester organogenesis in pregnancy because recent evidence suggests that methimazole (MMI) may be associated with congenital anomalies. However, PTU more commonly causes myeloperoxidase (MPO)-antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, which usually occurs during prolonged treatment, compared with MMI. We report a case of MPO-ANCA-associated vasculitis in a 35-year-old woman with Graves'disease. Although her thyroid function could be maintained euthyroid by MMI, her ATD was switched to PTU because she wished to become pregnant. The patient presented with flu-like symptoms 8 days after starting PTU and developed hemoptysis and dyspnea at 22 days. Her MPO-ANCA titer was 21 ELISA units (EUs) before PTU treatment but increased to 259 EUs at 22 days after PTU treatment. Her clinical condition improved with the discontinuation of PTU and with immunosuppressive therapy. This case indicated that MPO-ANCA vasculitis occurred within several weeks after the initiation of PTU and that this side effect could be caused by the change from MMI to PTU. Thus, our clinical observation suggests that patients treated with PTU should be carefully monitored for MPO-ANCA titers and variable manifestations of MPO-ANCA-associated vasculitis regardless of the period of administration.

Congenital thyroid hyperplasia in twins; report of a case following administration of thiouracil and iodine to mother during pregnancy.

Abstract: The purpose of this communication is to record the occurrence of hyperplasia of the thyroid in newborn twins following the administration of thiouracil and iodine to the mother during gestation. To our knowledge no other case of apparently induced hyperplasia of the thyroid in humans has been reported. Experimentally hyperplasia of the thyroid has been produced in puppies by thyroidectomy upon the mothers. In regions where endemic goiter prevails, the occurrence of spontaneous congenital enlargement of the thyroid is not rare. REPORT OF CASE History.— The first of normally delivered twin girls was stillborn. The mother, aged 36, who had previously borne six healthy children, was receiving treatment for thyrotoxicosis. For five months she had received strong iodine (Lugol's) solution, 10 drops three times daily, and propylthiouracil, 100 mg. four times daily, with amelioration of her symptoms and reduction of the basal metabolic rate from +36 to +11%. External Examination.—

Pituitary resistance to thyroid hormones: pathophysiology and therapeutic options

Abstract: Thyroid hormone secretion suppresses the expression of thyroid stimulating hormone (TSH), both of which are strictly controlled by a negative feedback loop between the hypothalamus-pituitary and thyroid. Pituitary resistance to thyroid hormone (PRTH) is defined as resistance to the action of thyroid hormone that is more severe in the pituitary than at the peripheral tissue level. Although the molecular basis of PRTH is not well understood, the clinical issue mainly involves imbalance between the hypothalamus-pituitary and peripheral thyroid hormone responsivity, which may induce peripheral thyrotoxic phenomena. Here, we review the pathogenesis and molecular aspects of PRTH, present a single case with inappropriate TSH secretion suffering from thyrotoxicosis treated with PTU, and discuss the possible choice of therapeutic options to correct the imbalance of thyroid hormone responsivity in both the hypothalamus–pituitary and peripheral tissues.