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PubMed1992

Nodular vasculitis associated with propylthiouracil therapy.

Cutaneous vasculitis is a rare complication of propylthiouracil therapy. We describe a patient who presented with lower extremity subcutaneous nodules, hemorrhagic bullae, and necrotic ulcers during treatment with this agent. Examination of a skin biopsy specimen revealed nodular vasculitis. This type of vasculitis has not been described in association with propylthiouracil therapy before. Nodular vasculitis not associated with the drug is characterized by a chronic protracted course, whereas in the patient reported the lesions rapidly regressed when use of the drug was discontinued.

Aged↗
PubMed1991

Critical analysis of the histomorphometry of rat thyroid after treatment with thyroxin and propylthiouracil.

The morphological variations of rat thyroid follicles after treatment with either thyroxin or propylthiouracil were evaluated by histomorphometry. A silver impregnation technique allowed a precise visualization of thyroid follicles on histological sections. The histomorphometric values (cell height, follicular diameter, percentage of epithelial cells) were obtained using a semi-automatic image analyser. The statistical tests used were analysis of variance (Fisher's test) and the Newman-Keuls tests. The results obtained showed that thyroxin treatment did not lead to any modification in histomorphometric values. Propylthiouracil, on the contrary, caused profound alterations in the morphology of thyroid follicles and in particular an increase in the height of the follicular epithelium. These changes were induced by a deficiency in thyroid hormones leading to an increase in thyroid-stimulating hormone (TSH) release. This study shows that with rigorous methodology, histomorphometry is adaptable to the requirements of a simple and reproducible evaluation of substances capable of causing functional perturbations and their effects on the thyroid gland.

Animals↗
PubMedDate not supplied

Propylthiouracil hepatotoxicity: two pediatric cases and review of the literature.

We have observed isolated hepatotoxicity in two children treated with propylthiouracil (PTU) for hyperthyroidism. Neither patient had risk factors for or clinical evidence of preexisting liver disease. In one patient the drug was promptly discontinued when signs of liver disease were noted. This patient quickly recovered. The second patient continued to receive PTU for several days after developing symptoms. Her illness progressed to fulminant hepatic failure with encephalopathy, and she died. These are the third and fourth pediatric cases reported, and there have been 10 cases reported in adults in the English language literature. Thirteen of the 14 patients are female. The literature regarding all these patients is reviewed. Propylthiouracil may cause lethal hepatic damage. This drug should be discontinued immediately if signs or symptoms of hepatic injury are detected.

Adolescent↗
PubMed1987

Cutaneous vasculitis associated with propylthiouracil therapy.

Cutaneous vasculitis is an uncommon complication of propylthiouracil therapy. Its pathogenesis has been related to the presence of circulating immune complexes. The lesions may be purpuric or bullous hemorrhagic, possibly evolving into necrotic ulcerations. Usually, lesions develop on the extremities and earlobe. The vasculitis has been related to the duration of the treatment and disappears with the withdrawal of the drug, although a fatal case has been reported. Corticosteroid therapy is often prescribed, but its efficacy has not been demonstrated. We describe a patient in whom treatment with propylthiouracil for a year was associated with vasculitic lesions on the lower extremities and earlobe. Discontinuation of the drug was correlated with disappearance of the lesions.

Adult↗
PubMed1987

Propylthiouracil-induced fatal hepatic necrosis.

We present a fatal case of acute submassive hepatic necrosis occurring in a 42-yr-old black woman treated for hyperthyroidism with propylthiouracil for 1 yr. Alcohol and drug abuse were ruled out and all serological tests for hepatitis A and B, cytomegalovirus, and Epstein-Barr virus infection were negative. At autopsy the liver was shrunken and presented a yellow granular appearance. Microscopy disclosed submassive necrosis with bile stasis and severe chronic inflammation, as well as mild bile duct proliferation. Although non-A, non-B hepatitis cannot be ruled out (there was no transfusion of blood or its products), this is considered to be the third fatal case and ninth instance of propylthiouracil-induced hepatic necrosis.

Adult↗
PubMed1979

[Administration of equally divided doses of propylthiouracil every two-eight hours in hyperthyroidism].

Serum propylthiouracil semi splitting occurs in 1.1 and 1.65 hours when administered in a single dose. In this work treatment for hyperthyroid patients is described; 350 mg were administered daily in divided doses, every two and eight hours. In group A fifteen patients received 50 mg every two hours from 8:00 to 20:00 hs. and in group B nine patients were administered 100, 100 and 150 mg at 8 hour intervals. The patients were hospitalized the first seven days and during this time circulating triiodothyronine and thyroxine concentrations were measured daily at 8:00 and 20:00 hrs. and then at 8:00 hrs. at days 8, 14, 21 and 28. After almost one week of treatment, in group "A", seven patients (46.6 per cent p 0.05) had normal concentration levels in both hormones. In group "B" only one patient reached normal levels in the first eight days. The administration of propylthiouracil every two hours is a useful procedure to attain the euthyroid state in less time than with other therapeutic patterns without undesirable side effects.

Adolescent↗
PubMed1979

Kinetics of the human thyroid trap: effects of iodide, thyrotropin, and propylthiouracil.

Effects on the thyroidal pertechnetate trap of iodide, thyrotropin (TSH), and propylthiouracil (PTU), compared with duplicated control studies, were assessed in normal subjects using i.v. [Tc99m] pertechnetate, a multicrystal scintillation camera, and a compartmental model. Sodium iodide (1 g), administered orally on two occasions, 2 wk apart, caused an early drop in plasma clearance into the follicular cell (p less than 0.05), with later return to normal clearance 1 wk after the second NaI dose. In this later study, exit from the colloid was elevated (p less than 0.01). Plasma equivalent volume of the "colloid" compartment was reduced in both postiodine studies (p less than 0.05). Thyrotropin, 10 units intramuscularly, was followed by no significant changes in trap parameters at 2 hr. At 24 hr, plasma clearance had doubled (p less than 0.05), and the plasma equivalent "colloid" volume had tripled (p less than 0.01). Propylthiouracil was given as a single 1 g dose 1 hr before a trapping study followed by 200 mg PTU every 8 hr for 1 wk. The first dose resulted in apparent reduction in all of the rate constants for transport across the basal and apical thyroid follicular cell membranes; these rates returned toward control levels after 1 wk. The plasma equivalent "follicular cell" volume was reduced to 66% of controls levels (p less than 0.025) after 1 wk PTU. These effects must be taken into account in the interpretation of studies of the trap based on PTU pretreatment to inhibit organification.

Adult↗
PubMed1980

Hypothalamic somatostatin and pituitary and serum growth hormone concentrations during postnatal development in rats exposed chronically to propylthiouracil or a low iodine diet.

The developmental profiles of hypothalamic somatostatin and pituitary and serum growth hormone (GH) concentrations were examined in rats exposed chronically to a low iodine diet or propylthiouracil. Hypothalamic somatostatin and pituitary and serum GH concentrations were similar during development in control and low-iodine-diet animals. Propylthiouracil-induced hypothyroidism, however, was associated with reduced hypothalamic somatostatin and pituitary and serum GH concentrations, the latter being undetectable after 6 days. These data indicate that hypothalamic control of GH secretion is unaltered in low-iodine-diet rats who maintain an euthyroid status by preferential triiodothyronine (T3) production. The marked derangements observed in the hypothyroid animals indicate that thyroid hormones are critical for the postnatal maturation of the GH regulatory mechanism.

Animals↗
PubMed1984

2-Propylthiouracil does not replace glutathione for the glutathione transferases.

2-Propylthiouracil has been reported as replacing glutathione as a substrate for the glutathione transferases of rat liver. This observation has been examined with several homogeneous glutathione transferases that were prepared from human and rat liver by different methods in three laboratories. No evidence was obtained for 2-propylthiouracil as a substrate for glutathione transferase in the several reactions tested.

Animals↗
PubMed1981

Giant mitochondria in rat liver cells after short-term administration of propylthiouracil.

Chronic administration of propylthiouracil for five weeks to rats induced marked ultrastructural changes in their liver mitochondria, consisting in round or oval transformation as well as in the presence of a few giant mitochondria per cell section. A decreased number of cristae was a common feature of both types of mitochondria. The more enlarged mitochondria frequently contained filaments within intracristal spaces or between the inner and the outer mitochondrial membranes. These structures were formed by helices, 35-45 A thick, with helical diameter and pitch about 130-150 A. The round or oval transformation of mitochondria and the decreased number of cristae are probably the morphological counterpart of the antithyroid effect of the drug. The formation of giant mitochondria may well represent a hepatotoxic action of propylthiouracil. The possibility of a relation between the helical filaments and abnormal lipidic composition of mitochondrial membranes is favoured.

Animals↗
PubMed1997

Propylthiouracil-induced alveolar haemorrhage associated with antineutrophil cytoplasmic antibody.

Propylthiouracil (PTU) is known to cause vasculitis as a rare complication. We report the case of a patient who developed alveolar haemorrhage and haematuria whilst treated with PTU. The serum was positive for antineutrophil cytoplasmic antibody (ANCA) with myeloperoxidase (MPO) specificity (MPO-ANCA). All symptoms resolved completely after discontinuation of PTU. Alveolar haemorrhage or pulmonary-renal syndrome associated with antineutrophil cytoplasmic antibody with myeloperoxidase specificity may be a new complication of propylthiouracil therapy.

Adult↗
PubMed1997

Propylthiouracil-induced cutaneous vasculitis.

Cutaneous reactions to propylthiouracil and methimazole occur in 3%-5% of adults. Generalized maculopapular and papular purpuric eruptions are perhaps the most common thionamide-induced reactions. We report 3 patients who developed cutaneous vasculitis which is a rare and serious side-effect during antithyroid drug therapy. The observation of cutaneous vasculitis during administration of propylthiouracil suggested that clinical awareness of this complication should be of considerable importance.

Adult↗
PubMed1984

Granulocytotoxic antibodies in a patient with propylthiouracil-induced agranulocytosis.

Agranulocytosis developed in a patient who was receiving propylthiouracil. Using a microgranulocytotoxicity assay, serum taken from the patient was shown to be strongly granulocytotoxic when tested against the patients granulocytes and those obtained from two of eight normal subjects. Tests for granulocyte agglutinins and for lymphocytotoxicity were negative. Granulocytotoxic activity decreased as the patient's peripheral granulocyte count recovered. Cytotoxicity was shown to be mediated by a complement-dependent IgM antibody.

Adult↗
PubMed1987

Remission in children with hyperthyroidism treated with propylthiouracil. Long-term results.

We treated 69 hyperthyroid children with propylthiouracil, of whom 53 remained under surveillance. Of these children, 34 (64%) had an initial remission, but relapses were frequent (47%). At this writing, 24 patients (45%) were in remission, with a mean duration of remission of 55 months (range, ten to 132 months). We found that the triiodothyronine level took significantly longer than the thyroxine (T4) level to return to normal. Thus, based on the T4 level alone, treatment may have been stopped prematurely in some patients, causing the relapse rate to be falsely high. The response to therapy did not depend on the size of the goiter nor on the initial levels of T4 or triiodothyronine. Six patients had adverse reactions, which were serious in two patients.

Adolescent↗
PubMed1995

Neonatal hypothyroidism causes delayed Sertoli cell maturation in rats treated with propylthiouracil: evidence that the Sertoli cell controls testis growth.

BACKGROUND: The testes of rats treated neonatally with propylthiouracil (PTU) grow to almost twice their normal size. The cause of testicular enlargement has been suggested to be the result of delayed maturation of Sertoli cells, allowing Sertoli cell division to occur beyond the 15th postnatal day, the commonly recognized cutoff date for Sertoli cell divisions. It has been shown that an increased population of Sertoli cells in postnatal development supports increased numbers of germ cells in adult animals. After examining developing rats treated neonatally with PTU, we hypothesized that an approximate 10-day delay in maturation was occurring and proceeded to test this hypothesis experimentally. Thus the purpose of this report was to determine if a 10-day delay in maturation could explain the increased numbers of Sertoli cells and increased testis size in PTU-treated animals. METHODS: Both control animals and animals treated neonatally with PTU N = 5/group were sacrificed at 15 and 25 days of age and prepared for electron microscopy. RESULTS: Micrographs show and morphometric ultrastructural analysis of numerous parameters demonstrated at the 95% probability level that Sertoli cells from 25-day-old PTU animals are not different in size and most constituents (volume and surface area) from 15-day-old control animals and are less mature than 25-day-old control animals. Mitosis of Sertoli cells was observed in PTU-treated animals in 25-day-old animals but not in age-matched controls. The number of Sertoli cells in 25-day-old PTU-treated animals is significantly increased over age-matched controls. Micrographs show the presence of immature Sertoli cell nuclei in 25-day-old animals receiving PTU as well as increased germ cell degeneration in this group. Sertoli cell tight junction formation is also delayed in PTU-treated animals as compared with controls. CONCLUSIONS: Together, the data show that delayed maturation of Sertoli cells occurs in treated animals that corresponds to a minimum of 10 developmental days. In the immature state, Sertoli cells continue to divide. Data presented herein and published data related to PTU treatment indicate that delayed maturation of the Sertoli cell results in delayed maturation and proliferation of other testicular cell types. From this and from published data, the hypothesis is presented that the Sertoli cell is responsible for the overall control of testis development.

Animals↗
PubMed1988

Dose-dependent induction of anti-native DNA antibodies in cats by propylthiouracil.

Cats receiving propylthiouracil (PTU) develop antinuclear antibodies (ANA) and an immune-mediated disease syndrome characterized by anorexia, lymphadenopathy, weight loss, and Coombs-positive hemolytic anemia. Investigation of the ANA specificity indicated that the predominant ANA activity consistent of anti-native DNA (nDNA) antibodies. The formation of anti-nDNA antibodies and immune-mediated disease syndrome appeared to be dose-dependent, even in cats in which a response had been induced on 4 prior occasions. These results supply further evidence that PTU-induced autoimmunity is not the result of a simple drug allergy. Rather, it appears that PTU induces a lupus-like syndrome, including the hallmark sign of systemic lupus erythematosus, anti-nDNA antibodies.

Animals↗
PubMed1979

Long-term effects of propylthiouracil-induced neonatal hypothyroidism.

Hypothyroidism was induced in neonatal Sprague-Dawley rats by adding propylthiouracil to the lactating female's food and water. Behavioral evaluation on a 6-item battery occurred from 70 to 114 days of age. Results indicated long-lasting behavioral changes in the neonatal hypothyroid animals characterized by increased activity and decreased performance on avoidance and escape learning. Serum thyroxine levels were reduced in the hypothyroid animals throughout the 120-day period. Experimental animals also had fewer synaptic contacts in the cerebellar cortex when analyzed at 90 days of age.

Animals↗
PubMed2005

Comparison of potential protective effects of melatonin, indole-3-propionic acid, and propylthiouracil against lipid peroxidation caused by potassium bromate in the thyroid gland.

Potassium bromate (KBrO3) is a prooxidant and carcinogen, inducing thyroid tumors. Melatonin and indole-3-propionic acid (IPA) are effective antioxidants. Some antioxidative effects of propylthiouracil (PTU)--a thyrostatic drug--have been found. The aim of the study was to compare protective effects of melatonin, IPA, and PTU against lipid peroxidation in the thyroids, collected from rats treated with KBrO3, and in homogenates of porcine thyroids, incubated in the presence of KBrO3. Wistar rats were administered KBrO3 (110 mg/kg b.w., i.p., on the 10th day of the experiment) and/or melatonin, or IPA (0.0645 mmol/kg b.w., i.p., twice daily, for 10 days), or PTU (0.025% solution in drinking water, for 10 days). Homogenates of porcine thyroids were incubated for 30 min in the presence of KBrO3 (5 mM) plus one of the antioxidants: melatonin (0.01, 0.1, 0.5, 1.0, 5.0, 7.5 mM), or IPA (0.01, 0.1, 0.5, 1.0, 5.0, 7.5, 10.0 mM), or PTU (0.01, 0.1, 0.5, 1.0, 5.0, 7.5, 10.0 mM). The level of lipid peroxidation products (MDA + 4-HDA) was measured spectrophotometrically in thyroid homogenates. In vivo pretreatment with either melatonin or with IPA or with PTU decreased lipid peroxidation caused by KBrO3--injections in rat thyroid gland. Under in vitro conditions, PTU (5.0, 7.5, and 10.0 mM), but neither melatonin nor IPA, reduced KBrO3-related lipid peroxidation in the homogenates of porcine thyroids. In conclusion, melatonin and IPA may be of great value as protective agents under conditions of exposure to KBrO3.

Animals↗