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PubMed1984

Relationship between leukopenia and bone marrow myeloperoxidase in the rat treated with propylthiouracil.

The relationship between the toxic effect of propylthiouracil (PTU) and myeloperoxidase activity of rat bone marrow was examined. The administration of PTU for 1 or 2 weeks caused a decrease in leukocyte count with the concomitant inhibition of the activity of myeloperoxidase in the bone marrow. The decreases in both leukocyte counts and myeloperoxidase activity were restored to control levels at 2 weeks after the discontinuation of the administration. PTU treatment did not affect the affinity of H2O2 for the enzyme; however, an increase in the Km value for guaiacol was seen. PTU, incubated with bone marrow peroxidase in vitro increased the Km value of the enzyme for guaiacol, but had no effect on the Km value for H2O2. The results suggest that the mechanism of inhibition of myeloperoxidase activity by PTU given in vivo or incubated with the enzyme in vitro may be the same. The activity of bone marrow glutathione peroxidase was not influenced by PTU treatment.

Animals↗
PubMed1993

Eosinophilic pleuritis due to propylthiouracil.

We report a patient who developed eosinophilic pleuritis due to propylthiouracil. Although immunologic side effects associated with thionamides previously have been described, this is the first reported case of an isolated eosinophilic pleural reaction.

Emergencies↗
PubMed1999

Diffuse alveolar hemorrhage and pulmonary capillaritis due to propylthiouracil.

Propylthiouracil (PTU) has recently been observed to be associated with antineutrophil cytoplasmic antibody (ANCA)-positive small vessel vasculitis, resulting in crescentic glomerulonephritis and, infrequently, diffuse alveolar hemorrhage (DAH). We describe a case of a 23-year-old pregnant woman who developed a perinuclear ANCA and antimyeloperoxidase-positive small vessel vasculitis manifesting as DAH and crescentic glomerulonephritis after she began taking PTU. An open lung biopsy was consistent with pulmonary capillaritis. She responded to corticosteroid therapy and discontinuation of PTU. DAH can be caused by pulmonary capillaritis, bland hemorrhage, or diffuse alveolar damage. To our knowledge, this represents the first documentation of an underlying pulmonary capillaritis in a case of PTU-induced DAH.

Adult↗
PubMed1996

Blockade of the estrogen induced increase in progesterone receptor caused by propylthiouracil, an anti-thyroid drug, in a transplantable pituitary tumor in rats.

It is well known that estrogen (E2) induces progesterone receptor (PR) in the uterus and the mammary gland. In MtT/F84, a pituitary tumor, which was established in our laboratory and has been maintained with in vivo passages, we investigated the PR regulation by E2 in relation to the host's thyroidal status. The PR level in the tumor had increased five fold 48 h after an E2 injection. When the host rats were treated with propylthiouracil (PTU), an anti-thyroid drug, the induction of PR after an E2 injection was completely blocked. This result is consistent with our previous findings indicating that E2 responsiveness in the tumor may be under the control of thyroid hormones. The estrogen receptor (ER) level in the tumor treated with PTU was 15% of the control. This low ER level may account for the blocking of PR induction after an E2 injection. When the host animals were continuously treated with various doses of E2, the PR level in the tumor rose in correlation with the E2 doses. PTU administration, however, did not prevent long term induction of PR by continuous E2 treatment. Our findings suggest that PTU lower the ER level and suppresses the short term estrogenic actions such as PR induction after an E2 injection.

Animals↗
PubMed2000

Altered CD15 glycolipid expression in the developing rat cerebellum following treatment with antithyroid drug, propylthiouracil.

Thyroid hormone plays an important role during central nervous system (CNS) development. Experimentally-induced perinatal hypothyroid rats show abnormal cerebellar cytoarchitecture, but the underlying mechanism is not fully understood. Altered cell-cell interactions may contribute to such abnormalities, since the expression of NCAM is increased in hypothyroid animals. In the present study, we examined the expression of carbohydrate epitope 3-fucosyl-N-acetyl-lactosamine (CD15 antigen), that can be localized on both astrocytes and neurons in the developing brain, and is considered to play an important role in glial-neuronal interaction and cell migration. Newborn rats were treated with an antithyroid drug, propylthiouracil (PTU) and the CD15 glycolipid levels in the cerebellum were examined by enzyme-linked immunosolvent assay (ELISA) using 7A monoclonal antibody raised against rat forebrain antigen. A transient elevation of CD15 level was observed on postnatal day 10 in PTU-treated animals. Analysis of neutral glycolipids on high performance thin layer chromatography (HPTLC), revealed two distinct immunoreactive bands, corresponding to Fuc-nLc6 and Fuc-nLc4. The Fuc-nLc4 is preferentially increased in the PTU-treated group. These results suggest that a transient increase in CD15 glycoconjugates with isoform-specific manner induced by PTU may contribute to morphological abnormalities in hypothyroid rat cerebellum affecting granule cell migration.

Animals↗
PubMed2002

Prevalence of serum anti-myeloperoxidase antineutrophil cytoplasmic antibodies (MPO-ANCA) in patients with Graves' disease treated with propylthiouracil and thiamazole.

Patients with Graves' disease (n = 61) treated with propylthiouracil (PTU) or thiamazole (MMI) were studied retrospectively to investigate differences in the prevalence of anti-myeloperoxidase anti-neutrophil cytoplasmic antibodies (MPO-ANCA) in relation to treatment with anti-thyroid drugs. The patients were divided into two groups: PTU-treated group (n = 32) and MMI-treated group (n = 29). There were no significant differences between the two groups in terms of age, gender distribution, or duration of treatment. In the PTU group, 8/32 (25%) patients were positive for MPO-ANCA, whereas in the MMI group, 1/29 (3.4%) patients were positive. There were no significant differences in age, duration, or dosage between the MPO-ANCA positive and negative patients. Most of the MPO-ANCA positive patients were asymptomatic, except for two patients in whom rheumatic arthritis or membranous glomerulonephritis developed. None of the MPO-ANCA positive patients were diagnosed as having classical ANCA-associated vasculitis. Thus, there is a high frequency of MPO-ANCA in patients with Graves' disease treated with PTU, compared with patients treated with MMI, although classical ANCA-associated vasculitis develops in only a few MPO-ANCA positive patients.

Adult↗
PubMed2002

A successful pregnancy and delivery case of Graves' disease with myeloperoxidase antineutrophil cytoplasmic antibody induced by propylthiouracil.

A 30-year-old female patient, diagnosed as having Graves' disease in 1996, was treated with propylthiouracil (PTU) for 4 years. She developed a low-grade fever from December 1999. As myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA) vasculitis is one of the adverse effects of PTU, we examined serum MPO-ANCA level and found it was positive, but cytoplasmic-ANCA (c-ANCA) was negative. There were no symptoms that indicated other diseases associated with MPO-ANCA. She was confirmed to be at 6 weeks gestation, and thyroid hormone levels were elevated at that time. We discontinued PTU and gave methyl-mercaptoimidazole (MMI), and the titer of MPO-ANCA fell along with fever. Therefore we estimated the case as probable MPO-ANCA positive vasculitis induced by PTU. MMI was also suspended because of the development of hepatic dysfunction. After thyroid function was normalized by administration of potassium iodide, she underwent subtotal thyroidectomy, and delivered a 2350 g infant at 38 weeks' gestation, which was less than the normal birth weight of 2400 g. MPO-ANCA is considered to be one reason of low birth weight infant including hyperthyroidism. It is necessary to consider the appearance of the possibility of MPO-ANCA positive vasculitis in patients who are treated with PTU.

Adult↗
PubMed1978

Effect of active and passive immunization with TRH on plasma TSH response to propylthiouracil.

The role of thyrotropin-releasing hormone (TRH) in the secretion of TSH from the anterior pituitary was investigated in rats by active and passive immunization with TRH. The plasma TSH response to propylthiouracil (PTU) in TRH-bovine serum albumin (BSA)-immunized rats was significantly lower than that of BSA-immunized or non-immunized rats. Similarly, the increased plasma TSH level following PTU treatment was significantly suppressed after iv injection of antiserum to TRH. However, the decline in plasma TSH levels was not complete. The results of the present study indicate, at least in part, the physiological significance of endogenous TRH in the regulation of pituitary TSH secretion.

Animals↗
PubMed1980

Effect of propylthiouracil on nycthemeral and sex related variation of plasma TSH in rats.

Studies of the effect on feedback mechanisms in nycthemeral fluctuation of plasma TSH and of its sex-related variation were carried out on normally fed (Purina) and propylthiouracil (PTU) treated rats. Plasma TSH concentration of purina fed rat was significantly higher in males than in females (M = 96 +/- 14, F = 49 +/- 3 microunits/ml, P less than 0.01). Plasma T4 concentration also showed a high tendency in males compared to females (M = 7.4 +/- 0.5, F = 5.8 +/- 1.0 micrograms/dl, 0.05 less than P less than 0.1) but the statistical difference was not significant. Plasma TSH demonstrated a typical periodicity characterized by a zenith at 1200 hr and a nadir at 1800 hr as in the previous reports. Plasma TSH concentrations rose apparently after the diet was switched to the one containing 0.15% of PTU. On the other hand, plasma T4 concentrations decreased to the very low levels following PTU administration. Concerning to the nycthemeral fluctuation and its sex related variation following PTU administration, nycthemeral fluctuation in male rats disappeared rapidly, whereas it was preserved in female rats. These facts showed that it kept more persistent fluctuation in female rats than in male rats under the high plasma TSH levels. Furthermore, female rats showed higher concentration of plasma TSH after PTU treatment compared to male rats. These results suggest that the nycthemeral fluctuation of plasma TSH was abolished or masked by the feedback mechanism of hypothalamo-pituitary-thyroid axis and there was a sex-related difference.

Animals↗
PubMed1983

Studies on the T3 suppression test by the 24-hour thyroidal 131I uptake in patients with Graves' disease: comparison of the effects of propylthiouracil and methylmercaptoimidazole.

The T3 suppression test by the 24-hr thyroidal 131I uptake was reevaluated in patients with Graves' disease before and after withdrawal of antithyroid drug. Fifty patients had been treated with propylthiouracil (PTU) or methylmercaptoimidazole (MMI) for 12 to 70 months. They were prescribed a maintenance dose of antithyroid drug (PTU, 50 mg/day; MMI, 5 mg/day) at the time of investigation and regarded as euthyroid on the basis of serum T3, T4 and TSH levels. Each patient was given 75 micrograms T3 daily for 8 days in conjunction with PTU or MMI. The 24-hr thyroidal 131I uptake was then measured (post T3 uptake). In 30 patients whose post T3 uptake was below 35%, treatment was stopped and the T3 suppression test was repeated at one and 3 months later. During the two-year follow up, 24 remained well, while 6 relapsed within 4 to 12 months. In patients with sustained remission, the post T3 uptake was significantly lower in the MMI-treated group (13 cases, 7.7 +/- 1.0%) than in the PTU-treated group (11 cases, 18.6 +/- 1.9%). MMI withdrawal produced a marked rebound in the post T3 uptake, whereas none of the patients showed the rebound after PTU withdrawal. In patients who relapsed later, there was no difference in the post T3 uptake during treatment and the rebound occurred in the both groups following goitrogen withdrawal. Serum T3, T4 and TSH levels were within normal ranges at one and 3 months after cessation of antithyroid drug. From the results of the present study, it is concluded that criteria for T3 suppressibility by the 24-hr uptake should be determined by the antithyroid drug employed and by the time of investigation. There is a dissociation in the post T3 uptake values following withdrawal of the two different antithyroid drugs.

Antithyroid Agents↗
PubMed1975

Role of growth hormone in the enhancement of the propylthiouracil-induced goitrogenesis by small doses of thyroxine.

The potentiation of the propylthiouracil (PTU)-induced goitrogenesis after chronic administration of small doses of thyroid hormone has been attributed to the high circulating level of thyrotrophin (TSH) or to the re-instatement of insulin. In re-examining this problem radioimmunoassayable concentrations of TSH, thyroxine (T4), insulin, and growth hormone (GH) were observed in sera of rats at sequential intervals after surgical or chemical thyroidectomy and after thyroidectomy and replacement therapy with GH or T4. In addition, TSH, GH or a combination of both hormones were injected into hypophysectomized recipients in a further attempt to delineate the effect of either hormone on the thyroid. As expected, the rate of body growth was inversely proportional to the apparent severity of the hypothyroidism achieved in the several experimental groups. Goitrogenesis was enhanced after T4 treatment but evidently was not the exclusive result of increased blood levels of TSH or insulin. Evidence is presented that suggest the enhancement of goitrogenesis may be a growth phenomenon involving the additive or synergistic action of GH and TSH and possible of other hormones.

Animals↗
PubMed1975

Binding of the 35-s of 35-s-propylthiouracil by follicular thyroglobulin in vivo and in vitro.

Radioactivity was found bound to follicular thyroglobulin after administration of 35-S-propylthiouracil (PTU) to rats. Denaturation of the thyroglobulin using various procedures could not separate the 35-S from the protein; it was concluded that the 35-S is bound to thyroglobulin covalently. Fractionation of saline-soluble thyroid proteins was performed by ultracentrifugation on sucrose gradients. The PTU-sulphur/thyroglobulin (S/Tg) molar ratio was calculated in all fractions. One hour after the injection of PTU the S/Tg molar ratio was the same for 19S thyroglobulin from rats on stock diet and 18S thyroglobulin from rats on low iodine diet. Injection of KI to the animals before administration of 35-S-PTU significantly reduced the ratio. The highest S/Tg ratio 1.10 was noted at 19S thyroglobulin, 17 h after a single injection of PTU. Daily injection of PTU for six days increased the S/Tg ratio to 3.3. Inverse relationship between dose of PTU and S/Tg ratio was noted at one hour. In animals injected with large dose of 35-S-PTU and sacrificed several hours later the S/Tg was higher at the 12S subunits than at the 19S protein. The amount of PTU bound to 3-8S subunits was minimal. Sulphite liberated 64 percent of the 35-S bound to thyroglobulin which appeared as four compounds on thin layer chromatography plates. The main 35-S compound liberated by sulphite was sulphate.

Animals↗
PubMed1977

Divergent effects of 6-propylthiouracil on 3,3',5'-triiodothyronine (RT3) serum levels and in man.

The effect of 6-propylthiouracil (PTU) on the peripheral conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3 rT3) was investigated by assessments of the concentrations of T4 T3 and rT3 in peripheral venous blood from T4-treated healthy volunteers given PTU, 4 X 150 mg daily. Within on day of PTU administration, serum T3 concentrations were reduced, and those of rT3 enhanced. These deviations lasted as long as PTU was given (five days), and there was a rapid return towards normal within one day after PTU administration ceased. It seems probable that, in man, PTU can evoke a diversion of T4 monodeiodination, less being converted to the metabolically active T3 and more to the metabolically inactive rT3. It is ppossible that the rapidity whereby PTU can reduce T3 levels can offer an advantage in the treatment of hyperthyroidism.

Female↗
PubMed1978

Extrathyroidal effects of propylthiouracil and carbimazole on serum T4, T3, reverse T3 and TRH-induced TSH-release in man.

A possible extrathyroidal effect of propylthiouracil (PTU) and carbimazole on serum levels of thyroxine (T4), triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3) and on thyrotrophin-releasing hormone (TRH) induced thyrotrophin (TSH) release was estimated in 19 patients with severe hypothyroidism treated with T4. During PTU medication a significant decrease in serum T3 from 90 +/- 16 (SD) to 79 +/- 23 ng/100 ml (P less than 0.01) and a reciprocal increase in serum reverse T3 from 51 +/- 14 (SD) to 58 +/- 20 ng/100 ml (P less than 0.025) were found. No significant changes in serum T4, basal serum TSH or response to TRH could be demonstrated. Carbimazole did not change any of the parameters studied.

Adult↗
PubMed1979

Effects of methylmercaptoimidazole (MMI), propylthiouracil (PTU), potassium perchlorate (KClO4) and potassium iodide (KI) on the serum concentrations of thyrotrophin (TSH) and thyroid hormones in the rat.

Male Sprague-Dawley rats were given graded doses of methylmercaptoimidazole (MMI), propylthiouracil (PTU), KClO4 or KI in drinking water for 4 days, or the lowest effective dose of each drug for various times. The rats were sacrificed at 1--2 p.m. and serum T3, T4 and TSH concentrations were measured by radioimmunoassays. It was found that administration of 5 mg/l of MMI, 10 mg/l of PTU and 100 mg/l of KClO4 for 4--14 days induced a transient rise in serum TSH and a fall in serum T3 or T4 or in both. The effects of KI were not consistent. In another series of experiments, PTU (10 mg/l) was given in drinking water for 4 days, and then graded doses of T3 or T4 were given iv, or 100 ng of TRH was injected into a tail vein, or the animals were exposed to 4 degrees C for 30 min. The initial high TSH levels were further increased by TRH and cold and decreased by T3 and T4. The PTU-treated animals had goitres after 4 days. We infer that low doses, that is to say 10--100 times lower than previously described, of antithyroid drugs induce a hypothyroidism characterized by an increased TSH level and a decreased serum T3 or T4 level or both. A 4 days' treatment with PTU (40 mg/l in tap water) is a suitable tool for studying the effect of various conditions on TSH secretion.

Animals↗
PubMed1980

Effects of propylthiouracil and relatively small doses of iodide on early phase treatment of hyperthyroidism.

In order to compare the acute effects of three methods of treatment in hyperthyroid patients with diffuse goitre, values of thyroxine (T4), triiodothyronine (T3) in serum, T3-resin uptake (T3-U), free thyroxine index (FT4I) and free triiodothyronine index (FT3I) were employed as thyroid function parameters. In iodide (I-) group given iodine (3 or 6 mg/day) as iodinated lecithine once daily, the parameters were reduced acutely within one week after the start of treatment, reaching a plateau during the next week. In contrast to the changes in I- group, the thyroid function was decreased gradually and consistently for two weeks in the propylthiouracil (PTU 300 mg/day) group. In PT1+I- (300 mg/PTU plus 3 or 6 mg/iodide/day) group, the parameters were reduced acutely and progressively for two weeks. These results indicate that PTU+I- therapy is much more effective than PTU or I- alone in early phase treatment of hyperthyroidism. Another new finding was that the thyroid function increased again during the later addition of PTU (300 mg/day) in the patients treated with I- (3 or 6 mg/day) for one or two weeks. The well-known escape phenomenon from iodide inhibition took place counteracted the effect of PTU. Since blocking of thyroidal secretion by I- is only transient while synthesis of T3 and T4 continues, leading to greater amount of hormone stored in the gland, the treatment of hyperthyroidism with I- alone is a risky procedure.

Adolescent↗
PubMed1982

A prospective study of the differential changes in serum thyroglobulin and its autoantibodies during propylthiouracil or radioiodine therapy of patients with Graves' disease.

Measurement of serum thyroglobulin (Tg) and its autoantibody (TgAb) by radioimmunological methods was performed in 48 patients with Graves' disease during treatment with radioiodine (n = 16) or propylthiouracil (PTU) (n = 32). Twenty-five of the 48 patients were TgAb positive, their sera being inaccessible to measurement of serum Tg. TgAb showed only minor changes during PTU treatment, whereas TgAb fell rapidly after radioiodine, in 5 of 16 patients to unmeasurable levels, followed by a secondary rise to 4.5 times pre-treatment level after 20 weeks. Serum Tg showed a steady increase during the first weeks after radioiodine treatment, but fell to lower levels after one year. PTU caused only minor changes in the serum Tg concentration. There was no shift in molecular sizes of either Tg or TgAb during the course of the treatments. Five of 16 131I-treated patients developed myxoedema, 4 of whom were TgAb positive. Another 3 patients had high increases in TgAb without myxoedema. Six of 18 patients had relapse of thyrotoxicosis after withdrawal of PTU-treatment. There was no significant difference in serum concentrations of TgAb or Tg between those developing relapse and those remaining in remission, and it is concluded that serum Tg is a poor predictor of relapse in medically treated thyrotoxicosis.

Adult↗