Should a woman taking propylthiouracil breast-feed?
Thyroid function was tested in mother and her son. The mother was taking propylthiouracil for treatment of hyperthyroidism, and she was breast-feeding. Thyroid function was normal in both.
Adult↗
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Scintigraphic study of propylthiouracil induced submassive hepatic necrosis.
Drug induced hepatitis is a rare complication of thiourea antithyroid drugs. In some patients, the hepatotoxicity may be severe and lead to submassive hepatic necrosis (SHN). Submassive hepatic necrosis is a potentially fatal complication which is usually recognized on the liver biopsy and histological examination or autopsy. In the case presented here, SHN was identified on Tc-99m SC liver images. Sharply defined intrahepatic photopenic abnormalities without significant colloid shift were noted. SPECT images were most remarkable and exhibited extensive liver necrosis. Resolution of hepatic abnormalities correlated with clinical and biochemical resolution of SHN. In patients with propylthiouracil hepatotoxicity, serial liver SPECT images with Tc-99m SC appear helpful for the diagnosis and follow up of SHN and, in an appropriate clinical context, may obviate the need for liver biopsy.
Adult↗
Time interval between the last dose of propylthiouracil and I-131 therapy influences cure rates in hyperthyroidism caused by Graves' disease.
PURPOSE: To examine the effects of propylthiouracil (PTU) pretreatment on the outcome of initial I-131 therapy for Graves' disease. DESIGN: A retrospective chart review was done. PATIENTS AND METHODS: The authors studied 106 patients in an outpatient nuclear medicine setting who were given initial I-131 therapy for Graves' disease from September 1989 to March 1993 and followed for at least 6 months after therapy. These patients were divided into groups based on whether they had ever received PTU or, if they had received PTU, the length of time between the last dose of PTU and the I-131 therapy dose. Measured failure rates of initial I-131 therapy were based on recurrent or continued hyperthyroidism. RESULTS: Treatment failure rates increased markedly from 2.5% in non-PTU-treated patients (n = 80) to 23.1% (n = 26) in patients pretreated with PTU (P = 0.003). Although not significant, two PTU-pretreated subgroups showed a trend toward increased failure rates. The failure rate was 15.4% (n = 13) in patients whose last dose of PTU was 7-14 days before I-131 therapy, and it increased further to 30.8% (n = 13) in patients whose last dose of PTU was within 1 week of I-131 therapy. CONCLUSIONS: PTU pretreatment within 2 weeks of I-131 treatment is a strong independent risk factor in failure rates after initial I-131 therapy in patients with Graves' disease. Patients should be free of PTU for 2 weeks before I-131 therapy if they are able to tolerate it, otherwise the dose of I-131 may need to be adjusted upward to diminish the risk that the initial I-131 therapy will fail.
Adult↗
Severe hepatotoxicity on beginning propylthiouracil therapy.
We report a case of propylthiouracil (PTU)-induced cholestatic hepatotoxicity in Graves' disease that developed 1 day after beginning PTU. After clinical recover, liver abnormalities persisted for 5 years. Percutaneous liver biopsy and the eventual normalization of enzyme levels excluded permanent liver damage as a result of PTU therapy. Thus prolonged elevation of serum enzymes is consistent with the diagnosis of PTU-induced hepatotoxicity, which may recover completely.
Antithyroid Agents↗
Bioavailability of propylthiouracil: Interindividual variation and influence of food intake.
The bioavailability of 6-propylthiouracil (PTU) has been examined in eight healthy volunteers, with respect to interindividual variation and influence of food intake. PTU was given as a single oral dose, both in a fasting state and together with a standardized breakfast. Numerous venous blood samples were taken during 5 hours after PTU ingestion, and the concentration of unmetabolized PTU in serum was determined by a specific gas-chromatographic technique. The observations indicate that the amount of PTU absorbed is subject to a large interindividual variation, and that concomitant food intake may exert a minor and non-systematic influence on PTU absorption. Hence, the major issue in PTU therapy is the individualization of the size and interval of dosage. Testing of single-dose PTU kinetics in patients would apparently be helpful.
Administration, Oral↗
Serum protein binding of propylthiouracil.
Serum protein binding of propylthiouracil (PTU) was measured by ultrafiltration in healthy and hyperthyroid patients. The serum protein binding in 12 euthyroid subjects was 76.2 +/- 1.2% (mean +/- s.d.), not significantly different from the values in 10 hyperthyroid patients: 76.6 +/- 1.3% Binding was unaffected by incubation time and temperatures between 25 and 37 degrees C, but increased from 76.5 to 79.1% when pH changed from 7.4 to 7.9. PTU is predominantly bound to albumin with two classes of binding groups with different number of binding sites and affinity. Displacement experiments showed interaction with acetylsalicylic acid, warfarin and phenylbutazone, but not with antipyrine and nortriptyline or other basic drugs.
Adult↗
Agranulocytosis induced by propylthiouracil: evidence of a drug dependent antibody reacting with granulocytes, monocytes and haematopoietic progenitor cells.
A patient with agranulocytosis and myeloid marrow hypoplasia following a second exposure to propylthiouracil (PTU) was studied for antibodies against mature blood cells and bone marrow precursor cells. During the acute phase of the agranulocytosis, significant growth inhibition of the myeloid committed progenitor cells (CFU-GM) was found following incubation with complement, indicating the presence of in-vivo cell bound cytotoxic antibodies. Using immunofluorescence and complement dependent cytotoxicity techniques it was demonstrated that acute phase and recovery phase sera contained circulating antibodies, reactive not only with differentiated granulocytes and monocytes but also with myeloid and erythroid (BFU-E/CFU-E) progenitor cells. Complement dependent lysis of the progenitor cells was facilitated by preincubation with PTU. These results indicate that the agranulocytosis was mediated by a PTU dependent antibody that affected both mature blood cells and bone precursor cells.
Aged↗
Anti-myeloperoxidase antibodies in sera from patients with propylthiouracil-induced vasculitis might recognize restricted epitopes on myeloperoxidase molecule.
Myeloperoxidase (MPO) is one of the major target antigens of antineutrophil cytoplasmic antibodies (ANCA) in primary systemic vasculitis. It is known that propylthiouracil (PTU) could induce MPO-ANCA-positive vasculitis. The production of anti-MPO antibodies in patients with PTU-induced vasculitis may be different from that in patients with primary microscopic polyangiitis (MPA). One possible reason for this may be differences in epitope recognition. The aim of this study is to compare the epitopes of antibodies to MPO in sera from patients with PTU-induced vasculitis (n = 10) and MPA (n = 10). The sera were collected and used to inhibit monoclonal antibodies against human MPO (3D8 and 6B9) and affinity purified, horseradish peroxidase conjugated human anti-MPO antibodies (Pab1-HRP, Pab2-HRP) in a competitive inhibition enzyme-linked immunosorbent assay (ELISA) system using soluble human MPO as solid phase ligand. The Pab1-HRP and Pab2-HRP were affinity purified from plasma exchanges of a patient with PTU-induced vasculitis and a patient with MPA, respectively. The inhibition rates were evaluated and compared between the PTU and primary MPA groups. In the PTU group all 10 sera could inhibit 3D8: the average inhibition rate was 44.7% +/- 5.0%; 9/10 sera could inhibit 6B9: the average inhibition rate was 35.6% +/- 6.0%. However, in the MPA group all 10 sera could inhibit 3D8 and 6B9; the average inhibition rates were 68.4% +/- 16.1% (P < 0.01) and 62.2% +/- 17.2% (P < 0.01), respectively. Sera in both the PTU and MPA groups could inhibit Pab1-HRP and the inhibition rates were 81.4% +/- 9.4%versus 86.6% +/- 17.2% (P > 0.05). However, the average inhibition rate for Pab2-HRP in the MPA group was significantly higher than that in the PTU group (76.3% +/- 7.8%versus 58.9% +/- 15.5%, P < 0.01). We conclude that anti-MPO antibodies from patients with PTU-induced vasculitis and from patients with primary MPA could recognize more than one epitope on the native MPO molecule. Although the epitopes overlapped between the two groups, the epitopes of anti-MPO antibodies from patients with PTU-induced vasculitis might be more restricted.
Adult↗
Anti-endothelial cell antibodies (AECA) in patients with propylthiouracil (PTU)-induced ANCA positive vasculitis are associated with disease activity.
Increasing evidence has demonstrated that propylthiouracil (PTU) could induce ANCA positive vasculitis. However, our previous work has suggested that only one-fifth of the PTU-induced ANCA positive patients had clinical vasculitis and so the mechanism is not clear. Anti-endothelial cell antibodies (AECA) have been implicated in the pathogenesis of various vasculitides, including primary ANCA positive systemic vasculitis. The purpose of this study is to investigate the prevalence of AECA and their possible role in the pathogenesis of patients with PTU-induced ANCA positive vasculitis. Sera from 11 patients with PTU-induced ANCA positive vasculitis at both active and quiescent phases, and sera from 10 patients with PTU-induced ANCA but without clinical vasculitis, were studied. Sera from 30 healthy blood donors were collected as normal controls. Soluble proteins from 1% Triton-100 extracted in vitro cultured human umbilical vein endothelial cells were used as antigens and an immunoblotting technique was performed to determine the presence of AECA, and their specific target antigens were identified. In patients with PTU-induced ANCA positive vasculitis, 10 of the 11 patients in an active phase of disease were serum IgG-AECA positive and six protein bands of endothelial antigens could be blotted (61 kD, 69 kD, 77 kD, 85 kD, 91 kD and 97 kD). However, in the quiescent phase, seven of the 10 positive sera turned negative. None of the ANCA positive but vasculitis negative patients or normal controls were AECA positive. In conclusion, AECA could be found in sera from patients with PTU-induced ANCA positive vasculitis and were associated more closely with vasculitic disease activity.
Adolescent↗
Titre and affinity of propylthiouracil-induced anti-myeloperoxidase antibodies are closely associated with the development of clinical vasculitis.
Substantial evidences suggested that propylthiouracil (PTU) could induced anti-myeloperoxidase (MPO) antibodies in sera from patients with hyperthyroidism, however, only a subgroup of the PTU-induced anti-MPO antibody positive patients developed clinical evident vasculitis. The aim of this study is to compare the titres and affinities of PTU induced anti-MPO antibodies in sera from patients with hyperthyroidism with and without clinical vasculitis. Anti-MPO antibody positive sera from patients diagnosed hyperthyroidism with (n = 13) and without (n = 14) clinical evident vasculitis were collected. The titre was determined by MPO-ELISA and expressed as logarithm value (lgT). The affinity constant (aK) of anti-MPO IgG was measured by antigen inhibition assay. The titre and aK values were compared between patients with and without vasculitis. In patients with vasculitis, the mean lgT of anti-MPO antibodies was 3.62 +/- 0.66; the median aK was 4.47 x 10(7)M(-1). In patients without vasculitis, the mean lgT was 2.54 +/- 0.29; the median aK was 0.14 x 10(7)M(-1), and both were significant lower than those in patients with vasculitis (t = 5.464; P = 0.000 & z = -4.373; P = 0.000, respectively). We concluded that the titre and affinity of anti-MPO antibodies might be associated with the development of clinical vasculitis in patients with PTU-induced ANCA.
Adolescent↗
Influence of treatment with radioiodine and propylthiouracil on thyroid stimulating immunoglobulins in Graves' disease.
Thyroid stimulating immunoglobulins (TSAb) were measured in fifty-four patients with Graves' disease before treatment with either radioiodine (seventeen patients) or propylthiouracil (PTU) (thirty-seven patients), and followed during treatment. After radioiodine TSAb increased to levels exceeding pretreatment values, and became detectable in three of six originally TSAb negative patients. In most patients TSAb decreased during treatment with PTU, and became undetectable after a mean of 12 months in patients above 40 years, and after a mean of 6 months in patients below 40 years. In order to eliminate the presumed causative agent in Graves' disease, antithyroid treatment should be at least 18 months in patients above 40 years, and at least 12 months in patients below 40 years of age. In twenty-nine patients TSAb were measured at cessation of 2 years antithyroid drug therapy. Ten patients were TSAb positive and all except one relapsed. Five of nineteen TSAb negative patients relapsed. Although TSAb positivity predict relapse, it is not an ideal index of prognosis after antithyroid therapy.
Adult↗
The effect of amiodarone on the control of hyperthyroidism by propylthiouracil.
We studied the efficacy of amiodarone (800, 600, 400 and 200 mg orally daily during weeks 1, 2, 3 and 4, respectively) plus propylthiouracil (PTU, 100 mg orally every 8 h) in comparison to PTU alone in the early treatment (28 days) of Graves' disease patients. Circulating T3 and T4 decreased earlier and more markedly in the amiodarone plus PTU-treated group. An initial rise of circulating rT3 above the base-line value followed by a gradual decline was observed in the former group while only a decline below the base-line values was observed in the latter group. The resting pulse rate decreased and body weight increased significantly in the amiodarone plus PTU-treated group. In the PTU-treated group, significant weight gain was observed later in the course of treatment while no significant reduction in pulse rate was observed. No major side-effects of amiodarone were observed during the course of treatment. This study suggested that the combination of amiodarone and PTU was more efficacious than PTU alone in reducing circulating T3, T4 and clinical hyperthyroidism early in the course of treatment of patients with Graves' disease. This regimen has an additional potential advantage because of the antiarrhythmic property of amiodarone, especially in situations when a beta-blocker is contraindicated.
Adult↗
Comparison of single daily dose of methimazole and propylthiouracil in the treatment of Graves' hyperthyroidism.
OBJECTIVE: The present study was to compare the efficacy of a single daily dose of methimazole (MMI) and propylthiouracil (PTU) in the treatment of Graves' hyperthyroidism. BACKGROUND: Antithyroid drugs, MMI and PTU, are widely used in the treatment of hyperthyroidism. Previous studies in the treatment of hyperthyroidism with a single daily dose of antithyroid drugs have demonstrated a more favourable result with MMI. However, the efficacy of a single daily dose of PTU was inconsistent. In this study, we examined the therapeutic efficacy of single daily doses of MMI and PTU on the change of thyroid hormones and thyrotropin receptor antibodies (TRAb) levels. METHODS: Thirty patients with newly diagnosed Graves' hyperthyroidism were randomly divided into two groups, each receiving a single dose of either 15 mg MMI or 150 mg PTU daily for 12 weeks. The therapeutic efficacy was determined by serum total triiodothyronine (TT3), total thyroxine (TT4), thyrotropin (TSH), free thyroxine (FT4), and TRAb levels at baseline and at the end of 4, 8 and 12 weeks during the study period. RESULTS: There was no significant difference in baseline thyroid function parameters. Serum TT3, TT4 and FT4 levels in the MMI-treated group were significantly lower than those of the PTU-treated group after 4 weeks and through the end of the study. MMI also has superior effect on reducing serum TRAb levels than PTU after 8 weeks and at the end of the study. CONCLUSION: During the 12-week treatment of Graves' hyperthyroidism, a single daily dose of 15 mg MMI was much more effective in the induction of euthyroidism than a single daily dose of 150 mg PTU. In the doses used in this study, MMI is preferable to PTU when a once-daily regimen of antithyroid drug is considered for the treatment of Graves' hyperthyroidism.
Adolescent↗
The effect of combination therapy with propylthiouracil and cholestyramine in the treatment of Graves' hyperthyroidism.
OBJECTIVE: The study aims to evaluate the efficacy of combination therapy with propylthiouracil (PTU) and cholestyramine in the treatment of Graves' hyperthyroidism. BACKGROUND: Thyroxine (T4) is metabolized mainly in the liver by conjugation to glucuronides and sulphates that enter the enterohepatic circulation. Thyrotoxic patients have an abnormal increase in thyroid hormone in their enterohepatic circulation. Previous studies on combination therapy with methimazole and cholestyramine for Graves' hyperthyroidism have shown it to be an effective adjunctive treatment. In this study, we examined the efficacy of combination therapy with PTU and cholestyramine in the treatment of Graves' hyperthyroidism. METHODS: Thirty patients with newly diagnosed Graves' hyperthyroidism were randomly divided into two groups: group I (n = 15) received PTU 100 mg twice a day, propranolol 40 mg twice a day and cholestyramine 4 g twice a day for 4 weeks; group II (n = 15) received PTU 100 mg twice a day and propranolol 40 mg twice a day for 4 weeks. The therapeutic efficacy was determined by serum total triiodothyronine (TT3), free thyroxine (FT4) and TRAb levels at baseline, and at the end of 2 and 4 weeks during the study period. RESULTS: There was no significant difference in baseline thyroid function parameters. At the end of 2 and 4 weeks of the study period, serum TT3 and FT4 levels of group I were significantly lower than those of group II. No significant differences in the TRAb level were found between the two groups. CONCLUSION: Cholestyramine contributed to a more rapid and complete decline in thyroid hormone levels in patients with Graves' hyperthyroidism. It was thus proved to be an effective and well-tolerated adjunctive therapy.
Adolescent↗
Effect of hyperthyroidism and propylthiouracil treatment on liver biochemical tests.
Liver biochemical test (LBT) changes can be commonly observed in hyperthyroid patients. Those kinds of changes could also be observed because of propylthiouracil (PTU) therapy. We prospectively evaluated LBT changes because of PTU use for 1 year in patients who had been diagnosed with hyperthyroidism first. We studied 64 patients who had been diagnosed with hyperthyroidism. These patients took at least 1-year PTU treatment. We analysed LBT at diagnosis and after 2 and 12 months of treatment with PTU. Prior to PTU treatment, 30 (46.8%) of the 64 patients had at least one LBT abnormality. We observed at least one LBT abnormality in 11 (32%) patients after 2 months and nine (26%) patients after 12 months of treatment with PTU in 34 patients whose CBT were normal before treatment. We did not observe any deterioration in clinical picture and bilirubin levels. Elevated serum LBT during the pretreatment and PTU treatment period is common and usually transient and asymptomatic. PTU could be used for long times by lowering the dose and close follow-up in patients who have elevated LBT during the pretreatment and after PTU treatment period.
Adult↗
Propylthiouracil-associated liver failure presenting as probable autoimmune hepatitis in a child with Graves' disease.
This case describes a young girl with Graves' disease, who presented with fulminant hepatic failure 9 months into propylthiouracil (PTU) therapy. Her clinical presentation was consistent with 'probable autoimmune hepatitis,' as defined by the International Autoimmune Hepatitis Group scoring system. Despite discontinuation of PTU and high-dose steroid therapy, she required liver transplantation. Subsequent pathology could not definitively rule out autoimmune hepatitis. PTU is an important cause of drug-related liver failure in children, and clinicians should be mindful that it is frequently used in patients who already have an underlying risk of autoimmune liver disease.
Antithyroid Agents↗
Antineutrophil cytoplasmic antibody-positive crescentic glomerulonephritis associated with propylthiouracil therapy.
A teenage girl with crescentic glomerulonephritis had antineutrophil cytoplasmic antibody (ANCA) detected after she had received propylthiouracil (PTU) for hyperthyroidism without cutaneous vasculitis. ANCA was detected on admission; renal biopsy showed crescentic glomerulonephritis with focal necrotizing glomerulonephritis but no immune deposits. Administration of steroid and decreasing the dose of PTU produced a good clinical response and the ANCA disappeared. It was concluded that ANCA is closely related to the pathogenesis of crescentic glomerulonephritis and that treatment with PTU appeared to induce ANCA.
Adolescent↗
Amiodarone-induced hyperthyroidism: assessment of the predictive value of biochemical testing and response to combined therapy using propylthiouracil and potassium perchlorate.
In order to assess the value of thyroid function testing during amiodarone therapy, we reviewed all available tests in 128 patients treated with this drug. Nine patients (7.0%) developed biochemical hyperthyroidism with elevation of both free thyroxine index (FT4I) and free triiodothyronine index (FT3I) and marked suppression of serum thyroid stimulating hormone (TSH) after 1-46 months of therapy; six of these nine patients had clear clinical evidence of thyroid overactivity. Where serial tests were available before development of hyperthyroidism, this complication developed suddenly, despite previously stable normal indices of thyroid function, and could not be predicted by currently-available biochemical tests such as T4, T3, sensitive TSH, thyroglobulin or sex hormone binding globulin (SHBG) assays. Clinical features such as unexplained weight loss, proximal myopathy, exacerbation of arrhythmia, or heat intolerance appear to be the key to prompt diagnosis of this complication. Hyperthyroxinemia without T3 excess was found in 32.8% of patients without progression to true hyperthyroidism. Serum TSH remained detectable by sensitive assay in 17 out of 18 patients with amiodarone-induced euthyroid hyperthyroxinemia and was significantly higher than in patients with equivalent hyperthyroxinemia due to thyroxine therapy. Serial levels of SHBG were higher in patients with true hyperthyroidism than in those with euthyroid hyperthyroxinemia. The effect of combined treatment with propylthiouracil (800 mg/day) and potassium perchlorate (800 mg/day) was evaluated in five of the six clinically hyperthyroid patients. Biochemical euthyroidism was achieved after 7-19 weeks, a response slower than previously reported, indicating that this drug combination does not result uniformly in prompt resolution of amiodarone-induced hyperthyroidism.
Adolescent↗