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PubMed1997

Acute effects of propylthiouracil on hemodynamics and oxygen content in patients with alcoholic cirrhosis.

BACKGROUND/AIMS: The antithyroid drug propylthiouracil has been suggested for the treatment of alcoholic liver disease. Its beneficial effects could be due to either a decrease in hepatic oxygen consumption or an increase in hepatic blood flow. The aim of this study was to test these two hypotheses in patients with proven alcoholic cirrhosis. METHODS: The pharmacokinetic parameters after intravenous administration of 300 mg of propylthiouracyl were first determined in four patients. Then, the effects on systemic and splanchnic hemodynamics, and oxygen content were measured 45 and 90 min after the intravenous administration of 300 mg (n=6) or 600 mg (n=6) of propylthiouracil. RESULTS: Systemic hemodynamics (heart rate, arterial pressure, cardiac output and systemic vascular resistance) and splanchnic hemodynamics (hepatic venous pressure gradient, hepatic and azygos blood flows) were not modified 45 and 90 min after the administration of 300 mg or 600 mg of propylthiouracil. Moreover, neither oxygen content in the radial artery, pulmonary artery or hepatic vein, nor systemic oxygen uptake was modified after propylthiouracyl administration. The absence of effect of propylthiouracyl administration was also confirmed in patients with cirrhosis with proven acute alcoholic hepatitis (n=7). CONCLUSIONS: In patients with alcoholic cirrhosis, acute administration of propylthiouracyl has no effect on systemic and splanchnic hemodynamics or on oxygen contents. The presence of acute alcoholic hepatitis does not modify these results.

Adult↗
PubMed2002

Determination of propylthiouracil using 1,3-dibromo-5,5-dimethylhydantoin (DBH): analytical methods of pharmacopeias with DBH in respect to environmental and economical concern: part 9.

USP 2000 [The United States Pharmacopeia, Rockville USA, 24th ed., 2000, pp. 1436] and PH. EUR. 1997 [European Pharmacopoeia, third ed., Council of Europe, Strasbourg, 1997, p. 1401] determine propylthiouracil using neutralization titration, whereby 0.1 M silver nitrate and twice boiling is necessary. With the application of 1,3-dibromo-5,5-dimethylhydantoin (DBH), the assay of propylthiouracil can be performed easily, faster and friendlier to environment. A mean deviation of 0.03% and a relative standard deviation of 0.3% are obtained. 5-Bromo-6-propyluracil is formed, when propylthiouracil is determined with DBH.

Antithyroid Agents↗
PubMed2001

Treatment of acrodermatitis continua of Hallopeau with oral propylthiouracil and methotrexate.

A 71-year-old man with acrodermatitis continua of Hallopeau was treated successfully with a combination of oral propylthiouracil and methotrexate. After 14 weeks, he developed acute pancytopenia, an uncommon idiosyncratic side-effect of propylthiouracil, and presented with a life-threatening methicillin-resistant Staphylococcus aureus pneumonia. This illustrates the potential value and associated risks of propylthiouracil in the management of this difficult condition.

Acrodermatitis↗
PubMed2004

Propylthiouracil and carbimazole associated-antineutrophil cytoplasmic antibodies (ANCA) in patients with Graves' disease.

OBJECTIVE: Propylthiouracil treatment of Graves' disease has been postulated to provoke antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. We aimed to investigate whether carbimazole therapy was also associated with increased risk of ANCA. DESIGN: The occurrence of ANCA and the relationship to thionamide treatment was investigated in a cross-sectional study in a consecutive series of 407 patients' with Graves' disease, 200 with Hashimoto's thyroiditis and 649 normal euthyroid subjects. MEASUREMENTS: ANCA was measured by indirect immunofluorescence (IIF) and enzyme-linked immunosorbent assay (ELISA) for proteinase 3 and myeloperoxidase-ANCA. RESULTS: The prevalence of ANCA, as measured by IIF, was increased in the Graves' disease cohort (19.9%) compared with euthyroid controls (4.6%; P < 0.001). The prevalence of MPO-ANCA (measured by ELISA) was also increased in Graves' disease (P = 0.019). ANCA prevalence was more strongly associated with propylthiouracil treatment than carbimazole (P = 0.0265), although risk of ANCA was also higher in Graves' patients treated with carbimazole than controls (RR 2.2, P < 0.0001). ANCA positivity was not increased in patients with Hashimoto's thyroiditis. CONCLUSION: This study revealed a high prevalence of ANCA in treated patients with Graves' disease but not in those with Hashimoto's thyroiditis. Furthermore, within the Graves' disease population, ANCA development was associated with propylthiouracil usage to a greater extent than carbimazole. These findings suggest that the altered immune environment associated with autoimmune thyroid disease is not sufficient to develop ANCA but treatment with thionamides is important in promoting ANCA development.

Adult↗
PubMed2005

Propylthiouracil attenuates acetaminophen-induced renal damage in the rat.

BACKGROUND: To date, there is no specific antidote to acetaminophen poisoning. Propylthiouracil (PTU) has been shown to be protective against acetaminophen (APAP)-induced liver damage in rats; however, the nephroprotective effect of propylthiouracil has not been studied yet. METHODS: In order to verify this, rats were given different doses of PTU (100, 200 or 400 mg/kg per body weight, orally) 1 h before a nephrotoxic dose of APAP (1,000 mg/kg per body weight, intraperitoneally (i.p.)). RESULTS: Propylthiouracil pretreatment significantly reduced APAP-induced nephrotoxicity in a dose-dependant manner, as evidenced by reduction in plasma creatinine and by amelioration of renal pathology (interstitial congestion, tubular cell degeneration and necrosis). CONCLUSION: The mechanism of protection by PTU is probably not due to the sparing effect of non-protein thiol (approximately 95% of which is reduced glutathione), as similar depletion of renal glutathione was observed regardless of PTU pretreatment; other mechanisms are suggested.

Acetaminophen↗
PubMed1981

Hepatic microsomal ethanol-oxidizing system (MEOS): increased activity following propylthiouracil administration.

Treatment for 7 days with the thyreostatic drug propylthiouracil (5 mg/100 g of body weight) resulted in a hypothyroid hepatic state as shown by the marked decreased hepatic content of thyroxine and triiodothyronine. This regimen led to an enchanced activity of the microsomal ethanol-oxidizing system, whereas the activities of alcohol dehydrogenase and catalase remained unchanged. Moreover, a hyperthyroid hepatic state achieved following the daily administration of L-thyroxine (150 micrograms/100 g of body weight) or L-3,3', 5-triiodothyronine (10 micrograms/100 g body weight) for 7 days resulted in a similar increased activity of the microsomal ethanol-oxidizing system. Under these conditions, a decrease of alcohol dehydrogenase activity and an unaffected catalase activity was observed. These findings, therefore, show that the administration of either propylthiouracil or thyroid hormones results in an increased activity of the microsomal ethanol-oxidizing system, suggesting that the underlying mechanism for the induction of the microsomal ethanol-oxidizing system by propylthiouracil is independent of the action of thyroid hormones.

Alcohol Oxidoreductases↗
PubMedDate not supplied

Leukocytoclastic vasculitis: a rare manifestation of propylthiouracil hypersensitivity.

OBJECTIVE: We report a case of leukocytoclastic vasculitis as a manifestation of propylthiouracil hypersensitivity. CLINICAL PRESENTATION AND INTERVENTION: A 66-year-old woman with a history of a toxic adenoma was referred for evaluation of a purpuric rash on the legs and buttocks bilaterally. She was biochemically hyperthyroid. Biopsy of the skin lesions revealed leukocytoclastic vasculitis. Propylthiouracil therapy was discontinued, and methimazole started. The purpuric rash resolved and surgical treatment for toxic adenoma resulted in euthyroid state. CONCLUSION: This report indicated that leukocytoclastic vasculitis should be considered in the differential diagnosis of patients with a vasculitic rash. The discontinuation of the propylthiouracil was associated with disappearance of the lesions.

Adenoma↗
PubMed1996

Antineutrophil cytoplasmic antibodies (ANCA)-associated crescentic glomerulonephritis and propylthiouracil therapy.

Cutaneous vasculitis is an uncommon complication of propylthiouracil therapy. Although its pathogenesis remains to be established, detection of antineutrophil cytoplasmic antibodies (ANCA) in association with this type of vasculitis has recently been described. We report here 2 patients who developed ANCA-associated crescentic glomerulonephritis without evidence of cutaneous vasculitis during propylthiouracil treatment of hyperthyroidism. Improvement of the renal function and the disappearance of ANCA were correlately found after discontinuation of propylthiouracil and by corticosteroid therapy in both patients.

Adult↗
PubMed1981

Hyperthyroidism and propylthiouracil-induced agranulocytosis during chronic lithium carbonate therapy.

The authors describe the case of a 49-year-old woman who developed a goiter, mild symptoms of hyperthyroidism, and grossly elevated thyroid function tests after 2 years of treatment with lithium carbonate. Thyroid microsomal autoantibodies were also present. She was retreated with propylthiouracil and improved, but within 3 months she developed agranulocytosis. Propylthiouracil was discontinued, and the patient was treated with antibiotics and recovered. She was then given 131I to control her hyperthyroidism. The case is an example of the rare association of hyperthyroidism with lithium, which usually suppresses thyroid function, and demonstrates that lithium carbonate cannot prevent agranulocytosis caused by propylthiouracil.

Agranulocytosis↗
PubMed1980

Influence of cholera toxin on in vitro refractoriness to thyrotropin of thyroids from rats fed propylthiouracil.

Using an increase in the concentration of cAMP as an index of stimulation, we previously reported that in vitro thyroid tissue of rats fed a goitrogenic diet (0.1% propylthiouracil in Purina) were unresponsive to TSH. We now show that the addition of cholera toxin (0.1-1.0 microM) to fragments of normal thyroid enhanced the concentration of cAMP. Subsequent exposure of the tissue to TSH resulted in a further increase in the concentration of cAMP, and there was statistical evidence of interaction or potentiation between the effects of TSH (20 mU/ml) and cholera toxin (1.0 microM). With fragments of thyroid from animals fed propylthiouracil (i.e. unresponsive in vitro to TSH), an increase in the concentration of cAMP was effected by 1 or 9 microM cholera toxin, and prior exposure to 9 microM toxin caused the tissue to be responsive to TSH. Unresponsiveness of the goitrous tissue was associated with a reduced capacity of the membrane to bind [125I]iodo-TSH although the affinity of the binding sites was unaffected. Cholera toxin at 0.1 microM enhanced and at 1 microM diminished the binding of [125I]iodo-TSH to membranes from either normal or goitrous glands, and these effects also reflected influences on the capacity rather than on the affinity of the binding sites. It is postulated that the unresponsiveness to TSH of thyroid tissue from rats fed propylthiouracil represents a down-regulation of receptor capacity, and this is effected by the binding sites becoming relatively inaccessible, rather than nonexistent.

Adenylyl Cyclases↗
PubMed1992

Propylthiouracil-induced hypersensitivity vasculitis presenting as respiratory failure.

Hypersensitivity vasculitis associated with propylthiouracil therapy is a well-documented clinical entity. Although any organ system may be involved, it is most unusual for pulmonary manifestations to be the cardinal presenting features. We report a 72-year-old woman presenting with respiratory failure and hemoptysis following initiation of propylthiouracil therapy for Graves' disease. She had cutaneous stigmata of hypersensitivity vasculitis and diffuse pulmonary infiltrates. The infiltrates improved dramatically after discontinuation of the propylthiouracil therapy and initiation of intravenous corticosteroid therapy.

Aged↗
PubMed2003

Thyroid over-expression of type 1 and type 2 deiodinase may account for the syndrome of low thyroxine and increasing triiodothyronine during propylthiouracil treatment.

Although propylthiouracil inhibits type 1 deiodinase, leading to a more rapid fall in triiodothyronine (T(3)) than thyroxine (T(4)) levels in patients treated for hyperthyroidism, we report a patient with Graves' disease whose free T(3) paradoxically rose during such treatment, despite low free T(4) levels and increasing doses of propylthiouracil. A similar response has previously been associated with high levels of thyroid stimulating antibodies, but it has been unclear why there should be a dichotomy in the circulating thyroid hormone profile. Thyroid tIssue from our patient contained very high levels of type 1 and, especially, type 2 deiodinase, in contrast to other patients treated with Graves' disease, which were most likely secondary to high levels of thyroid stimulating antibodies. This unusual response to propylthiouracil is important to recognise therapeutically, and represents a further situation in which abnormal expression of deiodinase enzymes has clinical significance.

Adult↗
PubMed2006

[Antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis associated to the use of propylthiouracil. Report of four cases].

Antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis is an uncommon complication of the use of propylthiouracil. When it occurs, it affects multiple organs as any systemic vasculitis. We report three females and one male, aged 30, 40, 43 and 41 years respectively, that after a lapse of 12 to 28 months of propylthiouracil use, presented clinical signs of vasculitis. All had high titers of ANCA against myeloperoxidase. In three patients, a skin biopsy confirmed the diagnosis. The condition subsided when propylthiouracil was discontinued, but one female patient required the use of prednisone.

Adult↗
PubMedDate not supplied

Leukocytoclastic vasculitis: a rare manifestation of propylthiouracil allergy.

OBJECTIVE: To report a case of leukocytoclastic vasculitis as a manifestation of propylthiouracil allergy. METHODS: We present the history, findings on physical examination, and results of laboratory evaluation in a 25-year-old woman. Associated reports from the literature are reviewed. RESULTS: The patient, with a history of Graves' disease, was referred for evaluation of a purpuric rash on the pinnas and buttocks bilaterally. Findings included exophthalmos and bilateral goiter with neck bruits. She was biochemically hyperthyroid. Biopsy of the skin lesions revealed leukocytoclastic vasculitis. Propylthiouracil therapy was discontinued, and prednisone was prescribed. Treatment with radioactive iodine resulted in appreciably diminished skin lesions and reduction in the size of the thyroid gland, but thyroxine and triiodothyronine levels increased. Administration of a second, higher dose of radioactive iodine with concomitant lithium carbonate resulted in clinical and biochemical improvement. Six months after initial assessment, the rash had resolved, and the patient's free thyroxine value had normalized, although the thyrotropin level was still suppressed. CONCLUSION: Leukocytoclastic vasculitis, although rarely seen as a manifestation of propylthiouracil allergy, has been reported in the medical literature and should be considered in the differential diagnosis of patients with a vasculitic rash. Treatment consists of discontinuation of the offending medication and administration of a corticosteroid and, occasionally, cyclophosphamide or plasmapheresis.

Adult↗
PubMedDate not supplied

Propylthiouracil-induced perinuclear-staining antineutrophil cytoplasmic autoantibody-positive vasculitis in conjunction with pericarditis.

OBJECTIVE: To describe a case of propylthiouracil-induced vasculitis manifesting with pericarditis. METHODS: We present the first case report of a woman with hyperthyroidism treated with propylthiouracil in whom a syndrome of pericarditis, fever, and glomerulonephritis developed. Serologic testing and immunologic studies were done, and a pericardial biopsy was performed. RESULTS: A 25-year-old woman with Graves' disease had a febrile illness and evidence of pericarditis, which was confirmed by biopsy. Serologic evaluation revealed the presence of perinuclear-staining antineutrophil cytoplasmic autoantibodies (pANCA) against myeloperoxidase (MPO). Propylthiouracil therapy was withdrawn, and she was treated with a 1-month course of prednisone, which alleviated her symptoms. A literature review revealed no prior reports of pericarditis in anti-MPO pANCA-positive vasculitis associated with propylthio- uracil therapy. CONCLUSION: Pericarditis may be the initial manifestation of drug-induced vasculitis attributable to propylthio- uracil therapy.

Adult↗
PubMed2003

Kinetic-spectrophotometric determination of propylthiouracil based on its inhibitory effect on the reduction of neutral red by hypophosphite.

A new kinetic-spectrophotometric method for determination of propylthiouracil (PTU) is described. The proposed method is simple, rapid, inexpensive and sensitive for the determination of PTU in pure and tablet forms. This method is based on the inhibitory effect of propylthiouracil on the palladium(II)-catalyzed reaction between neutral red and hypophosphite ions. The effect of various parameters such as: dye, hypophosphite, and Pd(II) concentrations, pH, ionic strength, and temperature were optimized. Two distinct linear calibration graphs were observed in the ranges 0.006-0.033 (n = 6, r = 0.9991) and 0.033-0.300 ppm (n = 10, r = 0.9980). The variable time method was used. The limit of detection was 0.004 ppm. The proposed method was applied for the determination of propylthiouracil in pure and tablet forms.

Calibration↗
PubMed2005

[Anti neutrophil cytoplasmatic antibodies-positive vasculitis as a complication of hyperthyreosis treatment with propylthiouracil].

This paper describes a patient treated for 12 months with propylthiouracil for multinodular toxic goiter who developed vasculitis. The clinical picture consisted of nasal septal necrosis, pulmonary infiltrations and skin rash. Patient's serum were positive for anti neutrophil cytoplasmatic antibodies (c-ANCA). Histopathological examination revealed the presence of small vessel vasculitis without granuloma formation. This condition resulted in patient's critical state with respiratory failure and severe cardiovascular complications. The article also contains a brief review of available literature concerning this very rare complication. Conclusion. Propylthiouracil, a widely-used medicine, can cause severe life-threatening complication. It is associated with propylthiouracil-induced immunological disturbances.

Anti-Inflammatory Agents↗
PubMed1984

Propylthiouracil-induced diffuse interstitial pneumonitis.

Cough productive of sputum, exertional dyspnea, and hypoxemia developed in two patients with Graves' disease after six months (patient 1) or three weeks (patient 2) of treatment with propylthiouracil, 300 mg/day. Chest roentgenograms and transbronchial lung biopsy specimens revealed diffuse interstitial pneumonitis. Lymphocyte transformation by phytohemagglutinin was highly stimulated by propylthiouracil. Symptoms and signs improved after cessation of the drug therapy and administration of prednisolone acetate. These cases represent the first report of a complication of diffuse interstitial pneumonitis induced by propylthiouracil.

Aged↗