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PubMed2004

Serum TNF-alpha in psoriasis after treatment with propylthiouracil, an antithyroid thioureylene.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) and its receptors play important roles in the development and persistence of psoriatic plaques. The antithyroid thioureylenes, propylthiouracil and methimazole, are effective in the treatment of patients with psoriasis with a significant number of patients showing clearing or near clearing of their lesions after a several weeks of treatment. METHODS: The present study examined the effect of treatment with propylthiouracil, given in a dose of 100 mg every 8 hours for 3 months, on the serum levels of TNF-alpha in 9 patients with plaque psoriasis. RESULTS: Propylthiouracil therapy did not result in a significant decline in serum TNF-alpha concentrations. CONCLUSIONS: The findings suggest that the therapeutic effect of propylthiouracil in psoriasis appears not to be related to any change in the concentration of TNF-alpha but occurs via an anti-proliferative mechanism as we have previously speculated.

Adult↗
PubMedDate not supplied

[Acute cholestatic hepatitis induced by propylthiouracil. Case report].

Propylthiouracil is widely used to treat patients with hyperthyroidism. However, propylthiouracil-induced hepatitis is an uncommon entity. The case of a 15-year-old boy treated with propylthiouracil for hyperthyroidism who developed a cholestatic acute hepatitis is reported. Viral, metabolic and autoimmune liver diseases were excluded and liver biopsy showed a pattern suggestive of drug-induced cholestatic hepatitis. After discontinuing the drug, there was a progressive resolution of symptoms and normalization of liver biochemical tests. Despite its rarity, patients receiving propylthiouracil are exposed to develop severe hepatotoxicity.

Acute Disease↗
PubMed2002

Clinical features and outcomes in children with antineutrophil cytoplasmic autoantibody-positive glomerulonephritis associated with propylthiouracil treatment.

A retrospective investigation was conducted by members of the Japanese Society for Pediatric Nephrology from 1990 to 1997 to define the clinical features and outcomes in children with antineutrophil cytoplasmic autoantibody (ANCA)-positive glomerulonephritis associated with propylthiouracil treatment. Seven Japanese pediatric patients who had myeloperoxidase-specific ANCA-positive biopsy-proven pauci-immune necrotizing crescentic glomerulonephritis associated with propylthiouracil administration were entered in the study. Three patients had nephritis alone, and four had nephritis and extrarenal organ system vasculitis. Females predominated, and the mean age at onset was 14 yr. Propylthiouracil was reduced or discontinued in all patients and was switched to methimazole in three patients. For the treatment of nephritis, five patients received corticosteroids; three had pulse methylprednisolone, one had plasma exchange, and one had plasma exchange and pulse methylprednisolone before initiating oral prednisolone. The remaining two patients received cyclophosphamide and corticosteroids, one of whom had pulse methylprednisolone before initiating oral prednisolone and cyclophosphamide. All patients achieved remission. In general, ANCA titers correlated with the response to treatment and disease activity, with some exceptions. No patient progressed to end-stage renal disease, renal dysfunction, or death during the follow-up period (58 +/- 25 mo; range, 32 to 108 mo). All but one patient remained euthyroid. In conclusion, this experience suggests that the clinical disease spectrum of ANCA-positive disease associated with propylthiouracil treatment is similar in pediatric and adult patients and that the overall prognosis may be better than that in the non-drug-induced ANCA-positive disease.

Adolescent↗
PubMed1999

[Relapsing polychondritis developing in a patient with Graves' disease: a possible association with propylthiouracil].

A 31-year-old woman presented 1993 with fever, painful swelling of cartilaginous portions of the ears and the bridge of nose, polyarthralgia including costochondroral pains, and episcleritis. She has been taking propylthiouracil since 1991 when she was diagnosed as Graves' disease. Laboratory evaluations revealed an elevated erythrocyte sedimentation rate (ESR) of 133 mm/h, a high CRP level of 13.2 mg/dl and positive antinuclear antibodies and anti-type II collagen antibodies. Histopathological findings of the biopsy specimen from the auricular cartilage included chondrocyte degeneration, matrix destruction and inflammatory cell infiltration. She was diagnosed as RP and treatment with 30 mg/day of prednisolone dramatically improved all symptoms and signs, accompanied by a fall in ESR, CRP and autoantibodies. When prednisolone was tapered to 5 mg/day, a clinical relapse occurred. After discontinuation of propylthiouracil, she has been well without prednisolone. Propylthiouracil-induced SLE-like syndrome or antineutrophil cytoplasmic antibodies (ANCA) related angitis has been reported previously. In addition, recent studies demonstrated that about 20% of sera from patients with relapsing polychondritis are P-ANCA positive. This is the first report suggesting a possible association between the development of relapsing polychondritis and propylthiouracil.

Adult↗
PubMed1976

An increase of liver uptake of thyroxine, an initial step of an increased fecal loss of thyroxine in response to propylthiouracil in rats.

Propylthiouracil augmented fecal loss of thyroxine (T4), but methimazole was without effect in this respect in rats. In vitro uptake of labeled T4 by the liver was significantly enhanced by a small amount of propylthiouracil in the presence of dilute rat plasma. Methimazole was without effect under comparable conditions. In contrast, propylthiouracil and methimazole failed to affect in vitro uptake of labeled T4 by the kidney and diaphragm in the presence of dilute rat plasma. Since deiodination of T4 does not occur in the presence of dilute rat plasma, it is suggested that propylthiouracil specifically stimulates liver uptake of T4 as an initial step of an increase of biliary-fecal excretion of T4 in rats.

Animals↗
PubMed1976

Fulminant hepatitis and lymphocyte sensitization due to propylthiouracil.

Fulminant hepatic failure developed in a 24-year-old black woman who had been treated with propylthiouracil and propranolol for hyperthyroidism. Clinical and biochemical recovery followed discontinuation of drug therapy. Liver biopsy disclosed submassive hepatic necrosis. During the acute phase of the disease, lymphocyte transformation studies revealed sensitization of the patient's lymphocytes to propylthiouracil but not to propranolol. Sensitization remained demonstrable 2 months after cessation of the former drug. Lymphocytes obtained from a hyperthyroid patient treated with propylthiouracil without complications failed to show evidence of sensitization. These observations indicate that submassive hepatic necrosis may result from treatment with propylthiouracil and are consistent with the notion that sensitization mechanisms may be responsible for the hepatic injury induced by this drug.

Adult↗
PubMed1991

Treatment of supraventricular tachyarrhythmias associated with hyperthyroidism by radioiodine, amiodarone and propylthiouracil.

Beta-blockers and calcium antagonists have been advocated for thyrotoxicosis induced tachyarrhythmias. Amiodarone is generally considered as contraindicated because of its high iodine content. Since amiodarone combined with propylthiouracil induced a greater fall in serum thyroid hormone concentrations than propylthiouracil alone, we treated 2 hyperthyroid patients with supraventricular arrhythmias by radioiodine (day 0) followed after 24 h by amiodarone and propylthiouracil. Serum T3 was normalized on day 2 (patient 1) and 3 (patient 2). Effective t1/2 of intrathyroidal 131I were 6.6 and 4.3 days (versus 5.9 days for 131I given alone). In patient 1, atrial fibrillation, reverted to sinus rhythm after verapamil and digoxin, and did not recur. In patient 2, conversion of atrial fibrillation to sinus rhythm occurred on day 11; from day 0 to day 11, ventricular rate decreased and was significantly correlated to T3 (r = 0.82; p < 0.05). In conclusion, amiodarone may be beneficial in thyrotoxicosis associated tachyarrhythmias, given with propylthiouracil 24 h after radioiodine, it did not decrease thyroid irradiation and rapidly decreased serum T3.

Adult↗
PubMed1991

[Propylthiouracil in therapy of alcohol-induced liver damage?].

Propylthiouracil (Propycil Thyreostat) is presently being used in hyperthyroidism, thyroidectomy, and other diseases affecting thyroid gland metabolism. Canadian clinicians have published interesting reports showing that propylthiouracil can be used to successfully treat alcohol-induced liver damage. In two clinical trials (approximately 340 patients) it was shown that long-term treatment with propylthiouracil was associated with a significantly more favorable prognosis in cirrhosis of the liver and with a reduction in mortality. Preclinical studies suggest that alcohol abuse leads to a hypermetabolic status of the liver, which is similar to hyperthyroidism. The results of these studies suggest a rationale for the use of propylthiouracil in alcohol-induced liver cirrhosis.

Energy Metabolism↗
PubMed1979

Propylthiouracil and hepatitis: a case report.

A 10-year-old girl initially presented with clinical features and thyroid function tests consistent with hyperthyroidism. She was treated with propylthiouracil, 100 mg, three times a day. She developed jaundice and hepatitis following treatment with propylthiouracil for 40 days. Clinical features of hepatitis improved after the discontinuation of propylthiouracil and she became euthyroid. At this time, an immunofluorescent technique revealed antibodies consistent with autoimmune thyroiditis. From this report, it appears that hepatitis is one of the infrequent complications of treatment with propylthiouracil and transient hyperthyroidism may be associated with autoimmune thyroiditis.

Chemical and Drug Induced Liver Injury↗
PubMed1983

Pharmacokinetics of propylthiouracil in children and adolescents with Graves disease after a single oral dose.

Pharmacokinetics of propylthiouracil after a single oral dose were studied in six pediatric patients with Graves disease, with respect to influence of food intake. Propylthiouracil administration in the fasting state induced a rapid rise of plasma level reaching a peak of 30 to 60 min. Peak values ranged from 7.2 to 18 micrograms/ml with administered dose (100 to 280 mg/m2 BSA) and plasma half-life was 1.3 +/- 0.41 hr (mean +/- SD). Single compartment model with first order absorption showed excellent fit to the data obtained in the fasting state, but not in the fed state. Most individuals showed marked difference in the pattern of propylthiouracil concentration-time curves between the fasting and the fed state. Food intake prior to the drug ingestion was associated with lower and delayed peak and variable AUC values. These results indicate that propylthiouracil administration in the fasting state is more advisable for obtaining a consistent bioavailability.

Administration, Oral↗
PubMed1982

Double-blind, controlled trial of propylthiouracil in patients with severe acute alcoholic hepatitis.

Sixty-seven patients entered a double-blind, controlled trial to evaluate the efficacy of propylthiouracil treatment in severe alcoholic hepatitis. Twenty-three percent (7 of 31) given propylthiouracil and 19% (7 of 36) given placebo died during the 6-wk study. Propylthiouracil treatment did not reduce the frequency and incidence of complications in alcoholic hepatitis, but induced hypothyroidism in 4 patients. Treatment produced no beneficial effect on any of the hepatic biochemical tests. We were unable to show any beneficial effect of propylthiouracil treatment on morbidity and mortality in patients with severe acute alcoholic hepatitis.

Adult↗
PubMed1997

Case of propylthiouracil-induced vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA); review of literature.

A 39-year-old Japanese woman had been receiving propylthiouracil for 5 years for hyperthyroidism when she developed myalgia, scleritis, proteinuria, fever, and inflammation of the nose. Examination of a renal biopsy specimen showed focal segmental necrotizing glomerulonephritis. Indirect immunofluorescent staining showed a highly positive perinuclear pattern of anti-neutrophil cytoplasmic antibody (ANCA) in her serum. Enzyme-linked immunosorbent assay (ELISA) of the ANCA showed positivity for anti-proteinase 3, anti-myeloperoxidase, anti-leukocyte elastase, and anti-lactoferrin, but anti-cathepsin G and anti-lysozyme were negative. Because ELISA showed the titer of anti-leukocyte elastase antibody to be markedly elevated, we challenged this data by performing dot blot analysis. The patient's serum reacted with the native form, but not with denatured leukocyte elastase. Propylthiouracil-induced vasculitis was suspected. Symptoms abated within 2 weeks and all values of ANCA were reduced after the drug was withdrawn. Vasculitis is a rare side-effect of propylthiouracil therapy. Recently it was reported in association with ANCA. We present the findings of this patient and compare them with those described in 19 published cases of propylthiouracil-induced vasculitis associated with ANCA.

Adult↗
PubMedDate not supplied

An antineutrophil cytoplasmic autoantibody associated with a propylthiouracil-induced adult respiratory distress-like syndrome: report of a case and review of the literature.

OBJECTIVE: To report the first case of propylthiouracil-induced adult respiratory distress-like syndrome associated with the presence of an antineutrophil cytoplasmic autoantibody. METHODS: We describe the initial manifestations, laboratory findings, and clinical course in a patient and discuss underlying factors potentially contributing to her condition. RESULTS: A 57-year-old woman with hyperthyroidism had an influenza-like illness and vasculitis during propylthiouracil therapy. Three days after she was admitted to the hospital, an adult respiratory distress-like syndrome developed. Results of perinuclear antineutrophil cytoplasmic antibody (pANCA) and antimyeloperoxidase antibody studies were positive. Her condition improved after the introduction of glucocorticoid therapy and the withdrawal of propylthiouracil treatment. The pANCA level, however, remained unchanged 3 months after her dismissal from the hospital. CONCLUSION: The propylthiouracil-induced adult respiratory distress-like syndrome may be a hypersensitivity phenomenon, and the presence of the pANCA could be a marker of a common mechanism of injury that stimulates its production rather than a pathogenic factor responsible for vascular injury in our patient.

Journal Article↗
PubMed1980

Propylthiouracil-induced cutaneous vasculitis. Case presentation and review of the literature.

A patient had cutaneous vasculitis, leukopenia, and splenomegaly caused by the antithyroid drug, propylthiouracil. Histopathologic changes of acute vasculitis of the superficial and deep dermal blood vessels accompanied by fibrin thrombi formation were found in biopsy specimens of the cutaneous lesions. Direct immunofluorescence studies demonstrated IgM and C3 of the vessel walls suggesting immune complex deposition. The literature disclosed five cases with similar features associated with propylthiouracil therapy. Characteristic cutaneous findings include a recurrent, self-limited, symmetrical purpuric eruption that can involve the face or earlobes. Clinicians should recognize these changes as a cutaneous sign of a vasculitis associated with propylthiouracil therapy.

Adult↗
PubMed2005

Fulminant hepatic failure associated with propylthiouracil: a case report with treatment emphasis on the use of plasmapheresis.

Propylthiouracil is a commonly used medication for hyperthyroidism. Though propylthiouracil-induced hepatotoxicity is a rarely encountered problem, death due to fulminant hepatic failure may occur. In the English literature, only 34 cases have been described with severe hepatotoxicity secondary to this drug. Here we report a case of fulminant hepatic failure due to propylthiouracil and review the issues of treatment and management with special emphasis on the use of plasmapheresis in such situations.

Adult↗
PubMed1992

Intellectual capacity of subjects exposed to methimazole or propylthiouracil in utero.

Antithyroid drugs, considered the treatment of choice for hyperthyroidism during pregnancy, may have an adverse effect on intellectual development of the offspring. We examined the intellectual capacity of 31 subjects aged 4-23 years, born to women with Graves disease who received antithyroid drugs throughout pregnancy. Methimazole 40-140 mg/week (n = 15) or propylthiouracil 250-1400 mg/week (n = 16) was given. I.Q. was assessed using the Wechsler test appropriate for age. Twenty-five unexposed siblings served as controls. The exposed and unexposed groups did not differ with respect to the total I.Q. Both groups scored equally in verbal and performance skills and in each of six main subcategories of the tests. There was no difference between exposure to methimazole and propylthiouracil or between the higher (greater than 40 mg/week and greater than 600 mg/week, respectively) and lower dosages. All children were euthyroid at birth and none had goitre. We conclude that exposure to methimazole or propylthiouracil during pregnancy in doses sufficient to control maternal hyperthyroidism does not pose any threat to intellectual capacity of the offspring.

Adolescent↗
PubMed1991

Evaluation of the antioxidant properties of thyroid hormones and propylthiouracil in the brain-homogenate autoxidation system and in the free radical-mediated oxidation of erythrocyte membranes.

The antioxidant capacity of thyroid hormones and the antithyroid drug propylthiouracil was studied in three model systems, namely, autoxidation of rat brain homogenates and oxidation of rat erythrocyte plasma membranes (EPM) induced by either 2,2'-azobis-(2-amidinopropane) (AAP) thermolysis or by gamma irradiation. Thyroid hormones significantly inhibited the development of lipid peroxidation in these systems at micromolar concentrations, as assessed either by visible light emission, thiobarbituric acid reactive substances accumulation or oxygen uptake. This behaviour was not observed when L-3,3',5-triiodothyronine (T3) and L-thyroxine (T4) were assayed at nanomolar concentrations. In EPM exposed to AAP or gamma irradiation, propylthiouracil inhibited the induced lipid peroxidation, with Q1/2 values of 112-150 microM. It is concluded that the antioxidant capacity of thyroid hormones found in vitro may not be of relevance in physiological conditions, which exhibit variations of T3 and T4 levels in the nanomolar range. On the other hand, the behaviour of propylthiouracil as an inhibitor of EPM lipid peroxidation is observed at concentrations close to the therapeutic levels, thus representing a possible complementary action to its antithyroid activity.

Animals↗
PubMed1989

Induction of experimental thyroid dysfunction in rats with implantable pellets of thyroxine or propylthiouracil.

Subcutaneously implanted pellets containing the thyroid hormone thyroxine or the thyrotoxic agent propylthiouracil were used to induce hyper- or hypothyroidism in rats. The results obtained were compared to those produced by daily subcutaneous injection of these substances. The thyroxine pellets caused substantial elevation of serum thyroxine concentrations for at least 25 days, whereas the propylthiouracil pellets caused a pronounced decrease of serum thyroxine concentrations. Changes in heart weight and rectal temperature were consistent with the observed alterations of serum thyroxine concentrations. Treatment with propylthiouracil was associated with small elevations of serum total protein, urea nitrogen, and creatine concentrations regardless of the method of administration of this agent. It is concluded that implantable pellets are an effective and convenient means of administering drugs for producing thyroid dysfunction in rats.

Animals↗