propylthiouracil has been researched along with Syndrome* in 16 studies
3 review(s) available for propylthiouracil and Syndrome
Article | Year |
---|---|
[Syndrome of arthritis by antithyroid drugs].
Topics: Adult; Antithyroid Agents; Arthritis; Female; Graves Disease; Humans; Methimazole; Propylthiouracil; Syndrome | 2003 |
The thyroid gland 1998: new ideas about an ancient structure.
Topics: Female; Graves Disease; Humans; Hypothyroidism; Immunosuppressive Agents; Male; Methimazole; Mutation; Propylthiouracil; Receptors, Thyrotropin; Syndrome; Thyroid Gland; Thyroid Hormones | 1999 |
Hypokalaemic thyrotoxic periodic paralysis: case report and review of an Oriental syndrome.
Presentations of acute systemic weakness are rare and appear dramatic and frightening to both patients and physicians. Aetiologies are multifactorial and diverse. Morbidity and mortality are associated with the unrecognized disease. One of the underlying disorders is hypokalaemic thyrotoxic periodic paralysis (HTPP), an uncommon disorder. HTPP is characterized by periodic occurrences of muscle weakness during attacks of hyperthyroidism and appears predominantly in Orientals. This article describes a patient of Chinese origin with hyperthyroidism and attacks of paralysis and considers several problems: a lack of familiarity with the syndrome, increasing numbers of patients with this disease in European hospitals as a result of migration of populations, and the importance of patient compliance in therapeutic management. Finally, a review of the literature concerning presentation, differential diagnosis, pathophysiology, and therapeutic management is provided. Topics: Adrenergic beta-Antagonists; Adult; Anti-Inflammatory Agents; Antithyroid Agents; Humans; Hypokalemia; Male; Paralysis; Potassium Chloride; Prednisolone; Propranolol; Propylthiouracil; Syndrome; Thyrotoxicosis | 1996 |
13 other study(ies) available for propylthiouracil and Syndrome
Article | Year |
---|---|
Importance of low serum DNase I activity and polyspecific anti-neutrophil cytoplasmic antibodies in propylthiouracil-induced lupus-like syndrome.
To study the role of deoxyribonuclease (DNase) I activity and ANCA in propylthiouracil (PTU)-induced lupus-like syndrome (LLS).. We compared 36 SLE patients with 17 PTU-induced LLS patients diagnosed from 2008 to 2014. We studied ANCA profile (MPO, PR3, lactoferrin, CTG, elastase, bactericidal/permeability-increasing protein), anti-dsDNA, anti-ENA, anti-nucleosome, anti-histone, anti-C1q, anti-aCL, complement components, cryoglobulins and serum DNase I activity. Healthy persons and patients without LLS treated with PTU comprised the control groups. Twelve LLS patients were serologically and clinically followed for 4.1 (S.D. 2.0) years.. PTU-induced LLS patients less frequently had arthritis, renal and neurological manifestations, but more frequently had fever, purpura, urticarial-like vasculitis and ulceration (P < 0.01). PTU-induced LLS patients more frequently had polyspecific ANCA (anti-MPO, anti-elastase and anti-PR3 were most commonly detected) (P < 0.01). SLE patients more frequently had anti-dsDNA, anti-ENA, anti-nucleosome, anti-C1q (P < 0.01) and anti-histone antibodies (P < 0.05). PTU-induced LLS patients had lower DNase I activity than SLE patients and controls (P < 0.01). Discontinuation of PTU increased DNase I activity, although it did not reach the levels of controls (P < 0.01). After remission, MPO-ANCA decreased (P < 0.01), but persisted for a long time.. PTU, as a trigger, and low DNase I activity, as a predisposing factor, may lead to LLS. Polyspecific ANCAs are useful markers for differentiating SLE from PTU-induced LLS. Low DNase I activity might be an important prognostic biomarker for PTU-induced LLS. Monitoring of ANCA and DNase I activity may prevent long-lasting exposure to causal drugs, unnecessary immunosuppressive therapy and severe complications of LLS. Topics: Adolescent; Adult; Aged; Antibodies, Antineutrophil Cytoplasmic; Antithyroid Agents; Biomarkers; Case-Control Studies; Deoxyribonucleases; Female; Humans; Hyperthyroidism; Lupus Erythematosus, Systemic; Male; Middle Aged; Prevalence; Prognosis; Propylthiouracil; Retrospective Studies; Syndrome; Young Adult | 2015 |
Tubulointerstitial nephritis and uveitis syndrome complicated by IgA nephropathy and Graves' disease: a case report.
Tubulointerstitial nephritis and uveitis syndrome is a disorder characterized by a combination of acute tubulointerstitial nephritis and uveitis. Immunoglobulin A nephropathy is defined by the presence of immunoglobulin A deposits in glomerular mesangial areas. In this report, we describe a rare case of tubulointerstitial nephritis and uveitis syndrome complicated by immunoglobulin A nephropathy and Graves' disease, which was successfully treated with corticosteroids. To the best of our knowledge, this is the first time such a case has been documented since tubulointerstitial nephritis and uveitis syndrome was first described.. A 64-year-old Japanese woman presented with tubulointerstitial nephritis and uveitis syndrome accompanied by immunoglobulin A nephropathy and Graves' disease. She had renal dysfunction, proteinuria, and hematuria. Two weeks after her admission, she developed anterior chamber uveitis. She received corticosteroids, resulting in significant clinical improvement.. Tubulointerstitial nephritis and uveitis syndrome is a relatively uncommon cause of tubulointerstitial nephritis. Clinicians should recognize that tubulointerstitial nephritis and uveitis syndrome with immunoglobulin A nephropathy can occur in the presence of Graves' disease. Additionally, this report may provide important clues in terms of the management of a concomitant case of these diseases. Topics: Antithyroid Agents; Biopsy; Female; Glomerulonephritis, IGA; Glucocorticoids; Graves Disease; Humans; Kidney; Methylprednisolone; Middle Aged; Nephritis, Interstitial; Prednisolone; Propylthiouracil; Syndrome; Treatment Outcome; Uveitis | 2014 |
Propylthiouracil-induced DRESS syndrome confirmed by a positive patch test.
Topics: Adrenal Cortex Hormones; Adrenergic beta-Antagonists; Adult; Anti-Inflammatory Agents; Antithyroid Agents; Drug Hypersensitivity; Eosinophilia; Exanthema; Female; Humans; Patch Tests; Postpartum Thyroiditis; Propranolol; Propylthiouracil; Syndrome | 2010 |
Beneficial effects of propylthiouracil plus L-thyroxine treatment in a patient with a mutation in MCT8.
Mutations of the monocarboxylate transporter 8 (MCT8) gene determine a distinct X-linked phenotype of severe psychomotor retardation and consistently elevated T(3) levels. Lack of MCT8 transport of T(3) in neurons could explain the neurological phenotype.. Our objective was to determine whether the high T(3) levels could also contribute to some critical features observed in these patients.. A 16-yr-old boy with severe psychomotor retardation and hypotonia was hospitalized for malnutrition (body weight = 25 kg) and delayed puberty. He had tachycardia (104 beats/min), high SHBG level (261 nmol/liter), and elevated serum free T(3) (FT(3)) level (11.3 pmol/liter), without FT(4) and TSH abnormalities. A missense mutation of the MCT8 gene was present. Oral overfeeding was unsuccessful. The therapeutic effect of propylthiouracil (PTU) and then PTU plus levothyroxine (LT(4)) was tested. After PTU (200 mg/d), serum FT(4) was undetectable, FT(3) was reduced (3.1 pmol/liter) with high TSH levels (50.1 mU/liter). Serum SHBG levels were reduced (72 nmol/liter). While PTU prescription was continued, high LT(4) doses (100 microg/d) were needed to normalize serum TSH levels (3.18 mU/liter). At that time, serum FT(4) was normal (16.4 pmol/liter), and FT(3) was slightly high (6.6 pmol/liter). Tachycardia was abated (84 beats/min), weight gain was 3 kg in 1 yr, and SHBG was 102 nmol/liter.. 1) When thyroid hormone production was reduced by PTU, high doses of LT(4) (3.7 microg/kg.d) were needed to normalize serum TSH, confirming that mutation of MCT8 is a cause of resistance to thyroid hormone. 2) High T(3) levels might exhibit some deleterious effects on adipose, hepatic, and cardiac levels. 3) PTU plus LT(4) could be an effective therapy to reduce general adverse features, unfortunately without benefit on the psychomotor retardation. Topics: Adolescent; Antithyroid Agents; Humans; Intellectual Disability; Male; Monocarboxylic Acid Transporters; Muscle Hypotonia; Mutation, Missense; Propylthiouracil; Puberty, Delayed; Symporters; Syndrome; Tachycardia; Thyroid Hormone Resistance Syndrome; Thyroid Hormones; Thyroxine; Treatment Outcome | 2008 |
Hyper- or hypothyroidism: its association with the development of ascites syndrome in fast-growing chickens.
The ascites syndrome in broiler chickens is attributed to the progress in genetic selection for rapid growth, coupled with the metabolic burden imposed by exposure to a relatively low-ambient temperature (T(a)). The syndrome is mainly characterized by hematocrit elevation, decline in blood oxygen saturation, accumulation of fluid in the abdominal cavity, and finally, death. Ascitic chickens have demonstrated hypothyroidism coupled with a marked stress response (high corticosterone concentration) and reduction in the hemoglobin content. The objective of the present study was to examine the role of thyroid and corticosterone hormones in the development of the syndrome. Ascites was induced by exposure to a gradually declining T(a) and supplementation of a pellet-form diet. Exogenous thyroxin (T(4)) and propylthiouracil (PTU) (in Experiments 1 and 2, respectively) were supplemented in drinking water to induce hyper- or hypothyroidism, respectively. Ascites syndrome was developed in 21.5% and 23% of the birds exposed to ascites-induced conditions (Exps. 1 and 2, respectively). Excess T(4) (Exp. 1) significantly reduced the percentage of ascites (down to 7%), whereas PTU (Exp. 2) significantly increased the appearance of the syndrome (35%). In the T(4)-treated chickens, although the T(4) concentration reached pharmacological levels, the triiodothyronine (T(3)) concentration remained within physiological levels, whereas T(3) in the ascitic birds exhibited a reduction pattern similar to that observed in the ascitic non-supplemented ones. In the PTU-treated chickens, however, both ascitic and non-ascitic birds demonstrated significant reductions in both T(4) and T(3) concentrations. In both experiments, ascitic chickens exhibited a considerable stress response, characterized by a significant and persisted elevation in plasma corticosterone concentration, which was in accordance with a similar elevation of hematocrit, and the PTU-treated non-ascitic birds exhibited a similar stress response. At 5 weeks of age, ascitic birds and the PTU-treated non-ascitic ones exhibited significant reductions in the hemoglobin content of their red blood cells. It may be concluded that deficiency in the thyroid hormones and elevated corticosterone may play a key deleterious role in the development of the ascites syndrome. Topics: Aging; Animals; Ascites; Chickens; Corticosterone; Hematocrit; Hemoglobins; Hyperthyroidism; Hypothyroidism; Male; Poultry Diseases; Propylthiouracil; Syndrome; Thyroxine; Triiodothyronine | 2002 |
[Myeloperoxidase-antineutrophil cytoplasmic antibody positive alveolar hemorrhage during propylthiouracil therapy for hyperthyroidism].
A 62-year-old woman had been treated with propylthiouracil(PTU) for hyperthyroidism. Because bloody sputum, dyspnea, and severe hypoxemia developed, the patient was admitted to our hospital. Chest X-ray and chest computed tomographic (CT) films disclosed diffuse infiltrative shadows in both lung fields. Bronchoalveolar lavage revealed abundant hemosiderin-laden macrophages. Alveolar hemorrhage associated with myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) positive vasculitis syndrome was diagnosed because of the high serum level of MPO-ANCA. After the initiation of steroid therapy and termination of PTU, the infiltrative shadows in both lung fields disappeared, PaO2 improved, and MPO-ANCA decreased. There have been some reports of MPO-ANCA positive vasculitis syndrome developing during PTU therapy, but most were concerned with renal disease. We concluded that PTU and similar agents should be given consideration as one of the possible causes of MPO-ANCA-induced alveolar hemorrhage. Topics: Antibodies, Antineutrophil Cytoplasmic; Antithyroid Agents; Female; Hemorrhage; Humans; Hyperthyroidism; Lung Diseases; Middle Aged; Peroxidase; Propylthiouracil; Pulmonary Alveoli; Syndrome; Vasculitis | 2000 |
Insulin autoimmune syndrome: a rare cause of hypoglycaemia not to be overlooked.
We report the case of a Caucasian patient with insulin autoimmune syndrome (IAS), defined as the association of hypoglycaemic attacks with insulin autoantibodies in individuals not previously treated with exogenous insulin. This rare syndrome (more than 200 published cases) has been reported mainly in Japan. Most affected patients present with other autoimmune disorders, most often Graves' disease. In most cases, insulin autoantibodies appear a few weeks after the beginning of treatment with a drug containing a sulphyldryl group. A significant increase in insulin and C-peptide plasma concentrations and the presence of other antiorgan antibodies are observed. The susceptibility haplotype is present in the Japanese population, which may account for the high frequency of IAS. Spontaneous remission is observed in 80% of cases, with cessation of hypoglycaemic attacks and disappearance of insulin autoantibodies some months after withdrawal of the drug. This rare cause of hypoglycaemia in Caucasian subjects should be considered in aetiologic investigation of spontaneous hypoglycaemia. Topics: Antithyroid Agents; Autoantibodies; Autoimmune Diseases; C-Peptide; Carbimazole; Humans; Hyperthyroidism; Hypoglycemia; Insulin; Japan; Male; Middle Aged; Morocco; Paris; Propylthiouracil; Syndrome; White People | 1999 |
Decreased peripheral 3,5,3'-triiodothyronine (T3) production from thyroxine (T4): a syndrome of impaired thyroid hormone activation due to transport inhibition of T4- into T3-producing tissues.
T4, rT3, and T3 kinetic studies have been performed in a T4-substituted female who showed an increased serum T4/T3 ratio and substantially increased rT3 serum levels in the presence of normal serum thyroid hormone binding properties. The kinetic studies were performed to discriminate between T4 transport inhibition into plasma T3-producing tissues and inhibition of extrathyroidal T4 to T3 conversion. The principal findings were that both T4 and rT3 transport were inhibited into the rapid equilibrating pool (REP), which mainly consists of the liver. The plasma T3 production rate was decreased. Despite an elevated serum free T4 level, serum TSH was elevated, pointing to T4 transport inhibition at the level of the thyrotroph as well. Transport of T4 and rT3 was normal to the slowly equilibrating pool, whereas no transport inhibition of T3 was found to either pool. Because T4 into T3 conversion efficiency in the REP (the main source of plasma T3 production) was normal, it was concluded that the lowered T3 production in the subject was caused by transport inhibition of T4 into the liver. Although the occurrence of the syndrome is rare, its significance is of general importance, in that it shows that transport of thyroid hormone may vary at the tissue level. Furthermore, as T3 is the principal biologically active thyroid hormone, regulation of transport of T4 into the REP may play a (patho)physiological role in the ultimate determination of thyroid hormone activity in the tissues. Topics: Aged; Biological Transport; Cells, Cultured; Female; Fibroblasts; Humans; Kinetics; Middle Aged; Propylthiouracil; Reference Values; Skin; Syndrome; Thyroid Hormones; Thyroxine; Triiodothyronine | 1993 |
Syndrome of generalized (peripheral tissue and pituitary) resistance to thyroid hormone.
Generalized resistance to thyroid hormone (GRTH), or Refetoff syndrome, is a disease in which peripheral tissues show resistance to thyroid hormone. Three patients with this disease were investigated. Cases 1 and 2 involved identical 7-year-old female twins and case 3, a 5-year-old girl. All three patients had goiters, and cases 1 and 2 had sensorineural deafness. In all three, the blood levels of T4, free T4, and T3 were high, while the blood levels of TSH were normal or slightly elevated. The responses shown by blood levels of the thyroid hormone and TSH to administration of propylthiouracil and T3 suggest that the regulating mechanism in the hypothalamic-pituitary-thyroid system was functional. Upon administration of T3, no sign of hyperthyroidism was observed. Topics: Child; Child, Preschool; Female; Goiter; Humans; Pedigree; Prednisone; Propylthiouracil; Syndrome; Thyroid Hormones; Thyrotropin; Triiodothyronine | 1989 |
Effects of antithyroid drugs on lymphocyte proliferative responses to lectins: relationship between insulin autoimmune syndrome and methimazole.
Using peripheral blood lymphocytes from 8 healthy individuals and 5 patients with untreated Graves' disease, direct effects of methimazole (MMI) and propylthiouracil (PTU) on lectin-induced lymphocyte proliferative response were studied. Lymphocytes were cultured for 72 hr in the presence of lectins and antithyroid drugs. Lymphocyte DNA synthesis was counted by incorporation of 3H-thymidine. MMI at 1,000 microM enhanced lectin-induced lymphoproliferation of peripheral blood lymphocytes from both patients with Graves' disease and healthy individuals, at every point of culture time, while PTU showed a tendency toward suppression. These results suggest that this lympho-stimulation by MMI may be a causative factor related to insulin autoimmune syndrome, as deduced from the clinical reports that insulin autoimmune syndrome is, sometimes, found in patients with Graves' disease treated with MMI. This lympho-stimulation was evident regardless of the time of MMI addition, thus indicating that MMI is, by its action, a lymphoid stimulator and may lead to the insulin autoimmune syndrome in predisposed subjects with underlying Graves' disease. Topics: Autoimmune Diseases; Concanavalin A; Graves Disease; Humans; Insulin Antibodies; Lymphocyte Activation; Methimazole; Phytohemagglutinins; Pokeweed Mitogens; Propylthiouracil; Syndrome | 1983 |
Thyroid steal syndrome?
A 57-year-old woman with hyperthyroidism had a loud to-and-fro bruit which persisted when the patient was inadvertently rendered hypothyroid with antithyroid drugs. Symptoms suggestive of transient cerebral ischemia prompted an angiographic study which demonstrated both normal cerebral circulation and an enormous increase in the size of thyroid vasculature. The possibility that the enhanced blood supply to the thyroid had compromised cerebral circulation (thyroid steal syndrome) was considered. The angiographic presentation of hyperthyroidism is reviewed, and the lack of specificity of thyroid bruits as a marker of hyperthyroidism in patients on antithyroid drugs is stressed. Topics: Carotid Arteries; Cerebrovascular Circulation; Female; Humans; Hyperthyroidism; Ischemic Attack, Transient; Middle Aged; Propranolol; Propylthiouracil; Radiography; Syndrome; Thyroid Gland | 1982 |
Transient superior vena cava syndrome due to propylthiouracil therapy in intrathoracic goiter.
Intrathoracic goiter is a rare cause of superior vena cava syndrome. We present the findings in a patient in whom the syndrome was precipitated by therapy with propylthiouracil and remitted on withdrawal of the medication. The superior vena cava syndrome did not recur on medical management, suggesting that surgery is not always indicated in this setting. Topics: Aged; Constriction; Female; Goiter, Substernal; Humans; Propylthiouracil; Syndrome; Vascular Diseases; Vena Cava, Superior | 1981 |
A case of the syndrome of inappropriate secretion of TSH.
A girl aged 4 years with goiter and accelerated physical and skeletal growth was found to be hyperthyroid on the basis of elevated serum thyroid hormone level, nevertheless both the basal TSH and TSH responsiveness to TRH were maintained within the normal range. Serum TSH was suppressed by exogenous T3 and dexamethasone administration, but not significantly changed after propylthiouracil (PTU) treatment. The diurnal rhythmicity of anterior pituitary hormones was preserved with the high nocturnal peak of TSH and prolactin. Clinically, neither thyrotoxic signs nor evidences of pituitary tumor were observed. Her accelerated growth and elevated thyroid hormone level appeared to be induced by inappropriate secretion of TSH. In view of the literature, this is the first case of the syndrome of inappropriate secretion of TSH excluding the neoplastic origin in Japan. Topics: Adrenocorticotropic Hormone; Child, Preschool; Dexamethasone; Female; Growth Hormone; Humans; Hyperthyroidism; Luteinizing Hormone; Prolactin; Propylthiouracil; Syndrome; Thyrotropin; Thyrotropin-Releasing Hormone; Thyroxine; Triiodothyronine | 1979 |