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antithyroid/nécrose
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Severe Gingival Ulceration and Necrosis Caused by an Antithyroid Drug: One Case Report and Proposed Clinical Approach
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Introduction: Diffuse gingival ulceration and necrosis is one of the major manifestations of neutropenia or agranulocytosis. Acquired neutropenia can be induced by many medications. Severe oral pain might induce a patient to seek the help
Suppression by antithyroid drugs of experimental hepatic necrosis after ethanol treatment. Effect on thyroid gland or on peripheral deiodination?
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Thionamides and analogues: a reapraisal of antithyroid and thyroid carcinogenic effects.
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As commonly depicted, in the thione form, thionamides (including thiourea and its derivatives) bear little resemblance to thyroid hormone. However, if placed in the thiol resonance form, these molecules are noted to structurally mimic the end of the tyrosine molecule (the precursor of thyroid
Extensive gingival necrosis and sequestration of the alveolar bone caused by methimazole-induced neutropenia and three-year follow-up.
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OBJECTIVE
Methimazole is an anti-thyroid drug that can cause life-threatening neutropenia in rare situations. The aim of this case report is to describe a set of oral complications associated with methimazole-induced neutropenia and the healing of the gingiva after proper treatment.
METHODS
A
Serum levels of interleukin 6 and tumor necrosis factor-alpha in hyperthyroid patients before and after propylthiouracil treatment.
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Contrary to the usual inhibitory role of tumor necrosis factor-alpha (TNF-alpha) in thyroid metabolism, it also has specific stimulatory effects in autoimmune thyroid disorders, including induction of HLA class II antigen-presenting cell-T cell interaction. Despite high intrathyroidal
Soluble tumour necrosis factor-alpha receptor I and interleukin-6 as markers of activity in thyrotoxic Graves' disease.
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Autoimmune thyroid diseases are thought to be mediated by pro-inflammatory cytokines such as TNFalpha and IL-6. Serum levels of cytokines may indicate activity levels of immune functions. We investigated serum levels of IL-6 and of the soluble receptor of TNFalpha in patients with newly diagnosed
Expression of tumor necrosis factor and c-fos genes in peritoneal macrophages of hypothyroid mice.
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It is well documented that hypothyroid patients are more susceptible to microbial infections. In order to study whether this impaired response is due to a decrease in production of antitumor molecules or an impaired ability to transmit information in the macrophage, a hypothyroid animal model was
Scintigraphic study of propylthiouracil induced submassive hepatic necrosis.
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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
Increased adipose tissue secretion of interleukin-6, but not of leptin, plasminogen activator inhibitor-1 or tumour necrosis factor alpha, in Graves' hyperthyroidism.
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OBJECTIVE
This study was designed to investigate adipose tissue secretion of interleukin-6 (IL-6), leptin, tumour necrosis factor alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) in Graves' hyperthyroidism.
METHODS
We studied 10 patients before and during (after 8 weeks) anti-thyroid
Unusual complications of antithyroid drug therapy: four case reports and review of literature.
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Two cases of propylthiouracil-associated acute hepatitis, one case of fatal methimazole-associated hepatocellular necrosis and one case of propylthiouracil-associated lupus-like syndrome are described. The literature related to antithyroid drug side effects and the mechanisms for their occurrence
Serum TNF-alpha in psoriasis after treatment with propylthiouracil, an antithyroid thioureylene.
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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
Two-step development of Hashimoto-like thyroiditis in genetically autoimmune prone non-obese diabetic mice: effects of iodine-induced cell necrosis.
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The administration of a high iodide dose (HID; 10 micrograms/day) to goitrous mice is known to induce thyroid cell necrosis and inflammation, which, in most strains, is transient. In this study, we analyzed the effects of iodide in autoimmune prone non-obese diabetic (NOD) mice. Control NOD mice fed
Role of the tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) axis in autoimmune thyroid disease.
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BACKGROUND
TNF-like weak inducer of apoptosis (TWEAK), its receptor fibroblast growth factor-inducible 14 (Fn14) and its scavenger receptor CD163 (sCD163) have known associations with many autoimmune diseases. However, the role of the TWEAK axis in autoimmune thyroid disease (AITD) remains unclear.
Anti-thyroid cancer properties of a novel isoflavone derivative, 7-(O)-carboxymethyl daidzein conjugated to N-t-Boc-hexylenediamine in vitro and in vivo.
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The incidence of thyroid cancer is up to 3 folds higher in women than in men, suggesting that estrogenic effects may be involved in the pathogenesis of this malignancy. Here, we explore whether or not human thyroid cancer cell growth can be curbed by a novel isoflavone derivative generated in our
Serum concentrations of interleukin (IL-)1alpha, 1beta, 6 and tumor necrosis factor (TNF-) alpha in patients with thyroid eye disease (TED).
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Serum proinflamatory cytokines were found to be altered in Graves disease (GD) and in TED. Serum values of IL1alpha, IL-1beta, IL-6, TNF-alpha were assessed in 22 patients with TED before and after treatment (aged 46.82 +/- 12.47, M:F=16:6). Free thyroxin was high, TSH low, thyroid ultrasound showed
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