methimazole has been researched along with Arthralgia* in 5 studies
5 other study(ies) available for methimazole and Arthralgia
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[Thiamazole-induced arthritis].
We report the case of a 42-year-old male patient with acute onset of asymmetrical polyarthritis of the medium and large joints as well as fever and elevated serological inflammation markers. The symptoms began shortly after initiation of thiamazole treatment for newly diagnosed Graves' disease. Antithyroid arthritis syndrome (AAS) is a rare but serious adverse side effect of antithyroid treatment with thioamides such as thiamazole. Clinically, AAS may present with myalgia, arthralgia, fever, exanthema and polyarthritis. In the case of suspected AAS, when possible the thionamide medication should be rapidly discontinued or modified in consultation with the endocrinologist. In some cases anti-inflammatory therapy with NSAID or corticosteroids may be required for symptom control.. Wir berichten über den Fall eines 42-jährigen Patienten mit akuter asymmetrischer Polyarthritis der großen und mittelgroßen Gelenke sowie Fieber und erhöhten serologischen Entzündungszeichen. Die Symptomatik begann kurz nach Beginn einer Thiamazol-Therapie bei neu diagnostiziertem Morbus Basedow. Eine durch Thionamide ausgelöste Arthritis wird auch als „antithyroid arthritis syndrome“ (AAS) bezeichnet und ist eine seltene unerwünschte medikamentöse Nebenwirkung. Klinisch kann sich das Krankheitsbild mit Myalgien, Arthralgien, Fieber, Hautausschlag und Polyarthritis präsentieren. Bei Verdacht auf ein AAS sollte die Thionamid-Medikation in Rücksprache mit dem Endokrinologen nach Möglichkeit zeitnah abgesetzt oder umgestellt werden. In einigen Fällen ist eine antiinflammatorische Therapie mit NSAR oder Glukokortikoiden zur Symptomkontrolle nötig. Topics: Adult; Antithyroid Agents; Arthralgia; Arthritis; Graves Disease; Humans; Male; Methimazole | 2021 |
Elevated levels of circulating fibroblast growth factor 23 with hypercalcemia following discontinuation of denosumab.
We report a case of a 47-year-old woman with hypercalcemia 6 months after discontinuation of denosumab. She underwent right mastectomy for breast cancer and had received aromatase inhibitor and denosumab therapy for 5 years. Thirst, appetite loss, and bilateral ankle pain began few months after cessation of denosumab. She was admitted to the hospital for hypercalcemia and hyperthyroidism 6 months after the last dose of denosumab. Laboratory investigations revealed hypercalcemia, normophosphatemia, normal renal function, and elevated levels of fibroblast growth factor 23 (FGF-23). Serum tartrate-resistant acid phosphatase 5b and urine N-terminal cross-linked telopeptide of type I collagen were both elevated, and bone scintigraphy revealed increase of whole bone uptake. Radiological examinations showed no recurrence of breast cancer or tumors that secrete intact PTH or FGF-23. Hypercalcemia, which lasted for 1 month, was refractory to discontinuation of the aromatase inhibitor, normalization of thyroid hormone levels, saline hydration, and calcitonin administration, but was effectively treated with zoledronic acid. Abnormal uptake on bone scintigraphy and ankle pain both resolved a few months after treatment, and hypercalcemia has not recurred in the ensuing 2 years. In conclusion, we found elevated levels of circulating FGF-23 with hypercalcemia following the discontinuation of denosumab. FGF-23 might be a surrogate marker for massive bone resorption triggered by discontinuation of long-term denosumab treatment. Topics: Ankle; Anorexia; Antithyroid Agents; Aromatase Inhibitors; Arthralgia; Bone Density Conservation Agents; Bone Neoplasms; Bone Resorption; Breast Neoplasms; Collagen Type I; Denosumab; Deprescriptions; Female; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Graves Disease; Humans; Hypercalcemia; Methimazole; Middle Aged; Parathyroid Hormone; Peptides; Potassium Iodide; Radionuclide Imaging; Tartrate-Resistant Acid Phosphatase; Thirst; Zoledronic Acid | 2020 |
An uncommon side effect of thiamazole treatment in Graves' disease.
Thionamides (such as thiamazole/methimazole) are a common first line treatment for Graves' disease. Common side effects include rash, urticaria, and arthralgia. However, thionamide treatment has also been associated with a variety of auto-immune syndromes. Here, we describe a patient presenting with mild arthritis after starting thiamazole. Although severe presentation warrants acute withdrawal of the causative agent, our case suggests that milder forms can be successfully treated with anti-inflammatory drugs alone. Recognition of the syndrome is key to warrant timely and effective treatment. Topics: Antithyroid Agents; Arthralgia; Graves Disease; Humans; Methimazole; Treatment Outcome | 2020 |
Antithyroid arthritis syndrome.
Antithyroid arthritis syndrome is a constellation of symptoms of myalgia, arthralgia, arthritis, fever and rash associated with the use of antithyroid medications. We report a case of a patient with severe hyperthyroidism likely secondary to Graves' disease who presented with the abovementioned symptoms after being treated with methimazole (antithyroid medication). Our aim is to increase awareness regarding this uncommon but disabilitating and life-threatening adverse effect of antithyroid medications among clinicians. We also discuss the proposed pathophysiology for this immunological reaction as well as management options in these patients. Topics: Antithyroid Agents; Arthralgia; Arthritis; Drug Eruptions; Female; Fever; Humans; Hyperthyroidism; Methimazole; Middle Aged; Syndrome | 2017 |
Cryofibrinogenemia with polyarthralgia, Raynaud's phenomenon and acral ulcer in a patient with Graves' disease treated with methimazole.
Cryofibrinogenemia is a cryopathy in which hypersensitivity to cold is a prominent feature. Cryofibrinogenemia developed in an 18-year-old Japanese female patient during methimazole therapy for Graves' disease. She developed cryopathy (livedo reticularis, Raynaud's phenomenon and acral ulcer) and polyarthralgia during methimazole therapy, and we detected cryofibrinogen in her plasma. Her symptoms resolved after administration of prostaglandins and anticoagulants. Several reports indicate that methimazole therapy induces autoantibody-related disease. In the present case, we cannot exclude the possibility that methimazole therapy contributed to the cryofibrinogenemia. Topics: Adolescent; Anticoagulants; Antithyroid Agents; Arthralgia; Cryoglobulins; Female; Fibrinogens, Abnormal; Foot Ulcer; Graves Disease; Humans; Methimazole; Prostaglandins, Synthetic; Raynaud Disease; Skin Diseases, Vascular | 1997 |