Thiamazole 5mg tablets

Thyrotoxic periodic paralysis (TPP) is a potentially life-threatening complication of hyperthyroidism. It is characterized by hypokalemia-induced muscle weakness that typically begins in the proximal lower limbs and may progress to paralysis of all four extremities and involvement of the respiratory muscles. We present a case of a 37-year-old man with a history of TPP, presenting with acute muscle weakness and hypokalemia. The patient reported acute-onset bilateral lower extremity weakness from the previous day. Physical examination revealed normal deep tendon reflexes, but marked muscle weakness was observed in both lower limbs. Laboratory workup revealed severe hypokalemia at 2.1 mEq/L and thyrotoxicosis, while the electrocardiogram showed a prolonged QTc interval. The patient received thiamazole, potassium iodide, and propranolol for thyrotoxicosis and a total dose of 122 mEq of potassium repletion. His potassium level rose from 1.7 mEq/L to 5.6 mEq/L within six hours post-repletion cessation, highlighting the risk of rebound hyperkalemia and the importance of close monitoring. This case underscores the danger of rebound hyperkalemia after aggressive potassium repletion in TPP and supports a cautious, stepwise correction strategy.

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Graves' disease (GD) may increase the difficulty of glucose control in patients with type 2 diabetes mellitus (T2DM). Therefore, selecting a drug with limited blood glucose side effects is an important issue in patients with T2DM and GD. Antithyroid drugs (ATDs) including propylthiouracil (PTU), methimazole, and carbimazole are commonly prescribed for the treatment of GD. Here, we review and summarize the literature from the last 10 years and discuss the effects of current ATDs used for GD for blood glucose control in patients with T2DM. A search of the literature published between January 1, 2012 and December 1, 2022 was conducted using three major medical databases: Google Scholar, Ovid Medline, and Scopus. An initial search was conducted on PubMed using the MeSH terms "propylthiouracil," "methimazole," "carbimazole," and "hyperglycemia" or "hypoglycemia" in academic databases. All articles included "Graves' disease" and "type 2 diabetes mellitus" in the title. Based on the results of previous studies, the hyperglycemic and hypoglycemic side effects of ATDs can be explained by several possible mechanisms. The most widely accepted hypothesis is that sulfhydryl group drugs (e.g., methimazole and carbimazole) cleave the disulfide bond of insulin and enhance its immunogenicity, resulting in hypoglycemia. Moreover, some reports have indicated that methimazole is associated with hypoglycemia; therefore, if the patient has a history of autoimmune diseases, it is necessary to consider whether to change drugs or actively track the production of autoimmune antibodies. In non-diabetic and diabetic patients with GD, the hyperglycemic and hypoglycemic side effects of PTU (on glycemic variation) were less than that of thiamazole. However, as relatively few reports have investigated the side effects of blood sugar changes, further research is necessary to confirm these effects. In addition to autoimmune diseases, drug side effects may need to be considered. These findings provide considerations for clinicians to select more appropriate ATDs for patients with GD and T2DM, and implement improved care guidelines.

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Nonautoimmune hyperthyroidism (NAH), caused by constitutively active mutants of the thyrotropin receptor (TSHR) gene, is recommended to be treated with total thyroidectomy followed by radioiodine administration. Herein, we present a 39-year-old woman with sporadic NAH caused by a TSHR-L512Q mutation. At the age of 20 years, she presented with a large goiter of 370 mL, treated with thiamazole, and opted for radioiodine therapy as outpatient management. Over the next 17 years, she underwent 6 treatments of 13 mCi radioiodine each. She did not experience a relapse of hyperthyroidism, and thiamazole was reduced and later withdrawn during the final radioiodine treatment. The patient's goiter significantly reduced to 18 mL, and thyroid function tests showed that free thyroxine and free triiodothyronine levels were below the lower limit of the reference ranges, while TSH remained within the reference range for 20 months. Along with an almost normal TSH response to thyrotropin-releasing hormone stimulation, no pituitary atrophy was observed on magnetic resonance imaging. Contrary to the recommended treatment, this case showed that fractionated radioiodine therapy alone is effective in controlling thyroid function and in reducing goiter size. Low TSH levels during treatment should not be assessed as subclinical hyperthyroidism or as risk of relapse.

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Graves' disease and hyperthyroidism in women with childbearing potential are a challenge in pre-conceptional counseling. The non-surgical alternatives are radioiodine therapy or antithyroid drugs. Here, we focus on the TSH receptor antibody (TRAb) level-without or after radioiodine therapy-and the probability of fetal or neonatal hyperthyroidism. This immunological effect should be weighed against the risk of congenital malformation taking propylthiouracil during pregnancy. For up to 2 years after radioiodine therapy for Graves' disease, TRAb levels may remain above the pre-therapeutic level. The time of conception after radioiodine therapy and a high TRAb level are associated with the likelihood of neonatal hyperthyroidism: 8.8% probability if conception occurred 6-12 months after radioiodine therapy, with a 5.5% probability for 12-18 months, and 3.6% probability for 18-24 months. The TRAb value above 10 U/L in the third trimester is the main risk factor for neonatal hyperthyroidism. If a woman does not wish to postpone her family planning, the pre-conceptional counseling has to describe the risk of propylthiouracil, thiamazole, or of an uncontrolled hyperthyroidism. According to some national cohort studies (Danish, Swedish, Korean), the risk for fetal malformations (ear, urinary tract) under propylthiouracil is increased by 1.1-1.6%, in addition to the spontaneous risk for unexposed pregnant women. For thiamazole, the additional risk for fetal malformation was about 2-3%, depending on the dose of thiamazole. Propylthiouracil has posed a lower risk for congenital malformation than an uncontrolled hyperthyroidism. To minimize the risk for the newborn, women with Graves' disease and hyperthyroidism should offer a definitive therapy strategy (e.g., radioiodine therapy) long before planning a pregnancy.

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Background: Resistance to thyroid hormones (RTH) is a rare, genetically determined disease characterised by reduced tissue sensitivity to thyroid hormones (THs). It is caused by mutations in genes encoding the receptors for thyroid hormones, α (THRα) or β (THRβ), the distribution of which varies between tissues. Therefore, patients present with elevated TH levels with unsuppressed TSH levels, and symptoms of both hypothyroidism and hyperthyroidism may be present. Methods: Hence, we report the case of a boy with a complex, cyanotic, congenital heart defect who was also diagnosed with TH resistance syndrome. Results: Because of the clinical features of hyperthyroidism in preparation for cardiac surgery, thiamazole was administered, resulting in the normalisation of TH effects on the α-receptor for HTs. Due to the effectiveness of the proposed treatment, it was further introduced before the further stages of cardiac surgeries. Conclusions: The management of RTH is a constant challenge for clinicians and must be individualised.

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