Carbimazole induced cholestatic hepatitis (original) (raw)
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Carbimazole-Induced Jaundice in Thyrotoxicosis: A Case Report
2021
Carbimazole is a commonly used antithyroid drug in thyrotoxicosis. It is generally well tolerated, and its side effects include allergic skin reactions, gastrointestinal upset, agranulocytosis, and hepatotoxicity. Hepatitis is a rare but serious side effect. Here we report a case of carbimazole-induced hepatitis with severe cholestasis that was managed by switching to propylthiouracil. Most of the literature recommends radioiodine or surgery as the definitive treatment for hyperthyroidism in thionamide-induced hepatitis rather than switching to other thionamide. However, substitution of one thionamide for another can be tried as we did in this case, without any increased risk of hepatotoxicity as the mechanism of liver injury differs in both groups. A previously healthy 30-year-old lady who was diagnosed with thyrotoxicosis one month earlier that was treated with carbimazole 60 mg daily was admitted to the medical ward with yellowish discoloration of sclera, urine, and pruritus of o...
https://www.ijhsr.org/IJHSR\_Vol.7\_Issue.1\_Jan2017/IJHSR\_Abstract.044.html, 2017
Grave's disease is the most common cause of hyperthyroidism. Antithyroid drugs are usually well tolerated in majority of patients but dangerous adverse effects can occur in 3-12% of treated patients. Cholestatic jaundice is a rare but potentially fatal complication secondary to the use of antithyroid drugs like carbimazole and propylthiouracil. We report a case of 46 year old male patient who developed cholestatic jaundice following sequential administration of carbimazole and propylthiouracil treatment for thyrotoxicosis.
Carbimazole-induced cholestatic hepatitis in Graves′ disease
Indian Journal of Endocrinology and Metabolism, 2013
Antithyroid medications are one of the treatment options for Graves' disease. Carbimazole is widely used as the drug of choice, except in pregnancy, where propythiouracil is preferred by many. It is generally well-tolerated. Its side-effects include allergy, upper gastrointestinal upset, a rare occurrence of granulocytosis, and others. Hepatitis is another rare, but serious side-effect. We report a healthy 30-year-old male patient with Graves' disease, who developed cholestatic jaundice after Carbimazole therapy for four months. He made a full recovery after the drug was discontinued. An idiosyncratic mechanism seemed likely.
A Case of Carbimazole-Induced Hepatitis and Agranulocytosis
The Endocrinologist, 2005
Agranulocytosis and hepatitis resulting from thioamides are recognized as potentially fatal adverse effects. We describe a patient with recent-onset Graves disease who developed both of these rare complications as a result of carbimazole treatment. Prompt diagnosis led to early institution of appropriate supportive therapy and specific treatment with granulocyte colony-stimulating factor (G-CSF). Alternative therapies for thyrotoxicosis are discussed.
Hepatotoxicity Induced by Methimazole in a Previously Health Patient
Current Drug Safety, 2009
We report a case of hepatotoxicity induced by methimazole treatment in a patient affected by hyperthyroidism. A 54-year-old man, presented to our observation for palpitations, excessive sweating, weakness, heat intolerance and weight loss. On physical examination, his blood pressure was 140/90 mmHg and heart beat was 100/min regular. He had mild tremors and left exophthalmos. Laboratory test revealed a significant increase in serum thyroid hormone levels with a decrease in thyroid stimulating hormone levels. A diagnosis of hyperthyroidism was made and he began treatment with methimazole (30 mg/day). Fourteen days later, he returned for the development of scleral icterus, followed by dark urine, and abdominal pain in the right upper quadrant. Laboratory examinations and liver biopsy performed a diagnosis of cholestatic hepatitis, secondary to methimazole usage. Methimazole was promptly withdrawn and cholestyramine, ursodeoxycholic acid, and chlorpheniramine were given. After five days, abdominal pain resolved and laboratory parameters returned to normal. Naranjo probability scale indicated a probable relationship between hepatotoxicity and methimazole therapy. In conclusion physicians should be aware the risk of hepatotoxicity related with methimazole.
Liver dysfunction and anti-thyroid therapy
SAGE Open Medical Case Reports, 2015
Thioamides have been used in the management of hyperthyroidism for over 50 years. Liver dysfunction is a rare but important side effect associated with their use. Recently, cases of liver failure associated with propylthiouracil have prompted the Federal Drug Administration to issue a Boxed Warning to the label of propylthiouracil regarding its risk of potentially fatal liver injury and acute liver failure in adults and children. Herein, we present a case to underline the importance of recognising the similar potential for severe hepatic dysfunction with the use of other thioamides.
Journal of Medical Cases, 2015
Thyrotoxicosis is one of the most frequent endocrine disorders. Methimazole is the antithyroid drug for the treatment of hyperthyrodism. Methimazole is rarely associated with hepatic toxicity. We reported a case of 56-year-old woman who developed hepatotoxicity and anti-nuclear antibody positivity during methimazole treatment. Increased liver enzyme levels appeared after 1 month of the methimazole treatment. Viral hepatitis markers were negative. The radiological examinations were normal. According to the CIOMS/RUCAM scale, the score was 11 and the causal relationship of the hepatic adverse reaction by methimazole was highly probable. Methimazole-induced hepatotoxicity was considered and methimazole treatment was cancelled. The laboratory parameters returned to normal after 15 days. The mechanism of hepatotoxicity due to methimazole treatment was not fully understood. It has been hypothesized that there is a genetic predisposition, associated with a dose-dependent immune reaction. In conclusion, physicians should be aware the risk of hepatotoxicity related with methimazole treatment.
Endocrine Practice, 2016
Objective: Overt hyperthyroidism and methimazole (MMI) treatment are frequently associated with abnormal liver function tests (LFTs). We describe the serial changes of LFTs in MMI-treated hyperthyroid patients. Methods: We retrospectively analyzed all 77 patients presenting with newly diagnosed overt hyperthyroidism (59 Graves diseases, 11 toxic nodular goiters, 4 toxic adenomas, 3 amiodarone-induced thyrotoxicosis) between 2012 and 2014. All patients started MMI at 10 to 60 mg/ day that was gradually tapered. We measured thyroid-stimulating hormone, free thyroxine, alanine aminotransferase (ALT) and aspartate aminotrasnferase (AST) at baseline and at 6 weeks, 4.5 months and 10 months after starting the MMI treatment. The concomitant medication was stable during MMI treatment. Results: At baseline, 25 patients (32.5%) had abnormal LFT, of which 5 had ALT or AST levels >2× the upper limit of normal (ULN). In most patients with baseline abnormal LFT, MMI treatment resulted in a normalization of serum ALT and AST. Thirteen patients with normal baseline LFT had <2× the ULN elevations of LFT sometime during treatment. There was a case of significant hepatotoxicity. During treatment, there were no significant differences in LFT levels between patients with initially normal or abnormal LFT. In a Cox proportional hazard regression model, abnormal LFT at baseline, abnormal thyroid function at the last evaluation, and MMI dose were not predictors of abnormal LFT at the final evaluation. Conclusion: MMI treatment can induce insignificant LFT elevation, <2× the ULN. MMI can be safely administered in hyperthyroid patients with abnormal LFT, and normalization of increased AST and ALT levels should be anticipated.
Gut, 1975
On three occasions, a 63 year old housewife with hyperthyroidism developed a reaction which included fever, pruritus, malaise, and, on one occasion, jaundice one to 17 days after taking carbimazole. Challenge with carbimazole was followed within 12 hours by abdominal pain, pruritus, and increased serum transaminase levels. Light microscopy of a liver biopsy showed increase of portal zone cellularity over the control and the electron microscopy revealed fine structural changes compatible with drug-related liver injury.