carbimazole
Sources réglementaires consultées
Indications approuvées
- Hyperthyroïdie, préparation à la thyroïdectomie, récidive après thyroïdectomie et crise thyréotoxique.
Contre-indications
Absolues
- Insuffisance hépatique sévère, affection hématologique sévère préexistante, antécédent de pancréatite sous carbimazole/thiamazole ou hypersensibilité.
Mises en garde cliniques
- Mise en garde majeure · Il peut provoquer une agranulocytose mortelle. En cas de fièvre, mal de gorge, ulcères buccaux, saignement ou malaise, arrêter immédiatement et réaliser une numération sanguine urgente. — CIMA/AEMPS, ficha técnica 28996
- Mise en garde majeure · Arrêter en cas de pancréatite aiguë ou d’atteinte hépatique. Le surtraitement provoque une hypothyroïdie ; surveiller la fonction thyroïdienne. — CIMA/AEMPS, ficha técnica 28996
Interactions médicamenteuses
- SévèreWarfarine et autres anticoagulants oraux
Mécanisme: Le carbimazole antagonise la vitamine K et peut intensifier l’effet de la warfarine et des autres anticoagulants oraux.
Recommandation: Surveiller étroitement la coagulation et ajuster l’anticoagulant lors de l’instauration, de la modification ou de l’arrêt du carbimazole.
CIMA/AEMPS, ficha técnica 28996
- ModéréeThéophylline et bêtabloquants
Mécanisme: Avec le retour à l’euthyroïdie, leur exposition ou le besoin posologique peut changer.
Recommandation: Surveiller la réponse et ajuster selon la clinique.
CIMA/AEMPS, ficha técnica 28996
Effets indésirables
Communs (≥1%)
Nausées, céphalée, arthralgie, gêne gastrique, éruption et prurit
Rares mais graves
Agranulocytose, pancytopénie, pancréatite aiguë et atteinte hépatique
Grossesse et allaitement
Il peut provoquer des malformations. Traiter l’hyperthyroïdie maternelle avec la dose minimale efficace et une surveillance étroite ; éviter le traitement blocage-substitution. Les femmes en âge de procréer doivent utiliser une contraception. L’allaitement nécessite d’évaluer la dose et de surveiller la thyroïde du nourrisson.
Bibliographie récente (PubMed)
Hyperthyroidism caused by Graves' disease (GD) is a relatively rare disease in children. Treatment options are the same as in adults - antithyroid drugs (ATD), radioactive iodine (RAI) or thyroid surgery, but the risks and benefits of each modality are different. The European Thyroid Association guideline provides new recommendations for the management of pediatric GD with and without orbitopathy. Clinicians should be alert that GD may present with behavioral changes or declining academic performance in children. Measurement of serum TSH receptor antibodies is recommended for all pediatric patients with hyperthyroidism. Management recommendations include the first-line use of a prolonged course of methimazole/carbimazole ATD treatment (3 years or more), a preference for dose titration instead of block and replace ATD, and to avoid propylthiouracil use. Where definitive treatment is required either total thyroidectomy or RAI is recommended, aiming for complete thyroid ablation with a personalized RAI activity. We recommend avoiding RAI in children under 10 years of age but favor surgery in patients with large goiter. Pediatric endocrinologists should be involved in all cases.
The diagnosis of Graves' disease is mainly based on ultrasonography and laboratory diagnostics. This includes the determination of the TSH value and the peripheral thyroid hormones. TSH receptor antibody (TRAb) measurement is highly sensitive and specific for the detection of Graves' disease (GD) and helps to distinguish from autoimmune thyroiditis (AIT). However, as recent studies show, some may AIT patients may also reveal TRAb. Current guidelines recommend primarily the use of thiamazol/carbimazole in GD. Due to the comparatively higher hepatotoxicity, propylthiouracil is not recommended as first line therapy. In case of relapse during 12 up to 18 months of antithyroid drug therapy or after a frustrating attempt at cessation, definitive therapy should be considered. Alternatively, in accordance with the current recommendations of the European Thyroid Association, drug therapy may be continued for up to 12 months after initial diagnosis. The treatment of active GD during pregnancy is problematic due to diaplacental crossing of peripheral thyroid hormones, TSH receptor stimulating antibodies and antithyroid drugs. According to current guidelines, PTU is recommended during the first 16 weeks of pregnancy, whereas for the 2nd and 3 rd trimester no special recommendations are given. After that, you can choose which antithyroid drug might be used. The aim of antithyroid drug therapy during pregnancy is to achieve a suppressed TSH value together with normal or slightly increased fT4 while using lowest effective dose of antithyroid drug. The most common endocrine side effect with this therapy is thyroid dysfunction. Hyperthyroidism; occur most frequently in combination therapy (CTLA-4 / anti-PD-1 therapy) ICI mainly causes destructive thyroiditis with lymphocytic infiltration; GD is absolutely rare in this context and only few cases are described.
Graves' disease (GD) is the most common cause of hyperthyroidism in children. A common GD symptom is a goiter. The usual biochemical profile in children with GD is a decreased thyroid hormone stimulating hormone (TSH) level and high free thyroxine (FT4) and free triiodothyronine (FT3) concentrations. The presence of thyroid receptor antibodies (TRAb) is the most important specific immunological sign for diagnosing GD. The treatment choices for pediatric GD are anti-thyroid drugs (ATDs), radioiodine, and thyroidectomy, but the risks and benefits of each modality are different. Management recommendations include the first-line use of a prolonged course of ATDs for at least 3 years and potentially 5 years or more. Rituximab and Teprotumumab are new novel alternative medications for the treatment of adult patients with GD and Graves' orbitopathy respectively, but evidence of the efficacy and safety of these drugs in pediatric patients with GD is lacking.
The thionamide anti-thyroid drugs namely carbimazole, methimazole, and propylthiouracil, have been the predominant therapy modality for Graves' hyperthyroidism for over 60 years. Although these agents have proven efficacy and favorable side-effect profiles, non-thionamide alternatives are occasionally indicated in patients who are intolerant or unresponsive to thionamides alone. This review examines the available non-thionamide drug options for the control of Graves' hyperthyroidism and summarizes their clinical utility, efficacy, and limitations. We reviewed existing literature on mechanisms, therapeutic utility, and side-effect profiles of non-thionamide anti-thyroid drugs. Established non-thionamide agents act on various phases of the synthesis, release, and metabolism of thyroid hormones and comprise historical agents such as iodine compounds and potassium perchlorate as well as drug repurposing candidates like lithium, glucocorticoids, beta-blockers, and cholestyramine. Novel experimental agents in development target key players in Graves' disease pathogenesis including B-cell depletors (Rituximab), CD40 blockers (Iscalimab), TSH-receptor antagonists, blocking antibodies, and immune-modifying peptides. Non-thionamide anti-thyroid drugs are useful alternatives in Graves' hyperthyroidism and more clinical trials are needed to establish their safety and long-term efficacy in hyperthyroidism control. Ultimately, the promise for a cure will lie in novel approaches that target the well-established immunopathogenesis of Graves' disease.