Carbiroid is indicated in the management of hyperthyroidism, thyrotoxicosis (including thyroid storm), and also for the preparation of patients for thyroidectomy. Carbiroid can also be used in combination with radio-active ablative therapy.
Carbimazole is an anti-thyroid substance which depresses the formation of thyroid hormone. It reduces the uptake and concentration of inorganic iodine by the thyroid but its main effect is to reduce the formation of di-iodotyrosine and thyroxine. Carbimazole is absorbed rapidly from the gastro-intestinal tract and is widely distributed throughout the body. Carbimazole is completely metabolised to methimazole and it is the metabolite that is responsible for its clinical activity. Carbimazole readily crosses the placental barrier and also attains a high concentration in the milk of lactating patients.
The initial dose : 20-60 mg, in 2-3 divided doses until the patient is euthyroid. Daily dosage should be divided. Maintenance regimen : The dose is gradually reduced to maintain a euthyroid state. The final dosage is usually in the range of 5-15 mg/day which may be taken as a single daily dose. Neonates & Children below 12 years : The usual initial dose is 250 mcg/Kg/day in divided doses. Duration of treatment : 18 to 24 months.
Side-effects may include rash, pruritis, skin pigmentation, paraesthesias, urticaria, headache, arthralgia, and gastro-intestinal disturbances (including nausea, vomiting and gastric discomfort), and abnormal hair loss. Drug fever, a lupus-like syndrome, vasculitis and nephritis, and hepatic disorders, most commonly jaundice, and taste disturbances following Carbiroid therapy have been reported.
Always consult a registered doctor before taking any medicine. This information is for general knowledge only.
Hypersensitivity to carbimazole or other thiourea antithyroid agents.
Carbiroid may interact adversely with other medicines. Iodine or iodine excess may decrease the response to Carbiroid, requiring an increase in dosage or longer duration of therapy with antithyroid agents. As thyroid and metabolic status of patient decreases toward normal, response to oral anticoagulants may decrease, however, if thioamide-induced hypoprothrombinemia occurs, anticoagulant effects may be enhanced. Adjustment of oral anticoagulant dosage on the basis of prothrombin time is recommended. Serum concentrations of digoxin and digitoxin have been reported to increase as the thyroid and metabolic status of patients taking antithyroid agents decreased, reduction in dosage of any digitalis glycoside may be necessary as patients become euthyroid.
Carbiroid should be given with the utmost caution, or not at all, if there is any degree of tracheal obstruction, as high dosages may produce thyroid enlargement and obstructive symptoms may become marked.