Hypothyroidism induced by antituberculosis drugs.
Keywords:antituberculosis drugs, hypothyroidism, rifampicin, ethionamide, prothionamide, paraaminosalicylic acid
Tuberculosis is an infectious disease that affects practically all organs, including the thyroid gland. In the same time, the hypofunction of the thyroid gland may increase susceptibility to infection with Mycobacterium tuberculosis. Antituberculosis treatment, especially with second-line drugs, can lead to hypothyroidism. It has been found that rifampicin, ethionamide, prothionamide and para-aminosalicylic acid are among the most common antituberculosis drugs responsible for the development of hypothyroidism. These preparations/agents can cause thyroid dysfunction by increasing the metabolism and clearance of thyroid hormones by inducing cytochrome P-450 enzymes, deregulating/ iodine uptake and synthesis of thyroid hormones, altering hormone receptor action and intracellular signal transduction. The treatment with these medications requires the monitoring of the function of the thyroid gland during the treatment, especially in the first 3 months, but also in the post-treatment period. The installation of clinical and/or subclinical hypothyroidism will require the use of appropriate doses of levothyroxine during antituberculosis treatment.
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