ABSTRACT
Introduction
Adverse reactions to tuberculosis treatment can impact patient adherence and prognosis. Hypothyroidism is a frequent adverse reaction caused using ethionamide, prothionamide, and para-aminosalicylic acid and is often underdiagnosed.
Areas covered
We searched Scielo, Scopus, and EMBASE databases, including 67 articles. Antitubercular drug-induced hypothyroidism has a prevalence of 17%. It occurs after 2 to 3 months of treatment and resolves within 4 to 6 weeks after discontinuation. It is postulated to result from the inhibition of thyroperoxidase function, blocking thyroid hormone synthesis. Symptoms are nonspecific, necessitating individualized thyroid-stimulating hormone measurement for detection. Specific guidelines for management are lacking, but initiation of treatment with levothyroxine, as is customary for primary hypothyroidism, is recommended. Discontinuation of antitubercular drugs is discouraged, as it may lead to unfavorable consequences.
Expert opinion
Antitubercular drug-induced hypothyroidism is more common than previously thought, affecting one in six MDR-TB patients. Despite diagnostic and treatment recommendations, implementation is hindered in low-income countries due to the lack of certified laboratories. New drugs for tuberculosis treatment may affect thyroid function, requiring vigilant monitoring for complications, including hypothyroidism.
Article highlights
One in six patients with multidrug-resistant tuberculosis develops drug-induced hypothyroidism.
Hypothyroidism is associated with para-aminosalicylic acid, ethionamide, and prothionamide.
Antitubercular drug-induced hypothyroidism emerges after 2-3 months of treatment and is reversible upon discontinuation of treatment.
The development of antitubercular drug-induced hypothyroidism is attributed to the inhibition of thyroid peroxidase and blocking of iodine organification.
Measurement of TSH levels should be conducted every 3-6 months to screen for this condition.
The treatment and follow-up of antitubercular drug-induced hypothyroidism parallel those of primary hypothyroidism.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Author contribution statement
JE Quiroz Aldave: conceptualization, methodology, investigation, writing – original draft, project administration. MC Durand-Vásquez: investigation, writing – original draft. ER Gamarra-Osorio: investigation, writing – review & editing. LA Concepción-Urteaga: writing – review & editing. S Pecho-Silva: writing – review & editing. LA Rodríguez-Hidalgo: writing – review & editing. MJ Concepción-Zavaleta: conceptualization, methodology, writing – review & editing, project administration.