Antitubercular drug (ATD)-induced hypovitaminosis D 3 and secondary hyperparathyroidism are less reported phenomena compared to other antitubercular therapy–induced adverse events. Rifampicin and isoniazid are often identified as the culprits in causing secondary hyperparathyroidism. The mechanism involved is CYP3A4 induction by rifampicin and isoniazid, which leads to hypovitaminosis D and hypocalcemia. In response, there is an increase in parathyroid hormone (PTH) secretion, leading to secondary hyperparathyroidism, which can cause bone decay, nephrolithiasis, and other complications. We report a case of a 43-year-old female who developed a nonhealing coccyx fracture following trivial trauma. She had been on antitubercular treatment for the past 5 months after being diagnosed with isoniazid monoresistant pulmonary tuberculosis. Her blood report showed increased PTH levels and decreased calcium and vitamin D 3 levels. Rifampicin was stopped, replaced it with linezolid, and the modified regimen was continued for a total of 9 months. The patient showed clinicoradiological improvement. Calcium, vitamin D 3 , and PTH levels were repeated and gradually normalized after stopping rifampicin. We conclude that regular monitoring of calcium and PTH levels during antitubercular treatment is important for early identification and management of potential vitamin D deficiency and secondary hyperparathyroidism.
Saha et al. (Thu,) studied this question.