Treatment failure and QTc interval prolongation: case reportA 47-year-old woman exhibited treatment failure during treatment with rifampicin and unspecified antitubercular drugs for pulmonary tuberculosis (TB). Additionally, she developed QTc interval prolongation during treatment with clofazimine and moxifloxacin for multidrug-resistant (MDR) pulmonary TB [not all routes, dosages and duration of treatments to reactions onsets stated].The woman, who had pulmonary TB, was treated with catgory 1 oral antitubercular therapy consisting of rifampicin and unspecified antitubercular drugs. However, this therapy failed to treat her pulmonary TB. GeneXpert examination showed rifampicin-resistant pulmonary TB. A confirmed diagnosis of MDR pulmonary TB was considered and she started receiving shortterm MDR-TB therapy with moxifloxacin 600mg, clofazimine 100 mg/day, kanamycin [kanamicin], ethionamide [ethionamid], isoniazid, pyrazinamide and ethambutol. However, after 1 week of therapy, she experienced prolonged QTc interval of 545 msec.The woman's moxifloxacin therapy was discontinued for 3 days. Following discontinuation of moxifloxacin, her QTc interval returned to normal at 411 msec.The woman was again initiated on moxifloxacin at a dose of 400mg. After 1 week, her QTc interval was 468 msec. Moxifloxacin dose was increased to 600mg. At the second month from initiation of treatment, her QTc interval was 471 msec. She started receiving advanced stage of therapy. However, at the fourth month from initiation of treatment, she again developed a prolonged QTc interval of 600 msec. Hence, moxifloxacin was temporarily discontinued. Subsequent laboratory examination showed mild hypokalaemia [aetiology not stated]. As a corrective measures, she received potassium therapy. After correction of hypokalaemia, the QTc interval returned to normal (443 msec). Moxifloxacin therapy was again started at a dose of 200mg for 7 days which was then increased to 400mg dose. At the fifth month of therapy, her QTc interval was 491 msec. However, at the seventh month of therapy, she again experienced a prolonged QTc interval of 539 msec. Moxifloxacin was continued. Clofazimine dose was decreased to 50 mg/day. After a week of evaluation, the QTc interval returned to normal (433 msec), and clofazimine dose was again increased to 100 mg/day until the end of treatment. She completed short-term MDR-TB therapy. Her TB was declared to have been resolved after completion of therapy. The QTc interval prolongation was considered to be secondary to clofazimine and moxifloxacin therapy.