Wernicke Encephalopathy as a Rare Complication of Antituberculosis Treatment: A Case Report

Wernicke encephalopathy (WE) is an acute neurological emergency caused by severe thiamine deficiency. Although classically associated with chronic alcoholism, it may also occur in nonalcoholic settings, including during prolonged antituberculosis treatment. We report the case of a 29-year-old woman treated for bacteriologically confirmed pulmonary tuberculosis who developed recurrent episodes of severe drug-induced hepatotoxicity, requiring treatment interruption and modification. Despite the introduction of an alternative antituberculosis regimen, she experienced persistent vomiting followed by the acute onset of cerebellar ataxia and ophthalmoplegia. Brain MRI revealed bilateral and symmetric fluid-attenuated inversion recovery hyperintensities of the medial thalami, the periaqueductal gray matter, and the mammillary bodies, consistent with WE. Plasma thiamine level was markedly reduced (55 nmol/L). High-dose IV thiamine (500 mg three times daily for five days), followed by oral supplementation, led to rapid and complete neurological recovery. WE is a rare but potentially severe complication in patients receiving antituberculosis therapy, particularly in the presence of persistent vomiting and hepatic toxicity. Early recognition and prompt treatment with thiamine are essential to prevent irreversible neurological sequelae. Preventive thiamine supplementation should be considered in high-risk patients.