Dear Sir, I read with interest the case report "Ethambutol-Induced Bilateral Retrobulbar Neuritis with Ceco-central Scotoma in Cervical Tuberculous Lymphadenitis Patient: A Case Report with Estimated Plasma Level Consideration" published ahead of print in your journal.[1] The authors have reported a case of tubercular lymphadenitis treated with a standard four drug regime, including ethambutol and subsequently patient developed decreased acuity of vision after 2 months. There is no mention of pupillary reflex to direct light or afferent pupillary defect. The case has not been worked up. Visual-evoked potentials, magnetic resonance imaging brain, and orbit were not done which are the primary investigations in all cases of optic neuropathy. Similarly, demyelinating optic neuritis which is very common was not excluded. The authors have presumed the cause to be ethambutol-induced optic neuropathy without excluding other causes. It would be preposterous to implicate ethambutol as an offending agent especially after only two months of treatment and normal plasma level of the drug. Although reports of early optic neuropathy in doses of 15 mg/kg have been reported in less than 1%of cases,[2,3] it is imperative to exclude other causes before implicating ethambutol as the offending drug. The term optic neuritis is normally reserved for inflammatory or demyelinating conditions. Optic neuropathy is the correct umbrella term under which all causes of involvement of the optic nerve including drugs and toxin-induced neuropathies are included. Author contribution Both the authors have contributed to writing comments on the published article in the journal. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
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Rohatgi et al. (2024) studied this question.
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