Abstract
In Reply.— De' Clari raises some interesting points regarding the potential awakening effect of pyridoxine and makes an argument for pyridoxine infusions in comatose isoniazid-poisoned patients. There are two likely mechanisms by which pyridoxine may reverse isoniazid-induced coma. First, pyridoxine is a cofactor in the transamination reaction between γ-aminobutyric (GABA) and a-ketoglutaric acid—a reaction responsible for GABA degradation. 1 The second mechanism is based on de' Clari's observation of a rapid efflux of isoniazid from the peripheral to the vascular compartment. This efflux would provide a mechanism for a reduction of central nervous system isoniazid levels. By binding to isoniazid (as pyridoxine is known to do), 2 the levels of active circulating isoniazid may be reduced. It is unknown to what degree these two mechanisms are operative in reducing the depth and duration of isoniazid-induced coma. We have some concerns regarding a continuous infusion of pyridoxine for comatose patients. One
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