Abstract
When isonicotinic acid hydrazide (INH) was first used for therapy of tuberculosis many patients developed peripheral neuritis resembling that of pyridoxine deficiency. Such patients exhibited increased urinary excretion of pyridoxine; administration of pyridoxine prevented the neuritis (1). In vitro studies have confirmed that INH inhibits pyridoxinedependent bacterial decarboxylases and transaminases (2, 21, 22). This inhibition could also be released more effectively with pyridoxal than with pyridoxine (2, 21). The structures of pyridoxal and its analog are illustrated in figure 1.
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