Isoniazid-induced psychosis in a patient on DOTS therapy

Isoniazid Induced Psychosis: A Case Report

“…5,8 Various mechanisms for this phenomenon has been suggested but the exact mechanism is not clearly understood, but INH is known to interfere with several metabolic pathways essential for normal neuronal functioning. 2 INH causes vitamin B6 deficiency by increasing its excretion. INH metabolites inhibit the activation of pyridoxine to pyridoxal 5-phosphate, which is a cofactor of the enzyme glutamic acid decarboxylase that catalyzes the conversion of glutamic acid to gammaaminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system.…”

“…Isonicotinic acid hydrazide (INH), also known as Isoniazid, has been in use since it was introduced by Robitzek in 1952 because of its potency, safety and low cost. 2 INH is a prodrug that must be activated inside M. tuberculosis by the catalaseperoxidase enzyme. Activation is associated with a reduction of the mycobacterial ferric KatG catalase-peroxidase by hydrazine and reaction with oxygen to form an oxy ferrous enzyme complex.…”

Isoniazid Associated Psychosis: A Case Series of 3 Patients

“…1 Isonicotinic acid hydrazide or isoniazid (INH) was first discovered in 1912 and was later introduced by Robitzek more than half a century ago in 1952 for the treatment of tuberculosis. 2,3 It is one of the first line agents used along with rifampicin (RIF), pyrazinamide (PZA), ethambutol (EMB) and streptomycin (STM) in the preven tion and treatment of Mycobacterium tuber culosis infection, 1 3 and it is the most potent, least toxic, and most cost effective of all anti tubercular drugs. 2 4,5 The common adverse drug reactions (ADRs) observed with INH include peripheral neuropathy, hepatitis, and rash.…”