Because isoniazid inhibits the synthesis of mycolic acid, it is used in the treatment of both latent and active tuberculosis. It can be used as a monotherapy for the treatment of latent tuberculosis but is commonly used in a four drug regimen including pyrazinamide, ethambutol, rifampin for active TB.
Isoniazid must be initially activated by bacterial catalase peroxidase enzyme because it is a pro-drug.
The mechanism of action is to inhibit the synthesis of mycolic acid, which is necessary for synthesis of the mycobacterial cell wall.
Isoniazid is metabolized in the liver via process of acetylation. There are two forms of the acetylator enzyme, a fast and slow form. The patients with the fast form metabolize the drug more quickly than the patients with the slow form.
Use of isoniazid can cause a B6 (pyridoxine) deficiency, which can lead to symptoms such as peripheral neuropathy and sideroblastic anemia.
Peripheral neuropathy and CNS effects are thought to be associated to vitamin B6 (pyridoxine) deficiency.
A well known drug side effect is hepatotoxicity, which can range from abnormal liver function tests to hepatitis.
Isoniazid, along with hydralazine and procainamide are associated with drug-induced lupus erythematosus. These drugs are thought to cause an autoimmune response which causes symptoms similar to lupus erythematosus.
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