Patients were admitted in the hospital for two days. On the study day ater an overnight fast, mg of rifampicin and mg of INH were administered orally with a glass of water. Group II Ten patients who were admitted in the hospital with a diagnosis of ATD induced hepatotoxicity and patients who got clinically detectable jaundice were enrolled in the study. Drug induced hepatotoxicity was established by casual assessment as described by WHO and was conirmed by dechallenge test i.
Blood samples were collected Figure 1: Flow chart indicating the methodology implemented in the present at the same time intervals as mentioned above ater the administration clinical study. Acocella et al.
On the other hand, plasma clearance decreased signiicantly indicating that INH metabolism decreased thus giving rise to higher level of INH, which may further add to hepatotoxicity.
Likewise, Cmax and AUC of rifampicin increased in group II as compared to group I while plasma clearance decreased signiicantly indicating decreased metabolism of rifampicin in these patients. Pharmacokinetic proile of DAH did not difer in two groups. Discussion Isoniazid and rifampicin both are metabolized in the liver and Figure 3: The plasma concentration time curve and values of pharmacokinetic both are known to cause hepatotoxicity.
Under such conditions, it is parameters of rifampicin in both groups of patients. Hepatotoxicity is dependent on further metabolism of MAH by 2. It has been shown Rifampicin-Induced release of hydrazine from lsoniazid. Since 3. Ann Int Med Science Hum Exp Toxicol 3: Ind J Tub Gut Clin Pharmacol Ther J Pharmacol Exp Ther Lukat-Rodgers, G. Rodgers, K.
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