Keywords : Hepatotoxicity
A study of hepatoprotective effect of N-acetyl cystein on the patient receiving ATT in tertiary care centre
European Journal of Molecular & Clinical Medicine,
2023, Volume 10, Issue 3, Pages 1169-1180
To hepatoprotective effect of N-acetyl cystein on the patient receiving at in tertiary care centre.
Material & Methods: Study will be conducted on 50 newly diagnosed pulmonary TB and treatment naïve patient from the Department of TB and CHEST at Index Medical College, Research centre and Hospital, Indore and all the tests will be performed with due permission from the Institutional Ethical Committee and informed consent from the subjects or their legal relatives. Subjects were included on the basis of their diagnosis of TB as per RNTCP guidelines. A rise of five fold in ALT over upper normal limit in the absence of symptoms and any increase in serum bilirubin.
Results: For the Sample size of 50 patients, 24 used the NAC drug & 26 were not administered NAC Drug. Without the use of NAC Drug : The Mean SGOT variation was observed from 40.23 to 123.65 from the 1st week to 3rd week, Mean SGPT from 34.31 to 77.38 and Mean Bilirubin variation was from 0.37 to 0.48. As per the study, to study the hepato-protective effect of N-acetyl cystein on liver injury induced by anti TB drugs 24 patients were administered NAC drug. It was observed & documented that Mean SGOT variation from the 1st week to the 3rd week, the change was from 26.92 to 29.92, Mean SGPT variation was from 23.67 to 29.0 and the Mean Bilirubin variation observed was from 0.40 to 0.46. The percentage change is very visible on comparison of the use of NAC drug vis-à- vis NAC drug not administered. The percentage change of SGOT was 111.15% in NAC used patients (p-value 0.0036) & 307.36% in patient not given NAC drug (p-value 0.0009). SGPT percentage change was 122.51% (p-value 0.0005) as compared to 225.56% for Patient not on NAC drug (p-value 0.0009) and Bilirubin percentage change was 115.30% for patient on NAC drug (p-value 0.0050) & 127.31% for patient not on NAC drugs (p-value 0.0301).
Conclusion: Isoniazid, rifampicin, and pyrazinamide, the first-line antituberculosis (anti-TB) drugs are associated with hepatotoxicity. Patients treated with antituberculosis drugs may experience hepatotoxicity ranging from simple hepatic enzyme elevations to severe clinical hepatitis. According to our study results, it could be concluded that NAC acts as an effective antioxidant in the prevention of ATT-induced hepatotoxicity. Administration of NAC produced a significant hepatoprotective effect and effectively reduced lipid peroxidation.
HEPATOPROTECTIVE EFFECT OF d-LIMONENE AGAINST ADRIAMYCIN INDUCED HEPATOTOXICITY IN EXPERIMENTAL RATS
European Journal of Molecular & Clinical Medicine,
2020, Volume 7, Issue 11, Pages 7712-7721
Objective: Monoterpenes plays an essential role to fight against various diseases. Among the various monoterpenes an efficientd-Limonene plays a fundamental role to fight against hepatotoxicity caused by cancer chemotheraphy treatment. Hence the presence study is to evaluate hepatoprotective function of d-limonene against adraimycin induced hepatotoxicity.
Methods: Male albino Wistar rats were administrated with ADR (15mg/Kg body weight) in six equal injection, and the protection efficacy of d-limonene (100mg/Kg body weight) was examined with reference to tissue AST level and the pathological studies was examined by microscopic study.
Results: Rats treated with ADR results in elevated level of liver AST marker enzymes, whereasthe level of AST was controlled when administrated with d-Limonene. However Histopathological proof added more protective role of rats treated with d-limonene against hepatotoxicity.
Conclusion:ADR administration of 15mg/Kg body weight of rats increase the level of hepatotoxicity by increasing the marker enzyme activity and show severe morphological changes. The final outcome from our result suggests that d-limonene (100mg/Kg body weight) a vibrant monoterpene act as latent hepatoprotective negotiator by attenuating ADR induced hepatotoxicity