Oral Amiodarone-induced liver Injury, especially Gamma Glutamyl Transferase Elevation: A Case Report

This study was conducted as a trail to abrogates acrylamide induced hepatotoxicity in male rats by administration of copper (I) nicotinic acid complex. Animals were divided into 4 groups ;GI: control kept on balanced diet and tap water , GII: Acrylamide group received acrylamide in drinking water (7.5 mg/kg b.w.) for 30 days. GIII: treated with copper (I)-nicotinate complex (400 μg/kg b.w.) after acrylamide intoxication for 30 days and GIV the complex then acrylamide (prophylactic). Results showed significant increase in serum levels of AST, ALT, ALP, GGT and total antioxidant capacity (TAC) in acrylamide group. Moreover a significant increase in tumer markers AFU and TNF-Alpha. while Levels of each of S. total protein and S. albumin were significantly decreased in ACR group compared with control. Histological study showed congestion of central vein in liver section and vacuolation of hepatocytes in ACR group. Anticancer activity using in-vitro cytotoxic assay of Cu (I) Nicotinate complex ; proves the anticancer properties of it comparing with doxorubicin. Treatment with Copper (I)-Nicotinate Complex restored tissue and serological indices concomitantly towards normal levels. These results revealed that Copper (I)-Nicotinate Complex is able to significantly alleviate the hepatotoxicity induced by AA in rats and could be utilized as a potent food additives.

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Copper (I) Nicotinate complex Abrogates Acrylamide Induced Hepatotoxicity in Male Rats: Biochemical and Histological Studies

El-Sawi

Aldajani

Mohamed

et al. 2019

IJFNS

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Role of immune dysfunction in drug induced liver injury

Girish¹,

Sanjay²

2021

WJH

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Drug-induced liver injury (DILI) is one of the leading causes of liver failure and withdrawal of drugs from the market. A poor understanding of the precipitating event aetiology and mechanisms of disease progression has rendered the prediction and subsequent treatment intractable. Recent literature suggests that some drugs can alter the liver’s repair systems resulting in injury. The pathophysiology of DILI is complex, and immune dysfunction plays an important role in determining the course and severity of the disease. Immune dysfunction is influenced by the host response to drug toxicity. A deeper understanding of these processes may be beneficial in the management of DILI and aid in drug development. This review provides a structured framework presenting DILI in three progressive stages that summarize the interplay between drugs and the host defence networks.

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Oral Amiodarone-induced liver Injury, especially Gamma Glutamyl Transferase Elevation: A Case Report

Cited by 2 publications

References 14 publications

Copper (I) Nicotinate complex Abrogates Acrylamide Induced Hepatotoxicity in Male Rats: Biochemical and Histological Studies

Copper (I) Nicotinate complex Abrogates Acrylamide Induced Hepatotoxicity in Male Rats: Biochemical and Histological Studies

Role of immune dysfunction in drug induced liver injury

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