Drug-induced liver disease

Lewis, James H.; Ahmed, Moustafa; Shobassy, Ahmed; Palese, Caren

doi:10.1097/01.mog.0000218958.40441.fd

Cited by 30 publications

(31 citation statements)

References 110 publications

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“…Specific liver injury inducible by phytochemical agents includes elevation in transaminases (Zhu et al, 2004; Saleem et al, 2010), acute and chronic hepatitis (Stedman, 2002; Pierard et al, 2009), liver failure (Durazo et al, 2004), veno-occlusive disorders (DeLeve et al, 2002), liver cirrhosis (Lewis et al, 2006), fibrosis (Chitturi and Farrell, 2000), cholestasis (Chitturi and Farrell, 2008), zonal or diffusive hepatic necrosis (Savvidou et al, 2007), and steatosis (Wang et al, 2009). Mechanism of liver injury may include bioactivation of CYP, oxidative stress, mitochondrial injury, and apoptosis (Cullen, 2005).…”

Section: Resultsmentioning

confidence: 99%

An Overview of the Evidence and Mechanisms of Herb–Drug Interactions

Fasinu¹,

Bouic²,

Rosenkranz³

2012

Front. Pharmacol.

205

140

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Despite the lack of sufficient information on the safety of herbal products, their use as alternative and/or complementary medicine is globally popular. There is also an increasing interest in medicinal herbs as precursor for pharmacological actives. Of serious concern is the concurrent consumption of herbal products and conventional drugs. Herb–drug interaction (HDI) is the single most important clinical consequence of this practice. Using a structured assessment procedure, the evidence of HDI presents with varying degree of clinical significance. While the potential for HDI for a number of herbal products is inferred from non-human studies, certain HDIs are well established through human studies and documented case reports. Various mechanisms of pharmacokinetic HDI have been identified and include the alteration in the gastrointestinal functions with consequent effects on drug absorption; induction and inhibition of metabolic enzymes and transport proteins; and alteration of renal excretion of drugs and their metabolites. Due to the intrinsic pharmacologic properties of phytochemicals, pharmacodynamic HDIs are also known to occur. The effects could be synergistic, additive, and/or antagonistic. Poor reporting on the part of patients and the inability to promptly identify HDI by health providers are identified as major factors limiting the extensive compilation of clinically relevant HDIs. A general overview and the significance of pharmacokinetic and pharmacodynamic HDI are provided, detailing basic mechanism, and nature of evidence available. An increased level of awareness of HDI is necessary among health professionals and drug discovery scientists. With the increasing number of plant-sourced pharmacological actives, the potential for HDI should always be assessed in the non-clinical safety assessment phase of drug development process. More clinically relevant research is also required in this area as current information on HDI is insufficient for clinical applications.

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Section: Resultsmentioning

confidence: 99%

An Overview of the Evidence and Mechanisms of Herb–Drug Interactions

Fasinu¹,

Bouic²,

Rosenkranz³

2012

Front. Pharmacol.

205

140

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“…Hypertransaminasemia of biliary etiology is remarkably more mild and presents with simultaneous elevation of GGT and alkalin phosphatase and, very often of bilirubin levels [10]. Conversely, the maintenance of a combined therapy with somatostatin analogs and pegvisomant does not explain the changes in gall blader contractility which could have provoked the propulsion of gallstone into the biliary duct.…”

Section: Discussionmentioning

confidence: 97%

“…Toxicity due to reactive metabolites is the most common mechanism and may be due to the existence of free radicals created during the biotransformation of the drug or by toxic metabolites which bind to certain molecules or cellular structures altering their structure, integrity and activity. The effects of such indirect aggressions are varied and include lipidic degeneration and hepatocellular necrosis [10]. Hypertransaminasemia associated to pegvisomant therapy seems to be the result of a toxic reaction produced by reactive metabolites (idiosincrasic) and not the result of a direct toxic mechanism.…”

Section: Discussionmentioning

confidence: 99%

Self-limited acute hepatotoxicity caused by pegvisomant

et al. 2009

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We present a case of acute severe hepatitis in a patient with acromegaly receiving combination therapy with somatostatin analogs and pegvisomant. Hepatitis resolved completely 18 weeks after diagnosis of hypertransaminasemia without discontinuation of therapy and with a close clinical and biochemical follow-up. In this case, despite the severity of the hepatitis, therapy could be continued as hypertransaminasemia was gradually decreasing after the maximum peak. We also review the literature on toxic hepatitis associated to pegvisomant therapy analyzing the etiology, clinical predisposing factors and natural evolution.

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“…However, a contributory role of paracetamol in liver injury in these cases cannot be ruled out [22]. …”

Section: Discussionmentioning

confidence: 99%

Paracetamol in therapeutic dosages and acute liver injury: causality assessment in a prospective case series

et al. 2011

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BackgroundAcute liver injury (ALI) induced by paracetamol overdose is a well known cause of emergency hospital admission and death. However, there is debate regarding the risk of ALI after therapeutic dosages of the drug.The aim is to describe the characteristics of patients admitted to hospital with jaundice who had previous exposure to therapeutic doses of paracetamol. An assessment of the causality role of paracetamol was performed in each case.MethodsBased on the evaluation of prospectively gathered cases of ALI with detailed clinical information, thirty-two cases of ALI in non-alcoholic patients exposed to therapeutic doses of paracetamol were identified. Two authors assessed all drug exposures by using the CIOMS/RUCAM scale. Each case was classified into one of five categories based on the causality score for paracetamol.ResultsIn four cases the role of paracetamol was judged to be unrelated, in two unlikely, and these were excluded from evaluation. In seven of the remaining 26 cases, the RUCAM score associated with paracetamol was higher than that associated with other concomitant medications. The estimated incidence of ALI related to the use of paracetamol in therapeutic dosages was 0.4 per million inhabitants older than 15 years of age and per year (99%CI, 0.2-0.8) and of 10 per million paracetamol users-year (95% CI 4.3-19.4).ConclusionsOur results indicate that paracetamol in therapeutic dosages may be considered in the causality assessment in non-alcoholic patients with liver injury, even if the estimated incidence of ALI related to paracetamol appears to be low.

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Drug-induced liver disease

Abstract: Drug-induced liver disease remains an important cause of acute liver failure, and research efforts by the National Institutes of Health and others are underway to better determine the risk factors and other host susceptibilities that will allow for the safer use of drugs in the future.

Cited by 30 publications

References 110 publications

An Overview of the Evidence and Mechanisms of Herb–Drug Interactions

An Overview of the Evidence and Mechanisms of Herb–Drug Interactions

Self-limited acute hepatotoxicity caused by pegvisomant

Paracetamol in therapeutic dosages and acute liver injury: causality assessment in a prospective case series

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