Acute cholestatic hepatitis in a child treated with famotidine

Jimenez-Saenz, Manuel; Argüelles-Arias, Federico; Durán-Quintana, J A; Herrerías-Gutiérrez, JM

doi:10.1016/s0002-9270(00)02199-7

Cited by 3 publications

(3 citation statements)

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“…To our knowledge there have been four cases reported where famotidine was responsible for hepatic failure [8-10]. In the above mentioned four cases, hepatitis was noted after a few weeks of famotidine.…”

Section: Discussionmentioning

confidence: 99%

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Hepatitis following famotidine: a case report

2009

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H2 receptor antagonists can rarely cause idiosyncratic drug reactions leading to acute hepatitis. Famotidine, however, is considered a relatively safe drug with regards to hepatotoxicity. We report a case of a 47 year old male with a history of hepatitis C who developed acute hepatitis on the third day of hospitalization with a dramatic rise in his liver enzymes from normal values at the time of admission. The acute rise in liver enzymes made us consider an adverse drug reaction and famotidine was discontinued. Subsequently his liver enzymes came back to normal in seven days. Thus, physicians should consider famotidine induced hepatitis as a possible etiology of acute liver dysfunction.

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Section: Discussionmentioning

confidence: 99%

“…We report a case of acute hepatic failure secondary to the use of famotidine. To our knowledge, there have only been 4 cases in the English literature where famotidine was responsible for hepatotoxicity [8-10]. …”

Section: Introductionmentioning

confidence: 99%

Hepatitis following famotidine: a case report

2009

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“…Out of the main three H2 antihistamines, cimetidine has the most frequent hepatotoxic effects even after a short period of treatment [15], compared with ranitidine and with famotidine [16,17]. A possible subacute liver failure has been reported after nizatidine.…”

Section: Sporadic Hepatic Dystrophic Changes Induced By Cimetidinementioning

confidence: 99%

Protective effect of cimetidine in carbon tetrachloride-treated rats.

Nedelcu¹,

Vlaicu²,

DumitraÈcu³

2019

biomedicalresearch

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Cimetidine may have hepatoprotective effects. We looked for the impact of cimetidine on the hepatic changes induced by carbon tetrachloride. Male Wistar-Bratislava albino rats were randomized into four groups. Group I, control (C) received physiologic saline solution (PSS) for 3 days. Group II (CT) received PSS but the last administration being followed by a carbon tetrachloride (CT) subcutaneous (sc) injection. Group III (CT+CM) received Cimetidine (CM); at the last dose of CM there was an injection of CT as for group II. Group IV was treated only with CM. The rats were weighted at the beginning of the treatment and at the moment of the euthanasia. Blood sampled were collected. The organs were removed and weighted. A sample of left lobe of the liver was taken for histological analysis. We have analysed morphometric characteristics of the organs, histological and biochemical changes. The acute hepatotoxicity effect of CCl 4 in rats after a single dose was demonstrated after 24 hours. CCl 4 (group II) increases the relative weight of the liver and histologically induces fatty dystrophy and extended centrilobular necrosis. The increase of ASAT and ALAT were massive. The preventive administered cimetidine, associated with CCl 4 (group III) has partially hepatic protection. The fatty infiltration is not present and the focal centrilobular necrosis is less extended. The effect of hepatic cytolysis enzymes is remarkable. Acute administering at rats, CCL 4 has a characteristic hepatotoxicity spectrum, induces fatty dystrophy, hepatic centrilobular necrosis and massive increases of transaminases. Cimetidine in subacute treatment, preventive, for 3 days has protective action relative to CCl 4 .

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The Role of Tumor Necrosis Factor Alpha in Lipopolysaccharide/Ranitidine-Induced Inflammatory Liver Injury

Tukov

Luyendyk

Ganey

et al. 2007

Toxicological Sciences

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Exposure to a nontoxic dose of bacterial lipopolysaccharide (LPS) increases the hepatotoxicity of the histamine-2 (H2) receptor antagonist, ranitidine (RAN). Because some of the pathophysiologic effects associated with LPS are mediated through the expression and release of inflammatory mediators such as tumor necrosis factor alpha (TNF), this study was designed to gain insights into the role of TNF in LPS/RAN hepatotoxicity. To determine whether RAN affects LPS-induced TNF release at a time near the onset of liver injury, male Sprague-Dawley rats were treated with 2.5 x 10(6) endotoxin units (EU)/kg LPS or its saline vehicle (iv) and 2 h later with either 30 mg/kg RAN or sterile phosphate-buffered saline vehicle (iv). LPS administration caused an increase in circulating TNF concentration. RAN cotreatment enhanced the LPS-induced TNF increase before the onset of hepatocellular injury, an effect that was not produced by famotidine, a H2-receptor antagonist without idiosyncrasy liability. Similar effects were observed for serum interleukin (IL)-1beta, IL-6, and IL-10. To determine if TNF plays a causal role in LPS/RAN-induced hepatotoxicity, rats were given either pentoxifylline (PTX; 100 mg/kg, iv) to inhibit the synthesis of TNF or etanercept (Etan; 8 mg/kg, sc) to impede the ability of TNF to reach cellular receptors, and then they were treated with LPS and RAN. Hepatocellular injury, the release of inflammatory mediators, hepatic neutrophil (PMN) accumulation, and biomarkers of coagulation and fibrinolysis were assessed. Pretreatment with either PTX or Etan resulted in the attenuation of liver injury and diminished circulating concentrations of TNF, IL-1beta, IL-6, macrophage inflammatory protein-2, and coagulation/fibrinolysis biomarkers in LPS/RAN-cotreated animals. Neither PTX nor Etan pretreatments altered hepatic PMN accumulation. These results suggest that TNF contributes to LPS/RAN-induced liver injury by enhancing inflammatory cytokine production and hemostasis.

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Acute cholestatic hepatitis in a child treated with famotidine

Cited by 3 publications

References 0 publications

Hepatitis following famotidine: a case report

Hepatitis following famotidine: a case report

Protective effect of cimetidine in carbon tetrachloride-treated rats.

The Role of Tumor Necrosis Factor Alpha in Lipopolysaccharide/Ranitidine-Induced Inflammatory Liver Injury

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