Nimesulide-induced acute hepatitis: evidence from six cases

Steenbergen, Werner Van; Peeters, Pascal; Bondt, Joris De; Staessen, Dirk; Buscher, H.-P.; Laporta, Thiery; Roskams, Tania; Desmet, Valeer

doi:10.1016/s0168-8278(98)80188-8

Cited by 92 publications

(43 citation statements)

References 19 publications

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“…Genetic factors and individual sensitivity are no doubt important factors in the Creatinin (mg/100 ml) 7.6 1.7 1.3 etiology of these symptoms and determine whether this potential toxicity will become clinically manifest (Robin et al, 1997;Boelsterli, 2002). Van Steenbergen et al (1998) stated that immunological and metabolic idiosyncratic reactions may be the pathogenic mechanisms of nimesulide-induced liver disease in humans. Renal adverse effects to these drugs are due to the inhibition of prostaglandin synthesis, an increase in renal vascular resistance with a concomitant decrease in diuresis, GFR, and renal blood flow acute reversible renal failure (Apostolou et al, 1997;Balasubramaniam, 2000;Prevot et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Nimesulide-induced acute biliary tract injury and renal failure in a kitten: a case report

Börkü¹,

Güzel²,

Karakurum³

et al. 2008

Vet. Med. - Czech

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ABSTRACT:A 3-month-old male kitten was presented to our clinic with malaise, vomiting and jaundice. In the anamnesis, we learned that the cat had a history of anorexia, sneezing, and nasal discharge and that the owner had administered 100 mg/day (t.i.d.) nimesulide orally for three days. In the laboratory study, high levels of serum alkaline phosphatase, γ-glutamyl transtransferase, total bilirubin, direct bilirubin, indirect bilirubin, urea, and creatinine were detected. All the clinical signs and laboratory abnormalities returned to normal levels after cessation of the nimesulide and supportive treatment. In this case, clinical and laboratory findings were thought to be compatible with nimesulide-induced acute biliary injury and renal failure. This case report indicates that the household pets are at risk of toxic drugs administered by their owners and great caution should be taken in administering NSAIDs in cats.

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Section: Discussionmentioning

confidence: 99%

Nimesulide-induced acute biliary tract injury and renal failure in a kitten: a case report

Börkü¹,

Güzel²,

Karakurum³

et al. 2008

Vet. Med. - Czech

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“…For instance, amoxicillin-clavulanate tends to produce cholestatic or mixed damage, although hepatocellular damage has been repor ted frequently as well [16,54] . Hepatocellular and cholestatic or mixed injury have been noted with nimesulide [55] or troglitazone [56,57] , among others. Hence it is important for gastroenterologists to view a suspicion of drug-induced hepatotoxicity with caution and with awareness that any given drug can produce diverse types of injury [58] .…”

Section: Cur Rently the Only Way To Confidently Confir M I D I O S Ymentioning

confidence: 99%

Assessment of drug-induced hepatotoxicity in clinical practice: A challenge for gastroenterologists

Andrade¹,

Robles²,

Fernández-Castañer³

et al. 2007

WJG

144

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Currently, pharmaceutical preparations are serious contributors to liver disease; hepatotoxicity ranking as the most frequent cause for acute liver failure and postcommercialization regulatory decisions. The diagnosis of hepatotoxicity remains a difficult task because of the lack of reliable markers for use in general clinical practice. To incriminate any given drug in an episode of liver dysfunction is a step-by-step process that requires a high degree of suspicion, compatible chronology, awareness of the drug's hepatotoxic potential, the exclusion of alternative causes of liver damage and the ability to detect the presence of subtle data that favors a toxic etiology. This process is time-consuming and the final result is frequently inaccurate. Diagnostic algorithms may add consistency to the diagnostic process by translating the suspicion into a quantitative score. Such scales are useful since they provide a framework that emphasizes the features that merit attention in cases of suspected hepatic adverse reaction as well. Current efforts in collecting bona fide cases of drug-induced hepatotoxicity will make refinements of existing scales feasible. It is now relatively easy to accommodate relevant data within the scoring system and to delete low-impact items. Efforts should also be directed toward the development of an abridged instrument for use in evaluating suspected drug-induced hepatotoxicity at the very beginning of the diagnosis and treatment process when clinical decisions need to be made. The instrument chosen would enable a confident diagnosis to be made on admission of the patient and treatment to be finetuned as further information is collected.

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“…lide-associated liver injury have exhibited features possibly consistent with an immunoallergic mechanism, hypersensitivity manifestations were absent in most patients, suggesting metabolic idiosyncrasy rather than immunoallergy (Van Steenbergen et al, 1998).…”

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confidence: 93%

The Anti-Inflammatory Drug, Nimesulide (4-Nitro-2-phenoxymethane-sulfoanilide), Uncouples Mitochondria and Induces Mitochondrial Permeability Transition in Human Hepatoma Cells: Protection by Albumin

Berson

Cazanave²,

Descatoire³

et al. 2006

J Pharmacol Exp Ther

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Like other nonsteroidal anti-inflammatory drugs, nimesulide (4-nitro-2-phenoxymethane-sulfoanilide) triggers hepatitis in a few recipients. Although nimesulide has been shown to uncouple mitochondrial respiration and cause hepatocyte necrosis in the absence of albumin, mechanisms for cell death are incompletely understood, and comparisons with human concentrations are difficult because 99% of nimesulide is albumin-bound. We studied the effects of nimesulide, with or without a physiological concentration of albumin, in isolated rat liver mitochondria or microsomes and in human hepatoma cells. Nimesulide did not undergo monoelectronic nitro reduction in microsomes. In mitochondria incubated without albumin, nimesulide (50 M) decreased the mitochondrial membrane potential (⌬ m ), increased basal respiration, and potentiated the mitochondrial permeability transition (MPT) triggered by calcium preloading. In HUH-7 cells incubated for 24 h without albumin, nimesulide (1 mM) decreased the ⌬ m and cell NAD(P)H and increased the glutathione disulfide/reduced glutathione ratio and cell peroxides; nimesulide triggered MPT, ATP depletion, high cell calcium, and caused mostly necrosis, with rare apoptotic cells. Coincubation with either cyclosporin A (an MPT inhibitor) or the combination of fructose-1,6-diphosphate (a glycolysis substrate) and oligomycin (an ATPase inhibitor) prevented the decrease in ⌬ m , ATP depletion, and cell death. A physiological concentration of albumin abolished the effects of nimesulide on isolated mitochondria or HUH-7 cells. In conclusion, the weak acid, nimesulide, uncouples mitochondria and triggers MPT and ATP depletion in isolated mitochondria or hepatoma cells incubated without albumin. However, in the presence of albumin, only a fraction of the drug enters cells or organelles, and uncoupling and toxicity are not observed.

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Nimesulide-induced acute hepatitis: evidence from six cases

Cited by 92 publications

References 19 publications

Nimesulide-induced acute biliary tract injury and renal failure in a kitten: a case report

Nimesulide-induced acute biliary tract injury and renal failure in a kitten: a case report

Assessment of drug-induced hepatotoxicity in clinical practice: A challenge for gastroenterologists

The Anti-Inflammatory Drug, Nimesulide (4-Nitro-2-phenoxymethane-sulfoanilide), Uncouples Mitochondria and Induces Mitochondrial Permeability Transition in Human Hepatoma Cells: Protection by Albumin

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