Outpatient Drug‐Induced Parenchymal Liver Disease Requiring Hospitalization

Beard, Keith; Belic, Lanie; Aselton, Pamela; Perera, David; Jick, Hershel

doi:10.1002/j.1552-4604.1986.tb02963.x

Cited by 32 publications

(10 citation statements)

References 23 publications

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“…Due to the lack of internationally accepted criteria for DILI, the overall incidence for DILI-ALF is variable [24,25]. For clinicians, DILI remains a diagnosis of exclusion, and the lack of experience with recognizing DILI may lead to delayed diagnosis and greater risks of severe or chronic liver injury [26].…”

Section: Discussionmentioning

confidence: 99%

Steroid and Ursodesoxycholic Acid Combination Therapy in Severe Drug-Induced Liver Injury

et al. 2011

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Background: Drug-induced liver injury (DILI) is the leading cause of acute severe liver disease in Western countries. Treatment strategies for DILI are still not well defined. Aim: We studied the safety and outcomes of steroid/ursodesoxycholic acid (UDCA) combination therapy in DILI patients. Patients, Materials and Methods: 15 consecutive patients with severe DILI were analyzed for clinical, biochemical and histological data. Nine patients were treated with a steroid step-down therapy with reduction of the daily dose over several weeks; 6 patients received a steroid pulse therapy for 3 days. UDCA was administered for several weeks in both groups. Results: Patients without histological signs of preexistent liver damage (n = 10) showed the most favorable clinical course. Bilirubin and serum transaminases dropped to <50% of peak values within 2 weeks, and normalized within 4–8 weeks. In contrast, patients with positive autoimmune antibodies (anti-nuclear antibodies and/or soluble liver antigen) and/or histological features of chronic hepatitis (n = 3) exhibited a slower reduction in bilirubin and serum transaminase levels. These patients were given immunosuppressants (steroids, azathioprine) for a further 6 months. Conclusion: Treatment of severe DILI with corticosteroids (both pulse and step-down therapy) and UDCA appears to be safe, and leads to a more rapid reduction in bilirubin and transaminases after DILI.

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Section: Discussionmentioning

confidence: 99%

Steroid and Ursodesoxycholic Acid Combination Therapy in Severe Drug-Induced Liver Injury

et al. 2011

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“…Trimethoprim-sulfamethoxazole (TMP-SMZ) is a widely used antibiotic combination effective in the treatment of a variety of pathogens causing urinary tract infections, upper respiratory infections and Pneurnocystis curinii pneumonia (1,2). TMP-SMZ is generally well tolerated when given orally or intravenously; it has a good safety record (3)(4)(5).…”

Section: ~342-347)mentioning

confidence: 99%

Intrahepatic cholestasis and phospholipidosis associated with the use of trimethoprim-sulfamethoxazole

1990

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Although liver injury after administration of the trimethoprim-sulfamethoxazole combination is rare, hepatocellular necrosis and cholestasis have developed in a few cases. We describe a patient who developed a severe, prolonged cholestatic reaction after trimethoprim-sulfamethoxazole administration. The findings from serial liver biopsy samples showed characteristic abnormalities of phospholipidosis that have not been previously described for trimethoprim-sulfamethoxazole-related hepatic injury. The most prominent finding on electron microscopic evaluation of the liver was the presence of prominent hepatocyte lysosomal inclusions characterized by concentric arrangements of membranous and lamellated structures. The patient improved after several courses of exchange plasmapheresis, which may have assisted in the removal of toxic drug-lipid complexes. The pathogenesis of this acquired secondary phospholipidosis is unknown. Possible mechanisms include generation of highly lipid-soluble metabolites and inhibition of the lysosomal enzyme phospholipase A1.

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“…The overall incidence of drug-induced liver injury (DILI) is variable,8 9 10 11 probably a reflection of the lack of internationally accepted criteria for DILI, under-reporting and selection bias 12. A meta-analysis from Canada reported the incidence of serious adverse reactions (ADRs) to drugs (defined as those that required hospitalisation, were permanently disabling, or resulted in death) as 6.7%, and of fatal ADRs as 0.32% of hospitalised patients 8.…”

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confidence: 99%

Diagnosis, management and prevention of drug-induced liver injury

Verma

Kaplowitz

2009

Gut

165

120

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Drug-induced liver injury (DILI) is increasingly being recognised as a significant cause of both acute and chronic liver disease. The most commonly implicated agents are paracetamol, antimicrobials, non-steroidal anti-inflammatory drugs, statins, isoniazid and herbal remedies. Drug-induced hepatotoxicity is generally idiosyncratic in nature. The pathogenesis of DILI remains enigmatic, but involves exposure to the toxic agent, mitochondrial injury, failure of adaptation, and innate and adaptive immune responses. Diagnosis of drug-induced liver diseases can be difficult, but the key to causality is to diligently exclude other causes of liver injury, and to identify a characteristic clinical drug-related signature. Management of drug-induced liver injury is symptomatic, with early referral to a liver transplant unit at the first hint of liver failure, especially in those with non-paracetamol-induced liver injury. Prevention of drug hepatotoxicity includes increased vigilance during pre-clinical drug development and clinical trials, alanine aminotransferase monitoring with certain drugs, better marketing strategies, and the future identification of both diagnostic and prognostic biomarkers.

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Outpatient Drug‐Induced Parenchymal Liver Disease Requiring Hospitalization

Cited by 32 publications

References 23 publications

Steroid and Ursodesoxycholic Acid Combination Therapy in Severe Drug-Induced Liver Injury

Steroid and Ursodesoxycholic Acid Combination Therapy in Severe Drug-Induced Liver Injury

Intrahepatic cholestasis and phospholipidosis associated with the use of trimethoprim-sulfamethoxazole

Diagnosis, management and prevention of drug-induced liver injury

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