Drug induced liver injury liver biopsy: Difference between revisions
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==Overview== | ==Overview== | ||
There are no specific liver biopsy findings diagnostic of drug induced injury, but there are several broad histological patterns that reflect the type of injury caused by the inciting drug | There are no specific liver biopsy findings diagnostic of drug induced injury, but there are several broad histological patterns that reflect the type of injury caused by the inciting drug. | ||
==Liver Biopsy== | ==Liver Biopsy== | ||
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Patients presenting with hepatocellular injury tend to have evidence of severe inflammation, necrosism, hemorrhage, and rosette formation on biopsy. Patients with cholestatic injury tend to have more bile plugs and duct paucity. Certain findings on biopsy are predictive of severe and even fatal hepatic injury, including higher degrees of necrosis, microvesicular steatosis, fibrosis, and duct reactions. In contrast, eosinophils and granulomas are associated with milder injury.<ref name="pmid24037963">{{cite journal| author=Kleiner DE, Chalasani NP, Lee WM, Fontana RJ, Bonkovsky HL, Watkins PB et al.| title=Hepatic histological findings in suspected drug-induced liver injury: systematic evaluation and clinical associations. | journal=Hepatology | year= 2014 | volume= 59 | issue= 2 | pages= 661-70 | pmid=24037963 | doi=10.1002/hep.26709 | pmc=3946736 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24037963 }} </ref> | Patients presenting with hepatocellular injury tend to have evidence of severe inflammation, necrosism, hemorrhage, and rosette formation on biopsy. Patients with cholestatic injury tend to have more bile plugs and duct paucity. Certain findings on biopsy are predictive of severe and even fatal hepatic injury, including higher degrees of necrosis, microvesicular steatosis, fibrosis, and duct reactions. In contrast, eosinophils and granulomas are associated with milder injury.<ref name="pmid24037963">{{cite journal| author=Kleiner DE, Chalasani NP, Lee WM, Fontana RJ, Bonkovsky HL, Watkins PB et al.| title=Hepatic histological findings in suspected drug-induced liver injury: systematic evaluation and clinical associations. | journal=Hepatology | year= 2014 | volume= 59 | issue= 2 | pages= 661-70 | pmid=24037963 | doi=10.1002/hep.26709 | pmc=3946736 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24037963 }} </ref> | ||
One example of a drug-specific histological finding is centrilobular necrosis characteristic of acetaminophen hepatotoxicity. | |||
==References== | ==References== |
Revision as of 21:35, 12 August 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rachita Navara, M.D. [2]
Overview
There are no specific liver biopsy findings diagnostic of drug induced injury, but there are several broad histological patterns that reflect the type of injury caused by the inciting drug.
Liver Biopsy
The most common histological patterns seen in the drug induced liver injury network are as follows:
- Acute hepatitis (21%)
- Chronic hepatitis (14%)
- Cholestatic hepatitis (29%)
- Acute cholestasis (9%)
- Chronic cholestasis (10%)
Patients presenting with hepatocellular injury tend to have evidence of severe inflammation, necrosism, hemorrhage, and rosette formation on biopsy. Patients with cholestatic injury tend to have more bile plugs and duct paucity. Certain findings on biopsy are predictive of severe and even fatal hepatic injury, including higher degrees of necrosis, microvesicular steatosis, fibrosis, and duct reactions. In contrast, eosinophils and granulomas are associated with milder injury.[1]
One example of a drug-specific histological finding is centrilobular necrosis characteristic of acetaminophen hepatotoxicity.
References
- ↑ Kleiner DE, Chalasani NP, Lee WM, Fontana RJ, Bonkovsky HL, Watkins PB; et al. (2014). "Hepatic histological findings in suspected drug-induced liver injury: systematic evaluation and clinical associations". Hepatology. 59 (2): 661–70. doi:10.1002/hep.26709. PMC 3946736. PMID 24037963.