Drug-induced liver injury (DILI) can be a diagnostic challenge for clinicians and pathologists due to its diverse histopathologic patterns, biochemical classifications, and an expanding list of causative drugs and supplements. This chapter covers frequently asked questions regarding DILI, including its classification, diagnostic approach, and histologic manifestations. Key topics include distinguishing intrinsic from idiosyncratic DILI, the role of liver biopsy, and the histologic features of various injury patterns, such as acute and chronic hepatitis, cholestasis, steatosis and steatohepatitis, granulomatous inflammation, and vascular injury. Specific drugs implicated in these histologic patterns, including immune checkpoint inhibitors and total parenteral nutrition, will be reviewed. Additional considerations include differentiating DILI from autoimmune hepatitis, the significance of eosinophils in DILI, stellate cell lipidosis, polypharmacy-induced injury, drug-related hepatic neoplasms, and drug-induced hemophagocytic lymphohistiocytosis.

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Drug-Induced Liver Injury

  • Sarah L. Zhang,
  • Xiaotang Alison Du,
  • Hanlin L. Wang

摘要

Drug-induced liver injury (DILI) can be a diagnostic challenge for clinicians and pathologists due to its diverse histopathologic patterns, biochemical classifications, and an expanding list of causative drugs and supplements. This chapter covers frequently asked questions regarding DILI, including its classification, diagnostic approach, and histologic manifestations. Key topics include distinguishing intrinsic from idiosyncratic DILI, the role of liver biopsy, and the histologic features of various injury patterns, such as acute and chronic hepatitis, cholestasis, steatosis and steatohepatitis, granulomatous inflammation, and vascular injury. Specific drugs implicated in these histologic patterns, including immune checkpoint inhibitors and total parenteral nutrition, will be reviewed. Additional considerations include differentiating DILI from autoimmune hepatitis, the significance of eosinophils in DILI, stellate cell lipidosis, polypharmacy-induced injury, drug-related hepatic neoplasms, and drug-induced hemophagocytic lymphohistiocytosis.