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Summary

This case study reports a rare instance of liver injury caused by denosumab, a medication used to treat low bone density. The patient experienced elevated liver enzymes and inflammation, suggesting an immune reaction to the drug.

Keywords:
cytokinedenosumabdrug-induced hepatotoxicityimmune hepatitisnecrosisnuclear factor-κB (NFκB)osteoporosisreceptor activator of nuclear factor-κB ligand (RANKL)

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Area of Science:

  • Endocrinology
  • Hepatology
  • Immunology

Background:

  • Denosumab (Prolia®, Xgeva®) is a monoclonal antibody targeting RANKL, used for osteoporosis and bone metastases.
  • Hepatotoxicity from denosumab is exceptionally rare, with only one prior case attributed to an immune response.
  • This report details a second documented case of denosumab-induced liver injury.

Observation:

  • A 43-year-old female with a history of breast cancer developed elevated liver enzymes (ALT, AST) ten times the upper limit of normal.
  • Liver biopsy revealed chronic inflammation, interface hepatitis, and plasma cell infiltration, indicative of drug-induced liver injury (DILI).
  • The patient had received denosumab for osteoporosis prevention following endocrine therapy for breast cancer.

Findings:

  • The patient presented with significant elevations in alanine aminotransferase and aspartate aminotransferase levels.
  • Histopathological examination of the liver showed immune-mediated inflammation, including plasma cells and lymphocytes.
  • These findings support a diagnosis of drug-induced liver injury (DILI) secondary to denosumab administration.

Implications:

  • This case highlights the potential for denosumab to cause rare immune-mediated hepatotoxicity.
  • Clinicians should consider DILI in patients presenting with liver enzyme abnormalities after denosumab treatment.
  • Further investigation into the immunological mechanisms of denosumab-induced liver injury may be warranted.