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A problem-oriented approach to liver disease in oncology patients
  1. G B McDonald1,2,
  2. D Frieze1,3
  1. 1
    Fred Hutchinson Cancer Research Center, Seattle Cancer Care Alliance, Seattle, USA
  2. 2
    University of Washington School of Medicine, Seattle, USA
  3. 3
    University of Washington School of Pharmacy, Seattle, USA
  1. Dr George B McDonald, Gastroenterology/Hepatology Section (D2-190), Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109-1024 USA

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Man sieht nur das, was man weiss – You only see what you know. (J.W. von Goethe, 1808)

The disciplines of oncology, clinical pharmacology, and hepatology have seen rapid growth in their respective literatures that deal with new anti-tumour agents; pharmacokinetics, pharmacodynamics and pharmacogenomics of cancer therapies; and the liver as a key organ in metabolism of these therapies as well as a frequent target of toxicity. The challenge for physicians caring for oncology patients is to integrate an understanding of this literature with practical considerations of how to prevent, diagnose and treat hepatobiliary problems that arise in the midst of therapy.


An ounce of prevention is worth a pound of cure. (Henry De Bracton, c. 1240)

Many underlying hepatobiliary problems become manifest only after anti-cancer therapy has begun. While the lack of recognition of underlying liver disease at baseline is perhaps understandable, some post-therapy liver problems can be prevented with forethought.

Hepatitis B infection

Patients with haematological malignancy, especially those treated with monoclonal antibodies that deplete lymphocytes (eg, rituximab and alemtuzumab), are at risk for fulminant hepatic failure caused by HBV if they habour HBV at baseline.14 Some patients with chronic HBV infection may have underlying fibrosis and portal hypertension, making them vulnerable to sepsis and decompensated liver disease. Baseline testing for HBV (HBsAg, anti-HBc, anti-HBs) should be routine, with polymerase chain reaction (PCR) for HBV DNA reserved for patients who are positive for these markers of HBV infection. There is a hierarchy of risk of fulminant hepatitis B after chemotherapy in the absence of antiviral drugs: high-titre viraemia at baseline > low level viraemia > surface antigenaemia > anti-core positivity > anti-surface antigen positivity (if acquired naturally) > birthplace in an HBV endemic area. Anti-HBc is a marker of prior HBV infection and latent virus; ∼4% …

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  • Funding: Our research in the field of liver toxicity is supported by grants from the U.S. National Institutes of Health, National Cancer Institute (CA 18029, CA 15704).

  • Funding: None.