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Blood, 1 April 2002, Vol. 99, No. 7, pp. 2310-2314
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Hepatic sinusoidal obstruction after gemtuzumab ozogamicin
(Mylotarg) therapy
Pankaj Rajvanshi,
Howard M. Shulman,
Eric L. Sievers, and
George B. McDonald
From the Gastroenterology/Hepatology, Oncology, and
Pathology Sections, Clinical Research Division, Fred Hutchinson Cancer
Research Center, and the University of Washington School of Medicine,
Seattle, WA.
Gemtuzumab ozogamicin (Mylotarg) targets leukemia cells expressing
the CD33 receptor by means of a monoclonal antibody conjugated to a
cytotoxic agent, calicheamicin. Treatment of acute myeloid leukemia
(AML) with gemtuzumab ozogamicin may result in liver injury. We
reviewed the course of 23 patients who were given gemtuzumab ozogamicin
for AML that had relapsed after hematopoietic cell transplantation.
Liver toxicity was assessed through physical examination, serum tests,
histologic examination, and hepatic venous pressure measurements. Liver
injury developed in 11 patients after gemtuzumab ozogamicin
administration; it was manifested as weight gain, ascites, and jaundice
in 7 patients. Seven patients died with persistent liver dysfunction
and either multiorgan failure or sepsis at a median of 40 days after
gemtuzumab ozogamicin infusion. Portal pressure measurements were
elevated in 2 patients. Results of liver histologic examination in 5 patients showed sinusoidal injury with extensive sinusoidal fibrosis,
centrilobular congestion, and hepatocyte necrosis. Six patients
experienced AML remission that was sustained for at least 60 days after
gemtuzumab ozogamicin infusion. In summary, hepatic sinusoidal liver
injury developed after gemtuzumab ozogamicin infusion.
Histology showed striking deposition of sinusoidal collagen, suggesting
that gemtuzumab ozogamicin targets CD33+ cells residing in
hepatic sinusoids as the mechanism for its hepatic toxicity.
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