Gemtuzumab ozogamicin-induced sinusoidal obstructive syndrome treated with defibrotide: a case report

J Clin Pharm Ther. 2006 Aug;31(4):389-92. doi: 10.1111/j.1365-2710.2006.00742.x.

Abstract

New treatments for relapse of acute myeloid leukaemia (AML), include gemtuzumab ozogamicin (GO), an anti-CD33 monoclonal antibody. We describe a second case of GO-induced sinusoidal obstructive syndrome (SOS) effectively treated with defibrotide (DF). No stem-cell transplantation was involved. On day 23 after the first GO dose, a patient presented with ascites, weight gain, liver enlargement and pain in the right upper quadrant. Sudden hepatic cytolysis (transaminases at six times the normal range: grade 3) and cholestasis [alkaline phosphatase ALP and gamma-glutamyltransferase (GGT) respectively at four and eight times the normal range: grade 2] were observed but there was no evidence of increase serum bilirubin. Treatment with DF (Prociclide), Crinos; 10 mg/kg/day, or 200 mg, q.i.d.) improved the hepatic abnormality within a few days (serum transaminases decreased from 312 to 103 IU/L for aspartate aminotransferase (AST) and from 141 to 80 IU/L for alanine aminotransferase (ALT) within 3 days ALP increased from 253 to 383 IU/L and gamma-GT from 238 to 417 IU/L 4 days after administration of DF. The clinical and biological features of our case suggest a direct involvement of GO in causing SOS, even when used as monotherapy, without allogenic stem-cell transplantation. Low dose DF (10 mg/kg/day) given early during the development of SOS associated with GO was effective. Unfortunately, in our case the patient eventually died of multi-organ failure probably because of failure of GO.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Fatal Outcome
  • Fibrinolytic Agents / therapeutic use
  • Hepatic Veno-Occlusive Disease / chemically induced*
  • Hepatic Veno-Occlusive Disease / drug therapy
  • Hepatic Veno-Occlusive Disease / physiopathology
  • Humans
  • Leukemia, Myeloid / drug therapy
  • Male
  • Polydeoxyribonucleotides / therapeutic use
  • Succinates / adverse effects*

Substances

  • Fibrinolytic Agents
  • Polydeoxyribonucleotides
  • Succinates
  • defibrotide
  • guanidinoethylmercaptosuccinic acid