Article Text

  1. J. Voss,
  2. L. Puneky
  1. Division of Oncology, University of Mississippi Medical Center, Jackson, MS


Purpose To investigate the incidence and etiology of acute thrombocytopenia due to fluorouracil (FU).

Patient Case A 76-year-old female with metastatic colorectal cancer was admitted for course number 17 of FOLFOX (FU/leucovorin/oxalaplatin) and 13 of bevacizumab. Within 36 hours of the start of chemotherapy, she developed gingival bleeding and melena. Her platelet count was 3,000 compared to 171,000 the previous day. PT, PTT, direct Coombs', fibrinogen, and peripheral smear were unremarkable. Her remaining chemotherapy was held, and 2 units of platelets were transfused with an appropriate incremental rise. She had a similar occurrence with the next 2 cycles of FOLFOX/bevacizumab as demonstrated by an acute fall of the platelet count within a 24-hour period. Thrombocytopenia was also experienced when FOLFIRI/bevacizumab (FU/leucovorin/irinotecan) was administered with a decline from 114,000 to 2,000 over an 8-hour period. To rule out other medications, Zofran and Decadron were given 8 hours prior to the chemotherapy. No adverse events were noted from these premedications. She has now tolerated a course of IROX (irinotecan/oxaliplatin) and bevacizumab without incident.

Summary After a literature review, reported cases of hemolysis and immune thrombocytopenia were found with irinotecan and oxaliplatin. However, no such reports were found for FU. This case demonstrates Level I evidence of drug-induced thrombocytopenia due to FU. Using modified antigen capture ELISA, convalescent serum tested positive for IgG against HPA 5a/5b platelet-specific antigen. However, there was no potentiation of reaction when serum was exposed to FU.

Conclusion It is proposed here that the effect of the patient's known antibody is potentiated in vivo when exposed to FU resulting in immune thrombocytopenia through a yet to be identified mechanism.

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