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CCNU Toxicity After an Overdose in a Patient with Hodgkin's Disease
Author(s) -
Hörnsten Per,
SundmanEngberg Britt,
Gahrton Gösta,
Johansson Bo
Publication year - 1983
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1983.tb02129.x
Subject(s) - bone marrow , medicine , chemotherapy , toxicity , platelet , cfu gm , absolute neutrophil count , white blood cell , in vivo , haematopoiesis , gastroenterology , pharmacology , immunology , neutropenia , stem cell , biology , microbiology and biotechnology , genetics
An overdose of CCNU (600 mg over a 15‐d period) was unintentionally ingested by a patient with advanced Hodgkin's disease subjected to combination chemotherapy. A severe bone marrow depression occurred 3 weeks after the start of the CCNU treatment. The nadir of the platelet count was reached after 4 weeks and that of the granulocyte count after 5 weeks. At the nadir of the white blood cell count, colony‐forming cells (CFU‐C) were found in significantly reduced numbers in the bone marrow, and were not found at all in the peripheral blood; the amount of colony‐stimulating activity (CSA) produced by peripheral blood cells was reduced. However, the cells producing CSA recovered earlier than the CFU‐C, and the CSA peak value was reached about 1 week before the peak value for CFU‐C in the bone marrow. Thus, in vivo CSA‐producing cells appeared to be more resistant to CCNU than were CFU‐C, and their recovery appeared to be a prerequisite for the recovery of CFU‐C and myelopoietic cells.