Background: Clinical reports emphasize the therapeutic usefulness of granul
ocyte colony-stimulating factor (G-CSF) in clozapine-induced granulocytopen
ia. Only sparse information exists, however on the natural course of endoge
nous G-CSF plasma levels in this condition.
Methods: We monitored G-CSF and white blood cell (WBC) counts in a 73-year-
old patient who developed granulocytopenia while being treated with clozapi
ne for schizoaffective disorder. Clozapine treatment was discontinued immed
iately, and G-CSF serum levels were determined repeatedly during the clinic
al course.
Results: Whereas WBC counts increased again within 6 days after discontinua
tion of clozapine, G-CSF level decreased significantly within the same peri
od. The rapid decrease of endogenous G-CSF levels paralleled by a normaliza
tion of neutrophil count was interpreted as the result of an intact regulat
ory mechanism of granulocytopoesis. Therefore G-CSF therapy was not initiat
ed. Owing to lack of therapeutic alternatives, it was decided to reintroduc
e clozapine. G-CSF levels decreased further, accompanied by an increase of
WBCs, indicating stable bone marrow functioning
Conclusions: Based on this observation, we assume that the course of G-CSF
and WBC counts indicated an abortive form of toxic bone marrow damage with
subsequent recovery. We conclude that monitoring of G-CSF levels may serve
as a useful tool in the follow-up of patients in whom clozapine-induced bon
e marrow damage is suspected. (C) 2000 Society of Biological Psychiatry.