Case report: We report the case of a 50-year-old man, treated with chlorpromazine for schizophrenia, who developed an agranulocytosis. Three mechanisms of drugs-induced agranulocytosis have been reported: toxic, genetic and immune. Phenothiazines are responsible for drug-induced agranulocytosis. This patient had been treated with first and second generation antipsychotic drugs during his life and had already been exposed to chlorpromazine or other phenotiazines without any signs of toxicity. However, two months after the introduction of chlorpromazine he presented an agranulocytosis (leukocytes 1.4G/L and neutrophils 0.2G/L). After discontinuation of chlorpromazine, blood count returned to normal. The role of chlorpromazine in inducing toxic agranulocytosis was based on: (i) normal blood count before the introduction of chlorpromazine; (ii) occurrence of agranulocytosis within the first weeks of chlorpromazine treatment; (iii) normal bone marrow and blood count after discontinuation of chlorpromazine; (iv) chlorpromazine was the only new drug prescribed to this patient at the time the agranulocytosis occurred. Risk factors for toxic agranulocytosis in this patient were: old age, association of phenothiazine with other drugs known to be able to induce agranulocytosis, and past history of use of high doses of chlorpromazine.
Discussion: This case report highlights the risk of chlorpromazine in inducing agranulocytosis, a risk underestimated in regard of the clozapine risk to induce agranulocytosis or neutropenia. For this reason, it seems reasonable to recommend performing a blood count before introduction of phenothiazine in patients with risk factors for toxic drug-induced agranulocytosis (old age, female, receiving other drugs with a high potential to induce agranulocytosis and having received high doses of phenothiazine for a long time).