We report a case of amodiaquine-induced agranulocytosis in a 60-year-old woman. Four months after the agranulocytosis episode we investigated the effect of the drug using in vitro agar culture techniques. Amodiaquine at increasing concentrations (0.005, 0.05 and 0.5 μg/ml) displayed an inhibitory effect, probably dose-dependent, on the growth of the patient’s bone marrow GM-CFU colonies in the absence of autologous serum. In contrast, no effect was found on the colony and cluster growth of bone marrow samples from 13 healthy controls. Though it has been shown in several cases that amodiaquine-induced agranulocytosis occurs via immune-mediated mechanisms, our data are in support of a direct toxic effect of the drug on abnormally sensitive myeloid progenitor cells.

Several haematological and immunological parameters were studied before and after a 4-week trial of oral levamisole (300 mg/week) in 15 patients with chronic lymphocytic leukaemia. We found no statistically significant difference in the mean peripheral blood counts of total lymphocytes, E-rosette-forming lymphocytes, monocytes, polymorphonuclear neutrophils, eosinophils and platelets. Mean serum levels of IgG, IgA, IgM, IgD, C3 and C4 were not statistically affected by levamisole nor was the mean lymphocyte stimulation modified by various mitogens (phytohaemagglutinin, concanavalin A, pokeweed mitogen, tuberculin, candidin). The mean IgE level was statistically increased (p < 0.05) after levamisole administration but remained below the normal upper limit. A high rate (46%) of clinical and haematological adverse reactions (1 patient developed thrombocytopenia) was associated with levamisole administration. These results suggest that levamisole, as given in this trial, has no obvious beneficial effect and cannot be recommended in patients with chronic lymphocytic leukaemia.

No abstract