As intravenous administration of deferoxamine is difficult in home dialysis patients we set out to determine the efficacy of intramuscular (i.m.) and intraperitoneal (i.p.) deferoxamine for removal of aluminium. Patients with serum aluminium levels greater than 90 μg/liter were studied in a paired fashion with each patient serving as their own control. Serum and peritoneal fluid aluminium were determined using flameless atomic absorption. In hemodialysis patients 2 g of intravenous deferoxamine increased serum aluminium from 124.7 ± 32.4 to 415 ± 192.4 μg/liter. One g of deferoxamine given intravenously or intramuscularly resulted in 76.8 ± 35.3% and 70.4 ± 23.2%, respectively, of the 2 g i.v. response. The rate at which serum aluminium increased following i.v. deferoxamine infusion was biphasic, with an initial rapid phase lasting 139 minutes followed by a much slower phase. The volume of distribution of aluminium following deferoxamine administration was 12.6 ± 1.61 and the half-life (t 1/2 ) for aluminium removal during hemodialysis was 9.0 ± 2.0 hours. The increase in serum aluminium following deferoxamine was not due to chelation of erythrocyte aluminium as erythrocyte aluminium remained constant over 24 hours. In patients on continuous ambulatory peritoneal dialysis, 2 g intravenous deferoxamine resulted in the removal of 560 ± 267 μg of aluminium over 24 hours while 2 g deferoxamine given intraperitoneally gave 91 ± 13% of the intravenous response. Aluminium clearance over 48 hours was twice that for 24 hours for both i.v. and i.p. deferoxamine. These results indicate that aluminium is chelated rapidly from tissues other than erythrocytes, and i.m. deferoxamine in hemodialysis patients and i.p. deferoxamine in CAPD patients is as efficacious and potentially safer than intravenously administered deferoxamine.
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