Pharmacokinetics of desferrioxamine and of its iron and aluminium chelates in patients on haemodialysis

Estimation of Statistical Moments for Desferrioxamine and Its Iron and Aluminium Chelates: Contribution to Optimisation of Therapy in Uremic Patients

“…The studies regarding the kinetics of DFO and its che lates in uremic patients are few and empirical [7,14], Only in 1992 was a paper published with well-formalized classical pharmacokinetics [9]. Since, to our knowledge, no other study was performed, we considered worthwhile to present our data, although this was not the main pur pose of the investigation.…”

“…No interference in the absence of DFO was ever demonstrated with iron added in excess in our laboratory. Another study was performed by Allain et al [7] using this method, and detectable DFO was found unchelated many hours after the infusion. This result does not preclude the possibility of a metabolic breakdown of the drug; in fact its level after 44 h is very low and this cannot be simply explained by chelation.…”

Iron chelators inhibit human platelet aggregation, thromboxane A2 synthesis and lipoxygenase activity

“…It should be noted, however, that DFO, Ll and possibly other chelators can only be used in the above conditions if sufficient therapeutic nontoxic concentration ranges are reached in vivo. The indications are that in some cases this may have occurred with DFO, where doses of up to 235 mg/kg were used in thalassaemia patients [26], since it is known that plasma concentrations exceeding 300 pmol/l could be achieved with a dose of DFO of 80 mg/kg in haemodialysis patients [27]. The design and screening of more chelators of the CYketohydroxypyridine or the desferrioxamine [31] classes, which could be more specific than Ll and DFO in inhibiting lipoxygenase and cyclooxygenase at lower doses and their interaction with other inhibitors of these enzymes, is currently under investigation.…”

Direct Effect of Deferoxamine on Hemoglobin Synthesis in Patients on Hemodialysis Treated with Recombinant Human Erythropoietin

“…Although unbound DFO results in an increment in TIBC [18], its levels48 h after DFO infusion were low [18,19], and, therefore, there were no significant changes in TIBC. In patients on HD treated with rHuEPO, there is a func tional iron deficiency, although sufficient stores as measured by ferritin, can be observed [11].…”

“…Feroxamine is the chelated product of D FO ; its intradialytic and interdialytic half-lives are 3.6 ±1.4 and 28 ± 3 h, respectively [19], so the persistence of high serum iron levels on day 14 after DFO does not seem related to the ferox amine persistence. It is possible that the iron released from its stores should be taken by transferrin and used in heme synthesis.…”