Advantages
of desferoxamine:
1.
Arrests the
progression of hepatic fibrosis to cirrhosis, even when administered in
regimens that stabilize, rather than reduce the body iron (Kwiatkowski, 2008).
2.
Early and intensive
administrations of desferoxamine therapy are associated with normal sexual
maturation but it apparently doesn't reverse established abnormalities (Bernard,
2000).
3.
Chelation therapy
with desferrioxamine prevents other organ toxicities such as diabetes mellitus (Kwiatkowski,
2008).
Adverse
reactions:
Local
infusion site reactions, including induration and erythema commonly are seen
with administration of deferoxamine. Low zinc levels also can develop with
deferoxamine use. Other adverse effects, include high frequency hearing loss,
ophthalmologic toxicity, growth retardation, and skeletal changes, including
rickets-like lesions and genu valgum, are more common when patients receive
high doses of deferoxamine relative to their total body iron burden and can be
minimized by maintaining an optimal chelator dose. Acute pulmonary toxicity
with respiratory distress and hypoxemia and a diffuse interstitial pattern on
chest roentgenogram is reported with the administration of high doses of
deferoxamine (10 to 20 mg/kg per hour). The major limitation to deferioxamine
is the need to administer the drug parenterally, which is painful and time
consuming. As a result, poor compliance remains a significant problem with
administration of this drug, and preventable, premature deaths related to iron
overload continue to occur (Kwiatkowski, 2008).
Characteristics
of an ideal chelator
The limitations of treatment with
deferoxamine have led investigators to search for more acceptable iron
chelators to be used in the management of iron overload. An optimal chelator
should have adequate gastrointestinal absorption to allow oral administration,
a long half-life permitting once or twice daily dosing, and a high affinity for
iron with lesser affinities for other metals. The chelator should be able to
induce iron excretion at rate of at least 0.5 mg/kg per day to offset the
amount of transfusional iron loading, and should be able to remove excess
cardiac iron. Finally, toxicities associated with the drug should be minimal
and manageable (Kwiatkowski, 2008).
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