Found this on iron overload and wanted to share.
Quote from Gene Reviews:
Prevention of Secondary Complications
Transfusional iron overload. The most common secondary complications are those related to transfusional iron overload, which can be prevented by adequate iron chelation. After ten to 12 transfusions, chelation therapy is initiated with desferrioxamine B (DFO) administered five to seven days a week by 12-hour continuous subcutaneous infusion via a portable pump. Recommended dosage depends on the individual's age and the serum ferritin concentration. Young children start with 20-30 mg/kg/day, increasing up to 40 mg/kg/day after age five to six years. The maximum dose is 50 mg/kg/day after growth is completed. The dose may be reduced if serum ferritin concentration is low. By maintaining the total body iron stores below critical values (i.e., hepatic iron concentration <7.0 mg per gram of dry weight liver tissue), desferrioxamine B therapy prevents the secondary effects of iron overload, resulting in a consistent decrease in morbidity and mortality [Borgna-Pignatti et al 2004].
Ascorbate repletion (daily dose not to exceed 100-150 mg) increases the amount of iron removed after DFO administration.
Side effects of DFO chelation therapy are more common in the presence of relatively low iron burden and include ocular and auditory toxicity, growth retardation, and, rarely, renal impairment and interstitial pneumonitis. DFO administration also increases susceptibility to Yersinia infections. The major drawback of DFO chelation therapy is low compliance resulting from complications of administration.
In clinical practice, the effectiveness of DFO chelation therapy is monitored by routine determination of serum ferritin concentration. However, serum ferritin concentration is not always reliable for evaluating iron burden because it is influenced by other factors, the most important being the extent of liver damage.
Determination of liver iron concentration in a liver biopsy specimen shows a high correlation with total body iron accumulation and is the gold standard for evaluation of iron overload. However, (1) liver biopsy is an invasive technique involving the possibility (though low) of complications; (2) liver iron content can be affected by hepatic fibrosis, which commonly occurs in individuals with iron overload and HCV infection; and (3) irregular iron distribution in the liver can lead to possible false-negative results [Clark et al 2003].
In recent years, MRI techniques for assessing iron loading in the liver and heart have improved [Anderson et al 2001, Wood et al 2004, St Pierre et al 2005]. T2 and T2* parameters have been validated for liver iron concentration. Cardiac T2* is reproducible, is applicable between different scanners, correlates with cardiac function, and relates to tissue iron concentration [Anderson et al 2001, Wood et al 2004]. Clinical utility of T2* in monitoring individuals with siderotic cardiomyopathy has been demonstrated [Anderson et al 2004]. Calibration of T2* in the heart will be available in the near future.
Magnetic biosusceptometry (SQUID), which gives a reliable measurement of hepatic iron concentration, is another option [Fischer et al 2003]; however, magnetic susceptometry is presently available only in a limited number of centers worldwide.
Two other chelators have been introduced into clinical use: deferiprone and desferrioxamine.
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Deferiprone (L-1), a bidentated oral chelator, available for several years in many countries, is administered in a dose of 75-100 mg/kg/day. The main side effects of deferiprone therapy include neutropenia, agranulocytosis, arthropathy, and gastrointestinal symptoms [Cohen et al 2003] that demand close monitoring. Recent findings seem to exclude any correlation between deferiprone treatment and progression of liver fibrosis [Wanless et al 2002]. The effect of deferiprone on liver iron concentration may vary among the individuals treated. However, results from independent studies suggest that deferiprone may be more cardioprotective than desferrioxamine; compared to those being treated with DFO, individuals being treated with deferiprone have better myocardial MRI pattern and less probability of developing (or worsening pre-existing) cardiac disease [Anderson et al 2002, Piga et al 2003]. These retrospective observations have been confirmed in a prospective study [Pennell et al 2006].
After many years of controversy, deferiprone is emerging as a useful iron chelator equivalent/alternative to desferrioxamine.
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Deferasirox recently became available for clinical use in patients with thalassemia. It is effective in adults and children and has a defined safety profile that is clinically manageable with appropriate monitoring. The most common treatment-related adverse events are gastrointestinal disorders, skin rash, and a mild, non-progressive increase in serum creatinine concentration. Post-marketing experience and several phase IV studies will further evaluate the safety and efficacy of deferasirox.
New strategies of chelation using a combination of desferrioxamine and deferiprone have been effective in individuals with severe iron overload; toxicity was manageable [Wonke et al 1998, Wu et al 2004, Tanner et al 2007