Pediatric Clinics of North America - CIPERJ

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ORAL IRON CHELATORS 467 Table 2 Comparison of iron chelators Property Deferoxamine Deferiprone Deferasirox Chelator:iron 1:1 3:1 2:1 binding Route of Subcutaneous or Oral Oral administration intravenous Usual dosage 25–50 mg/kg per day 75 mg/kg per day 20–30 mg/kg per day Schedule Administered Three times a day Daily over 8–24 hours, 5–7 days per week Primary route(s) of excretion Urine/feces Urine Feces Adverse effects Advantages Disadvantages Special monitoring considerations Local reactions Ophthalmologic Auditory Bone abnormalities Pulmonary Neurologic Allergic reactions Long-term data available Compliance problems may be greater Long bone films in growing children Annual ophthalmology exam Annual audiology exam Agranuloctyosis/ neutropenia Gastrointestinal disturbances Transminase elevations Arthralgia May be superior in removal of cardiac iron Not licensed for use in United States Variable efficacy in removal of hepatic iron Weekly complete blood count with differential Gastrointestinal disturbances Transaminase elevations Rise in serum creatinine Proteinuria Rash The only oral chelator licensed for use in United States Long-term data lacking Efficacy at cardiac iron removal not known Monthly blood urea nitrogen, creatinine, hepatic transaminases, and urinalysis Adapted from Kwiatkowski JL, Cohen AR. Iron chelation therapy in sickle cell disease and other transfusion-dependent anemias. Hematol Oncol Clin N Am 2004;18(6):1355–77; with permission.
468 KWIATKOWSKI [42]. Chelation therapy with deferoxamine prevents other organ toxicities, such as diabetes [37]. 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, including high frequency hearing loss, ophthalmologic toxicity [43], growth retardation, and skeletal changes, including rickets-like lesions and genu valgum [44], 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 [45]. 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) [46]. The major limitation to deferoxamine 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 [47,48]. 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 a 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. Deferiprone Pharmacology Deferiprone, or 1,2 dimethyl-3-hydroxypyrid-4-1 (Ferriprox), was the first orally active chelator studied extensively for the treatment of transfusional iron overload, introduced into clinical trials 20 years ago (see Table 2). Most studies have been open-label, noncomparative studies, often including patients who had a history of inadequate iron chelation, but a few randomized trials comparing deferiprone to deferoxamine are reported. A substantial amount of data on the safety and efficacy of the drug has been acquired, but considerable controversy surrounding the drug exists. In the European Union, deferiprone is approved for use for patients in whom deferoxamine therapy is contraindicated or inadequate, but the drug is not approved for
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Pediatr Clin N Am 55 (2008) xiii-xi
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Pediatr Clin N Am 55 (2008) 287-304
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DECISION ANALYSIS IN PEDIATRIC HEMA
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Nietert et al [30] Treatment of sic
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VENOUS THROMBOEMBOLISM IN CHILDREN
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PEDIATRIC ARTERIAL ISCHEMIC STROKE
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CARE OF PATIENTS WITH VASCULAR ANOM
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358 RODRIGUEZ & HOOTS Fig. 1. X-lin
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Table 1 Clotting factor concentrate
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Table 1 (continued ) Factor VIII (o
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364 RODRIGUEZ & HOOTS was administe
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366 RODRIGUEZ & HOOTS Antifibrinoly
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368 RODRIGUEZ & HOOTS infections an
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370 RODRIGUEZ & HOOTS Fig. 3. Schem
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372 RODRIGUEZ & HOOTS protein is no
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374 RODRIGUEZ & HOOTS [2] Berntorp
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376 RODRIGUEZ & HOOTS [42] Carcao M
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378 ROBERTSON et al von Willebrand
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380 ROBERTSON et al Fig. 2. A propo
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382 ROBERTSON et al a heterogenous
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384 ROBERTSON et al of considering
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386 ROBERTSON et al Type 2M Type 2M
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388 ROBERTSON et al Desmopressin is
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390 ROBERTSON et al References [1]
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392 ROBERTSON et al [46] Nesbitt IM
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394 BLANCHETTE & BOLTON-MAGGS A key
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396 BLANCHETTE & BOLTON-MAGGS recep
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398 BLANCHETTE & BOLTON-MAGGS and p
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400 BLANCHETTE & BOLTON-MAGGS Fig.
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402 BLANCHETTE & BOLTON-MAGGS in di
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404 BLANCHETTE & BOLTON-MAGGS the s
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406 BLANCHETTE & BOLTON-MAGGS findi
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408 BLANCHETTE & BOLTON-MAGGS as a
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410 BLANCHETTE & BOLTON-MAGGS splen
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412 BLANCHETTE & BOLTON-MAGGS with
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414 BLANCHETTE & BOLTON-MAGGS react
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Page 162 and 163: Pediatr Clin N Am 55 (2008) 447-460
Page 164 and 165: THALASSEMIA UPDATE 449 hypochromia
Page 166 and 167: THALASSEMIA UPDATE 451 Fig. 1. Chan
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Page 170 and 171: THALASSEMIA UPDATE 455 thromboses i
Page 172 and 173: THALASSEMIA UPDATE 457 On the basis
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Page 178 and 179: ORAL IRON CHELATORS 463 large iron-
Page 180 and 181: ORAL IRON CHELATORS 465 of 50 child
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Page 200 and 201: HYDROXYUREA FOR CHILDREN WITH SICKL
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518 TRACY & RICE [13] Bader-Meunier
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Pediatric Clinics of North America - CIPERJ

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