"Effect of the two chelators warrants further investigation"

This is EXACTLY how they stumbled across the cure in sickle.
Investigating chelators and cured the sickle patients.
Coincidentally close TO thalassemia.

"C-reactive protein decreased significantly"

Published online 10 May 2008
Haematologica, Vol 93, Issue 6, 817-825

--------------------------------------------------------------------------------

Original Article

Inflammation and oxidant-stress in β-thalassemia patients treated with
iron chelators deferasirox (ICL670) or deferoxamine: an ancillary
study of the Novartis CICL670A0107 trial
Patrick B. Walter1, Eric A. Macklin2, John Porter3, Patricia Evans3,
Janet L. Kwiatkowski4, Ellis J. Neufeld5, Thomas Coates6, Patricia J.
Giardina7, Elliott Vichinsky1, Nancy Olivieri8, Daniele Alberti9,
Jaymes Holland9, Paul Harmatz1 for the Thalassemia Clinical Research
Network
1 Children's Hospital & Research Center Oakland, Oakland, CA,USA;
2 New England Research Institutes, Watertown, MA, USA (current
address: Massachusetts General Hospital, Boston, MA);
3 University College London, London, UK;
4 Children's Hospital of Philadelphia, Philadelphia, PA;
5 Children's Hospital Boston, Boston, MA, USA;
6 Children's Hospital Los Angeles, Los Angeles, CA, USA;
7 New York-Presbyterian Hospital, New York, NY, USA;
8 University Health Network, Toronto, Canada and
9 Novartis Pharmaceuticals Corp., East Hanover, NJ, USA

Correspondence: Paul Harmatz, Children's Hospital & Research Center
Oakland, 747 52nd Street, Oakland, Ca, 94609, USA. E-
mail:pharmatz@mail.cho.org

Background:
We assessed whether oxidant-stress and inflammation in β-thalassemia
could be controlled by the novel oral iron chelator deferasirox as
effectively as by deferoxamine.

Design and Methods:
Forty-nine subjects were enrolled from seven sites and studied at
baseline, and after 1, 6, and 12 months of therapy. Malondialdehyde,
protein carbonyls, vitamins E and C, total non-transferrin bound iron,
transferrin saturation, C-reactive protein, cytokines, serum ferritin
concentration and liver iron concentration were measured.

Results:
Liver iron concentration and ferritin declined significantly in both
treatment groups during the study.
This paralleled a significant decline in the oxidative-stress marker
malondialdehyde (deferasirox -22%/year, deferoxamine -28%/year,
average decline p=0.006).
The rates of decline did not differ between treatment groups.
Malondialdehyde was higher in both treatment groups than in a group of
30 non-thalassemic controls (p<0.001).
The inflammatory marker high-sensitivity C-reactive protein decreased
significantly only in the group receiving deferasirox (deferasirox -
51%/year, deferoxamine +8.5%/year, p=0.02).
This result was confounded by a chance difference in the level of high-
sensitivity C-reactive protein between the two groups at baseline, but
analyses controlling for this difference suggested an equally large
treatment effect.

Conclusions:
Iron chelation therapy with deferoxamine or with deferasirox was
equally effective in decreasing iron burden and malondialdehyde. The
possible differential effect of the two chelators on inflammation
warrants further investigation.

Key words: iron overload, thalassemia, oxidative stress, inflammation,
hsCRP, C-reactive protein, malondialdehyde, lipid peroxidation,
vitamin E, vitamin C.

doi:10.3324/haematol.11755
Copyright (c) 2008 by Ferrata Storti Foundation

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