“Secondary lron overload: lmplications of Non-lnvasive Measurement”
Performer: John K. Olynyk,
School of Medicine & Pharmacology, University of Western Australia,
Fremantle Hospital Campus, Department of Gastroenterology, Fremantle Hospital,
Western Australia
Recent advances in the understanding of the regulation of iron transport have
substantially improved our knowledge of the pathogenesis of iron overload.
In normal circumstances, iron absorption and losses are in balance.
Iron is stored in the marrow and liver and levels of toxic non-transferrin
bound iron（NTBI） or labile plasma iron（LPI） are low.
When iron overload occurs as a result of increased absorption or exogenous
administration via blood products or parenteral iron, storage levels increase
along with NTBI and LPI.
The development of iron overload is associated with increased morbidity and
mortality.
NTBI and LPI play important roles in this process as storage iron in the form
of ferritin and haemosiderin may be biologically inert.
To reduce the risks of morbidity and mortality, accurate documentation of
iron load and treatment with iron chelators is required.
Whilst simple measures such as serum ferritin are useful, they are limited
by a lack of specificity for iron per se.
Noninvasive measurement using MRI technology has emerged as an excellent method
for accurate and specific measurement of iron stores, especially in the liver.
Chelators have been the principle methods of reduction of iron stores in secondary
iron overload related to haematological disorders.
These have evolved from parenteral to oral therapies, with the greatest recent
advance being the development of deferasirox（Exjade, Novartis）.
A combination of early assessment of iron overload and early introduction
of iron chelation offer the best prospects for prolonged survival in patients
with secondary iron overload.