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Remedy to improve anaemia treatment

Monday, 1 November, 2010

LOOK to the serum ferritin level first and last to confirm a suspected diagnosis of iron deficiency anaemia (IDA), a co-author of a clinical update on the management of IDA has recommended.

Consultant physician Dr Stephen Flecknoe-Brown said the serum iron level and parameters derived from it were unreliable ways to confirm a suspected IDA diagnosis.

He was commenting on the publication in the latest MJA of a clinical update on the diagnosis and management of IDA, described as an important public health problem in Australia and around the world.

The clinical update was written by a group of health professionals who are members of the Australian Iron Deficiency Expert Group.

Some of the major recommendations from the update include that patients with IDA be assessed for coeliac disease, that blood transfusion is inappropriate therapy for IDA and that oral iron therapy, in appropriate doses and for a sufficient time, is effective first-line treatment for most patients.

For example, the update said it is reasonable to replenish iron stores by continuing oral iron therapy for 3–6 months (2–3 months in children) beyond normalisation of haemoglobin concentrations.

Leading haematologist Associate Professor Anthony Dodds has welcomed the update, saying IDA is under-diagnosed and generally poorly treated in Australia.

Professor Dodds, Director of Haematology and Bone Marrow Transplantation, St Vincent's Hospital, Sydney, said the update gave clear guidelines for diagnosing, investigating and treating IDA in the groups at risk and for avoiding the use of unnecessary blood transfusions.

He said IDA was poorly treated in Australia for several reasons, including the mistaken assumption that a low serum iron level equalled iron deficiency. He said this could lead to inappropriate iron therapy.

Professor Dodds said some practitioners referred all cases of anaemia for endoscopic investigation when the presence of iron deficiency had not been determined.

“Patients presenting to hospitals with IDA are wrongly transfused when they are clinically stable and iron therapy would have been safer and more appropriate.”

Moreover, some patients with IDA were not treated with iron therapy long enough to correct the anaemia and fully replace iron stores, he said.

The update had also highlighted the growing acceptance of intravenous iron in selected cases of IDA, Professor Dodds said.

“There is one small omission [in the update] and that is the interaction between oral iron and other medications,” he said.

Dr Flecknoe-Brown told MJA InSight that the update offered a confident approach to the diagnosis of the commonest cause of anaemia and fatigue in the Australian community and world-wide.

“Some still believe that non-anaemic tissue iron deficiency is a harmless physiological state,” said Dr Flecknoe-Brown, a senior lecturer with the Broken Hill University Department of Rural Health, part of the School of Public Health at the University of Sydney.

“Reversible physical and cognitive impairment are known consequences of non-anaemic iron deficiency in adults and the RACP [Royal Australasian College of Physicians] warns us that irreversible damage to cognitive development can result from untreated iron deficiency in toddlers.”

Dr Flecknoe-Brown said an update was necessary because all the authors still saw far too many patients who had treatable iron deficiency which had been ignored for too long, inadequately treated, or the opportunities for finding treatable causes, such as a gastrointestinal lesion or coeliac disease, were missed.

“And iron deficiency anaemia is the commonest indication for transfusion in hospitalised patients — a practice which is both wasteful of voluntarily donated blood and needlessly hazardous to the patient,” he said.

He said intravenous iron complexes currently available in Australia were safer and more effective treatments of IDA than blood transfusion.

MJA 2010; 193: 525-532.

 

Posted 1 November 2010  

 

Comments

The problem with ferritin levels is that I think some patients have high ferritin levels because of chronic disease - but can still be Fe deficient. Chronic disease can also be associated with low transferrin. So serum Fe and saturation would need to be considered - and microcytosis.

The issue of a falsly elevated and thus 'normal' ferritin with inflammation or infection is a common one in paediatric patients who often have an intercurrent viral illness when bloods are taken.
Soluble transferrin receptor (STR) titres are useful in this situation as this protein is not an acute phase reactant and not materially altered by concurrent inflammation. The finding of elevated STR especially with a elevated transferrin level indicates low iron stores or deficiency even if ferritin levels are 'normal'.
Many factors affect blood iron levels independent of body iron status. The only clinical setting where I put any real store on iron levels are in suspected iron poisoning where elevated levels are useful.

three years ago i was operated on for pancreatic cancer.
basically i have been going o.k
recently i was prescribed iron tablets for a deficiency...
after three days i noticed that my urine was a very dark
brown colour with a very small trace of blood.....i immediately stopped taking the tablets and will not continue.
i am now eating liquorice/cashew nuts/almonds and dark chocolate....my red meat intake is very small....can you kindly assist me.
Rgards charles

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