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Iron deficiency predicts outcome in acute heart failure

  [ 2 votes ]   [ Discuss This Article ]
www.ProHealth.com • June 4, 2014


Press Release: European Society of Cardiology, May 17, 2014

Iron deficiency (ID), defined as a combination of depleted body iron stores and unmet cellular iron requirements, identified acute heart failure (AHF) patients with the worst outcomes, reported a Polish observational study in yesterday’s Late Breaking Trial session.

Iron is an essential micronutrient involved in cellular energy and metabolism. “In previous studies iron deficiency has been shown to be common in patients with chronic HF and to aggravate symptoms and worsen clinical outcomes,” explained study presenter Ewa Jankowska. The current study, she added, is the first to look at iron status in AHF.

Two major pools of iron are known to exist in the body: stored iron (hepatocytes, reticuloendothelial cells, and syderoblasts) and utilized iron (circulating iron and intracellular iron in virtually all cells). “Diagnosis of ID needs to take both these pools into consideration since they closely interact with each other and iron can be physiologically transferred between these departments,” explained Jankowska, from Wroclaw Medical University, Poland.

In the prospective study, 165 patients with a diagnosis of AHF as the primary cause of hospitalization had their serum hepcidin measured on admission as a marker for depleted iron stores, and serum soluble transferring receptor (sTfR) as a marker of unmet cellular iron requirements. The primary end-point was all-cause death, with 33 deaths occurring by 12 months follow-up.

Depleted body iron stores were diagnosed when serum hepcidin was <14.5 ng/ mL (the 5th percentile among healthy controls); while depleted utilized iron stores were diagnosed when serum sTfR was>1.59 mg/L (the 95th percentile among healthy controls). Four different groups of patients were defined: those with the most severe ID (low hepcidin and high sTfR); isolated low hepcidin; isolated high sTfR; and preserved iron status (neither low hepcidin nor high sTfR).

Results show iron deficiency (defined as low hepcidin and high sTfR) was demonstrated in 37% of patients (61), whereas isolated high sTfR was found in 29% (48) and isolated low hepcidin in 9 % (15). Mortality at 12 months was 41 % [95% CI 29-53%] for patients with low hepcidin and high sTfR compared to 15% [95%CI 5-25%] for patients with isolated low hepcidin levels and 0% for patients with preserved iron status (p<0.001).

“Indices of iron status were only weakly, if at all, associated with haemoglobin. Profound ID (low hepcidin and high sTfR) was seen in both anaemics and non-anaemics,” said Jankowska, adding that iron status appeared to be severely deranged as serum hepcidin levels were extremely low and serum sTfR high.

“Profound ID confirmed as depleted iron stores and iron avidity allows for the identification of AHF patients with particularly poor outcomes. This holds equally for both anaemic and non anaemic patients. Correction with iron supplementation may offer an attractive therapeutic option targeting abnormal metabolism in patients with AHF who still have unacceptably high mortality. We hope to initiate such a trial soon” said Jankowska.



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