The Role of Labile Plasmatic Iron (LPI) In the Assessment of Iron Overload In β-Thalassemic Patients and Its Correlation with MRI Findings
Authors: de Assis Reiĵne Alves , Espósito Breno Pannia , Kay Fernando Uliana , Baroni Ronaldo Hueb , Rosemberg Laercio Alberto , Nomura Cesar Higa , Ribeiro Andreza Alice Feitosa , Loggetto Sandra Regina , de Almeida Veríssimo Mônica Pinheiro , Junior Antonio Fabron , Araujo Aderson S , Baldanzi Giorgio Roberto , Nakashima Sandra Saemi , da Silva Diniz Michelli , Steagal Merula , di Sessa Velloso Claudia Angela Galenni , de Gusmão Funari Marcelo Buarque , Wood John , Hamerschlak Nelson 
Published: October 2019

Abstract
Abstract 2072

Introduction:
The labile plasmatic iron (LPI) represents part of non-transferrin-bound iron (NTBI) capable of entering the tissues and causing oxidative injury. It might be related to certain types of brain damage, especially in those with ischemia, cognitive defects in Alzheimer's disease, endothelial dysfunction in thalassemic children, complications in myelodysplastic syndrome (MDS), in particular infection and tissue injury, and to the increase in mortality rates in transfused and diabetic patients. LPI determination has been used by several authors as a means to monitor the efficacy of different protocols of iron chelation in thalassemic and MDS patients. Efficacy studies of vitamin C and E antioxidant activity, which blocks iron-induced oxidative damage, have also used this methodology. LPI has been suggested as an alternative method to assess iron load.

Objective:
Establish a correlation between LPI and serum ferritin levels and tissue iron estimated by magnetic resonance imaging (MRI) T2*/R2* in the heart, pancreas and liver.

Methods:
Data from 83 patients with thalassemia major were analyzed. LPI was measured using a fluorescent method and values <0.5μM were considered normal. Serum ferritin was measured by chemiluminescence and MRI was performed with a General Electric 1.5 T device. Cardiac, pancreatic and liver iron were determined by T2*/R2* methodology, and liver T2* was used to calculate the liver iron concentration (LIC). The statistical analysis was performed using ANOVA.

Results:
Eighty three patients were studied, of which 44.6% were males and 55.4% females. The median number of red blood cell packs used per year was 29.3±7.4. The mean LPI was 1.04±2.39μM (range 0.001 – 11.45). The mean LIC and serum ferritin were 8.96±3.35 mg/g dry liver weight (1.31-18.34) and 2,928.19 ± 2,398.4 ng/ml (101-12,958), respectively. Cardiac T2* values varied from 3.4 to 59.52ms, of which 33.7% (28) showed cardiac iron overload (T2*<20ms). Pancreatic R2*values varied from 19.8–500 Hz. Considering abnormal pancreatic R2*values >43Hz, 86.3% (69) were classified as pancreatic siderosis. After ANOVA analysis, we found a strong correlation between LPI and LIC (p<0.0007).

Conclusion:
A strong correlation was found between LPI and liver iron concentration. It is still premature to use this correlation as a predictor of iron overload. However, it might be useful as a complementary method to monitor chelation therapy and does not preclude the MRI studies to assess tissue iron in clinical practice.

Disclosures:
No relevant conflicts of interest to declare.