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Iron overload in children who are treated for acute lymphoblastic leukemia estimated by liver siderosis and serum
Päivi Halonen1, Jorma Mattila, Pauli Suominen
1Paediatric Research Centre, Medical School, University of Tampere, Tampere, Finland. paivi.halonen@kotiposti.net
Insights
Children treated for acute lymphoblastic leukemia often develop iron overload. Serum ferritin is a useful marker, but soluble transferrin receptor (sTfR) is not effective for detecting liver iron load.
Area of Science:
- Pediatric Oncology
- Hematology
- Clinical Biochemistry
Background:
- Children undergoing treatment for acute lymphoblastic leukemia (ALL) may develop secondary liver iron overload.
- Monitoring iron levels is crucial for managing long-term health outcomes in these patients.
Purpose of the Study:
- To evaluate the prevalence and progression of liver iron overload in children treated for ALL.
- To determine the utility of serum soluble transferrin receptor (sTfR) as a biomarker for detecting liver iron load in this population.
Main Methods:
- Liver biopsy specimens from 30 children near or at the end of ALL therapy were analyzed for iron content using the total iron score (TIS).
- Serum iron parameters and sTfR levels were measured concurrently and in a subset of patients during follow-up (1-3 years post-therapy).
Main Results:
- Moderate to severe liver iron overload (TIS >15) was observed in 63% of patients.
- Serum ferritin and transferrin saturation correlated significantly with liver iron content, while sTfR levels did not show significant differences.
- Iron parameters normalized in most patients post-therapy, but 14% had persistently high serum ferritin levels.
Conclusions:
- A significant proportion of children treated for ALL experience long-term iron overload.
- Serum ferritin is a reliable serologic marker for assessing liver iron overload in pediatric ALL survivors.
- Serum sTfR is not an appropriate marker for evaluating liver iron load in this patient group.
Objective:
To evaluate a secondary liver iron overload and its fate in children who are treated conventionally for acute lymphoblastic leukemia and to assess whether serum soluble transferrin receptor (sTfR) is useful in detecting iron load.
Methods:
Liver siderosis was estimated histologically from liver biopsy specimens of 30 children (aged 2.6-17.6 years) close to or at the end of therapy using total iron score (TIS). Serum iron parameters and sTfR were measured at the same time and in 22 patients 1 to 3 years after therapy.
Results:
In 19 (63%) of 30 patients, liver TIS was >15, indicating at least moderate iron overload. Serum ferritin, iron, and transferrin iron saturation levels were highest and transferrin level lowest in the patients with the highest liver iron content. Serum sTfR levels did not differ significantly between the patients with varying amounts of liver iron. TIS correlated most significantly positively with serum ferritin (r(S) = 0.899), transferrin iron saturation (r(S) = 0.764), and the amount of transfused red blood cells (r(S) = 0.783). Serum iron parameters normalized in most patients during the follow-up. In 3 (14%) of 22 patients, serum ferritin level remained high (>1000 microg/L).
Conclusions:
Long-term iron overload is detected in at least 14% of children after therapy for acute lymphoblastic leukemia. Serum sTfR is an inappropriate marker for liver iron overload, whereas ferritin seems to be the most useful serologic marker for it.
