Reticulocyte Hemoglobin Equivalent (Ret-He) Combined with Red Blood Cell Distribution Width Has a Differentially Diagnostic Value for Thalassemias

Abstract

As a type of congenital microcytic hypochromic anemia, thalassemia trait is often confused with other conditions, such as congenital sideroblastic anemia (CSA) and iron deficiency anemia, before a specific work-up is performed. However, these tests, including hemoglobin (Hb) electrophoresis, gene mutations and Prussian blue staining after bone marrow aspirate, are relatively expensive, time-consuming and invasive. To find labor-saving parameters to facilitate differential diagnosis, we retrospectively analyzed the routine blood indexes of 59 thalassemia trait cases [22 α-thalassemia (α-thal), 36 β-thalassemia (β-thal) and one α/β-thal], 21 CSA patients, and 238 iron deficiency anemia controls. Significantly higher reticulocyte Hb equivalent (Ret-He) and lower red blood cell (RBC) distribution width (RDW) were prominent in thalassemia trait. Furthermore, RDW-standard deviation (SD) was independent of the severity of anemia in thalassemia trait, similar to Ret-He in CSA. In the context of the same grades of anemia, Ret-He combined with RDW was powerful in differentiation of thalassemia from CSA and iron deficiency anemia. By receiver operation curve (ROC) analysis, Ret-He had a specificity of 67.06% and a sensitivity of 76.92% with a cutoff value of 20.9 pg for thalassemia trait in mild anemia and a specificity of 84.09% and a sensitivity of 68.42% with a cutoff value of 19.1 pg for thalassemia trait in moderate anemia. Regarding CSA, Ret-He had 92.94% specificity and 60.00% sensitivity in mild anemia, with a cutoff value of 18.1 pg. Overall, Ret-He and RDW are two convenient indexes able to differentiate thalassemia from the other two microcytic anemias, CSA and iron deficiency anemia.

Keywords:

• Congenital sideroblastic anemias (CSA)
• differential diagnosis
• red blood cell (RBC) distribution width (RDW)
• reticulocyte hemoglobin (Hb) equivalent (Ret-He)
• thalassemia trait

Acknowledgements

The authors acknowledge the team of researchers at the Clinical Laboratory Center Institute of Hematology and Blood Diseases Hospital, Tianjin City, People’s Republic of China, for their professional assistance. Y. Lian collected and analyzed the data and wrote the article; N. Nie, Z. Huang, Y. Shao, J. Huang, X. Li, M. Ge, P. Jin, M. Wang and Y. Zheng contributed to the data collection and diagnosis; J. Shi designed the research and wrote the article and approved the final manuscript.

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

Additional information

Funding

This study was supported by a grant from the National Natural Science Foundation of China [No. 81370606, 81670120], the CAMS Innovation Fund for Medical Sciences [CIFMS: 2017-I2M-3–018], and the National Key Research and Development Program of China [2016YFC0901503].