Diagnostic Availability of the Soluble Transferrin Receptor in RA Patients.
- Author:
Lae Hee CHUN
1
;
Think You KIM
;
Hye Rim LEE
;
Woong Soo LEE
Author Information
1. Department of Clinical Pathology, College of Medicine, Hanyang University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Soluble transferrin receptor (sTfR);
Rheumatoid arthritis (RA);
Anemia
- MeSH:
Anemia;
Anemia, Iron-Deficiency;
Arthritis, Rheumatoid;
Bone Marrow;
Chronic Disease;
Enzyme-Linked Immunosorbent Assay;
Ferritins;
Humans;
Iron;
Joint Diseases;
Outpatients;
Receptors, Transferrin*;
Reference Values;
Rheumatology;
Transferrin*
- From:Korean Journal of Clinical Pathology
1998;18(3):420-424
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The transferrin receptor (TfR) is expressed on almost all cellular surfaces and is shedded into the blood to form the soluble transferrin receptor (sTfR). The sTfR has been known to be a good marker to reflect cellular iron status and to differentiate between iron deficiency anemia (IDA) and anemia of chronic disease (ACD) without the need for a bone marrow aspiration in rheumatoid arthritis (RA) patients. So we aimed to evaluate the diagnostic availability of sTfR in patients with RA and degenerative joint disease (DJD). METHODS: Eighty-seven outpatients visiting the Department of Rheumatology at HYUH were studied and divided into anemic and non-anemic groups according to their Hb levels (female< 12 g/dL, male< 14 g/dL). The sTfR was measured by ELISA method (Quantikine IVDTM, R&D system). To differentiate whether the anemia was due to iron deficiency or other causes, we used the RBC parameters and a discriminant index which was calculated from serum iron, ferritin and TIBC instead of a bone marrow aspiration, an invasive procedure of which interpretation can be subjective. RESULTS: The median was higher (31.09 nM) than the normal reference values (9-28 nM) only in the anemic group of RA. The medians were within normal limit in all the other groups. sTfR levels were high in 15 of the 28 RA anemic patients which were composed of 10 patients with IDA, 4 with non-anemic RA and 1 with non-anemic RA & DJD. CONCLUSIONS: In the present study, sTfR was increased not only in IDA but also in ACD of RA patients and also in non-anemic patients, which showed that sTfR cannot be used to differentiate these two types of anemia by itself and the further tests are needed. We conclude that the expression of TfR in RA patients was dependent not only on iron deficiency but also on the disease itself.
