SERUM TRANSFERRIN RECEPTOR LEVELS IN ANEMIC PATIENTS WITH RHEUMATOID-ARTHRITIS

Citation
Oj. Nielsen et al., SERUM TRANSFERRIN RECEPTOR LEVELS IN ANEMIC PATIENTS WITH RHEUMATOID-ARTHRITIS, Scandinavian journal of clinical & laboratory investigation, 54(1), 1994, pp. 75-82
Citations number
16
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
00365513
Volume
54
Issue
1
Year of publication
1994
Pages
75 - 82
Database
ISI
SICI code
0036-5513(1994)54:1<75:STRLIA>2.0.ZU;2-9
Abstract
The value of s-Transferrin Receptor (s-TfR) measurements in recognizin g simultaneous iron deficiency in anaemia of chronic disease was exami ned in 35 anaemic patients with active rheumatoid arthritis. Based on a quantification of stainable bone marrow (marrow iron grade 0-4) and serum ferritin concentrations (levels < 60mug l-1) compatible with iro n deficiency) the anaemia was found to be aggravated by iron deficienc y in 19/35 or 54% of the patients. There was no significant difference between the mean s-TfR concentrations in patients with adequate iron in comparison to patients with iron depletion [2.9 (1.6) mg l-1 v. 2.7 (1.4) mg l-1; t = 0.273; p = 0.786; Student's t-test]. Mean s-TfR lev els in both patients with adequate iron and depleted iron stores were within the normal range, but tended to be higher than in normal indivi duals [mean (SD): 1.54 (0.43) mg l-1]. In patients with no stainable m arrow iron (MIG 0; N = 15) a significant inverse correlation was found between s-TfR concentrations and s-ferritin levels (r = 0. 57; p < 0. 05). 5/15 patients with MIG = 0 exhibited significantly raised concent rations of s-TfR values > 3.05 mg l-1 (the highest normal value of the normal range). Increases of s-TfR levels were consistently moderate, and never exceeded a level of 7 mg l-1, which is markedly lower than c oncentrations measured in patients with iron deficiency anaemia. In co ntrast to serum ferritin, serum TfR levels were clearly shown not to b e influenced by the activity of inflammatory disease, as evaluated bot h by ESR levels and serum concentrations of CRP. Thus the increase in s-TfR in iron deficient patients with active RA seems primarily to be a reflection of an iron deprived erythropoiesis. The measurement of s- TfR promises to possess a considerable discriminative power not only i n distinguishing between the anaemia of chronic disease and iron defic iency, but also by allowing the identification of iron depletion and f unctional iron deficiency in patients with an anaemia of chronic disea se accompanying an active inflammatory process.