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THU0112 Anaemia in rheumatoid arthritis
  1. P Athanassiou1,
  2. E Griva2,
  3. I Kostoglou-Athanassiou3,
  4. P Konstantopoulou1,
  5. S Papazoglou4,
  6. D Rontogianni5,
  7. G Vezyroglou1,
  8. T Kontomerkos4
  1. 1Department of Rheumatology, Asklepieion Hospital, Voula
  2. 2Department of Haematology
  3. 3Department of Endocrinology, Metaxa Hospital, Pireaus, Greece
  4. 4Department of Rheumatology
  5. 5Department of Histopathology, General Hospital of Athens “G. Gennimatas”, Athens


Background Rheumatoid arthritis (RA) is accompanied by haematological abnormalities. It is well known that anaemia in RA may have plural aetiology, however no correlation has been performed between anaemia and the morphology of blood cell precursors in the bone marrow in RA.

Objectives The aim was to investigate the aetiology of anaemia in RA by analysing blood, bone marrow aspirate and bone marrow biopsy findings.

Methods RA patients were included in the study, n = 51, aged 58.7 ± 1.2 (range 17–85) years. None of the patients was taking any disease modifying agents and 26 were newly diagnosed and had never taken any treatment for RA, duration of disease of the remaining being 9.1 ± 1.8 (range 0.5–35) years. In all patients antinuclear antibodies, anti-dsDNA antibodies and serum rheumatoid factor were measured. Haematocrit, haemoglobin, MCV, MCH, MCHC, serum iron, serum ferritin, serum iron-binding capacity, serum folate and vitamin B12 levels were also measured and indirect and direct Coombs’ test was performed. In all patients a bone marrow aspirate was obtained and a bone marrow biopsy was performed.

Results In 51 RA patients haemoglobin levels were 11.3+0.2 g/dl (mean ± SEM), haematocrit 35.0 ± 0.6%, MCV 80.5 ± 1.4 fl, MCH 25.9 ± 0.5 pg, MCHC 32.0 ± 0.1%, serum iron levels 72.9 ± 4.8 ?g/dl, serum iron-binding capacity 343.4 ± 7.4 ?g/dl, ferritin levels 119.5 ± 23.1 ?g/dl, folate 12.4 ± 1.9 ng/ml and vitamin B12 levels 722.6 ± 301.3 pg/ml. In 32 of 51 patients with haemoglobin 12 g/dl, hyperplasia of red blood cell precursors was noted in 12, megaloblastoid alterations in 4 and erythroblastic islets in 2 patients. No correlation was observed between the presence or absence of anaemia and the dysplastic alterations in the blood cell precursors in the bone marrow in the RA patients studied.

Conclusion The aetiology of anaemia in RA patients seems to be multifactorial. Dysplastic alterations in blood cell precursors were noted in all the groups of RA patients, irrespective of the presence of anaemia, indicating either that inflammatory cytokines may affect the microenvironment of the bone marrow in RA or that in RA the stem cell in the bone marrow is defective being implicated in the pathogenesis of the disease.

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