Abstract
Background Systemic lupus erythematosus (SLE) is accompanied by haematological abnormalities. A very common haematological abnormality observed in SLE is anaemia. It is well known that anaemia in SLE may have many causes, however no correlation has been performed between anaemia and the morphology of red blood cell precursors in the bone marrow in SLE. Objectives The aim was to investigate the aetiology of anaemia in SLE by analysing blood, bone marrow aspirate and bone marrow biopsy findings. Methods SLE patients were included in the study, n = 17, aged 40.9 ± 3.6 (range 18–36) years. None of the patients were taking any disease modifying agents and 11 were newly diagnosed and had never taken any treatment for SLE, duration of disease of the remaining being 5.7 ± 3.6 (range 1–23) years. In all patients antinuclear antibodies, anti-DNA 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 17 SLE patients haemoglobin levels were 11.4+0.4 g/dl (mean ± SEM), haematocrit 35.0 ± 1.3%, MCV 88.9 ± 1.2 fl, MCH 29.0 ± 0.4 pg, MCHC 32.7 ± 0.1%, serum iron levels 83.2 ± 7.2 ?g/dl, serum iron-binding capacity 359.0 ± 11.2 ?g/dl, ferritin levels 123.1 ± 65.3 ?g/dl, folate 6.4 ± 1.1 ng/ml and vitamin B12 levels 534.7 ± 79.4 pg/ml. In 10 of 17 patients with SLE haemoglobin levels were 12 g/dl, hyperplasia of red blood cell precursors was noted in all of them, megaloblastoid alterations in 3 and blasts of the red cell series in 2 patients. No correlation was observed between the presence or absence of anaemia and the dysplastic alterations in the red blood cell precursors in the bone marrow in the SLE patients studied. Conclusion The aetiology of anaemia in SLE patients seems to be multifactorial. Dysplastic alterations in red blood cell precursors was noted in all the groups of SLE patients, irrespective of the presence of anaemia, indicating either a primary defect of the stem cell in the bone marrow in SLE which is implicated in the pathogenesis of the disease or that inflammatory cytokines may affect the microenvironment of the bone marrow.
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