Anaemia May Predict Radiographic Damage in RA
Anaemia May Predict Radiographic Damage in RA
Objective: Anaemia in rheumatoid arthritis (RA) is prototypical of the chronic disease type and is often neglected in clinical practice. We studied anaemia in relation to disease activity, medications and radiographic progression.
Methods: Data were collected between 1996 and 2007 over a mean follow-up of 2.2 years. Anaemia was defined according to WHO (♀ haemoglobin<12 g/dl, ♂: haemoglobin<13 g/dl), or alternative criteria. Anaemia prevalence was studied in relation to disease parameters and pharmacological therapy. Radiographic progression was analysed in 9731 radiograph sets from 2681 patients in crude longitudinal regression models and after adjusting for potential confounding factors, including the clinical disease activity score with the 28-joint count for tender and swollen joints and erythrocyte sedimentation rate (DAS28ESR) or the clinical disease activity index (cDAI), synthetic antirheumatic drugs and antitumour necrosis factor (TNF) therapy.
Results: Anaemia prevalence decreased from more than 24% in years before 2001 to 15% in 2007. Erosions progressed significantly faster in patients with anaemia (p<0.001). Adjusted models showed these effects independently of clinical disease activity and other indicators of disease severity. Radiographic damage progression rates were increasing with severity of anaemia, suggesting a 'dose-response effect'. The effect of anaemia on damage progression was maintained in subgroups of patients treated with TNF blockade or corticosteroids, and without non-selective nonsteroidal anti-inflammatory drugs (NSAIDs).
Conclusions: Anaemia in RA appears to capture disease processes that remain unmeasured by established disease activity measures in patients with or without TNF blockade, and may help to identify patients with more rapid erosive disease.
Anaemia in rheumatoid arthritis (RA) is prototypical of anaemia of chronic disease (ACD), characterised by low serum iron concentrations in conjunction with normal or increased storage iron. ACD without functional iron deficiency is normochromic, normocytic, and usually mild. Haemoglobin concentrations were a component of earlier RA disease activity measures until they were omitted during validation of the original RA disease activity score (DAS) due to low correlation with other disease activity measures, despite moderate correlation with radiographic outcome.
The significantly higher need for joint replacements and higher mortality rates in the anaemic patients of the British early RA cohort (ERAS) challenged the concept of causal ACD treatment by aiming at remission only with synthetic disease-modifying antirheumatic drugs (DMARDs). Inhibition of human erythroid colony-forming units in the bone marrow downstream of tumour necrosis factor-α (TNF-α) and anemia is reversible upon TNF-α blockade, even in otherwise refractory RA patients. Here, we question whether anaemia in RA is still relevant in terms of prevalence and clinical consequences in the era of TNF-α blockade, one of the most efficacious and common biological RA treatments.
Abstract and Introduction
Abstract
Objective: Anaemia in rheumatoid arthritis (RA) is prototypical of the chronic disease type and is often neglected in clinical practice. We studied anaemia in relation to disease activity, medications and radiographic progression.
Methods: Data were collected between 1996 and 2007 over a mean follow-up of 2.2 years. Anaemia was defined according to WHO (♀ haemoglobin<12 g/dl, ♂: haemoglobin<13 g/dl), or alternative criteria. Anaemia prevalence was studied in relation to disease parameters and pharmacological therapy. Radiographic progression was analysed in 9731 radiograph sets from 2681 patients in crude longitudinal regression models and after adjusting for potential confounding factors, including the clinical disease activity score with the 28-joint count for tender and swollen joints and erythrocyte sedimentation rate (DAS28ESR) or the clinical disease activity index (cDAI), synthetic antirheumatic drugs and antitumour necrosis factor (TNF) therapy.
Results: Anaemia prevalence decreased from more than 24% in years before 2001 to 15% in 2007. Erosions progressed significantly faster in patients with anaemia (p<0.001). Adjusted models showed these effects independently of clinical disease activity and other indicators of disease severity. Radiographic damage progression rates were increasing with severity of anaemia, suggesting a 'dose-response effect'. The effect of anaemia on damage progression was maintained in subgroups of patients treated with TNF blockade or corticosteroids, and without non-selective nonsteroidal anti-inflammatory drugs (NSAIDs).
Conclusions: Anaemia in RA appears to capture disease processes that remain unmeasured by established disease activity measures in patients with or without TNF blockade, and may help to identify patients with more rapid erosive disease.
Introduction
Anaemia in rheumatoid arthritis (RA) is prototypical of anaemia of chronic disease (ACD), characterised by low serum iron concentrations in conjunction with normal or increased storage iron. ACD without functional iron deficiency is normochromic, normocytic, and usually mild. Haemoglobin concentrations were a component of earlier RA disease activity measures until they were omitted during validation of the original RA disease activity score (DAS) due to low correlation with other disease activity measures, despite moderate correlation with radiographic outcome.
The significantly higher need for joint replacements and higher mortality rates in the anaemic patients of the British early RA cohort (ERAS) challenged the concept of causal ACD treatment by aiming at remission only with synthetic disease-modifying antirheumatic drugs (DMARDs). Inhibition of human erythroid colony-forming units in the bone marrow downstream of tumour necrosis factor-α (TNF-α) and anemia is reversible upon TNF-α blockade, even in otherwise refractory RA patients. Here, we question whether anaemia in RA is still relevant in terms of prevalence and clinical consequences in the era of TNF-α blockade, one of the most efficacious and common biological RA treatments.
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