Does Anemia Independently Influence the Erythrocyte Sedimentation Rate in Rheumatoid Arthritis? A Multivariate Analysis From North India

TL;DR

This study from North India finds that anemia does not independently affect ESR in rheumatoid arthritis patients, while inflammation remains a key factor.

Contribution

The study provides new evidence on the independent influence of anemia and inflammation on ESR in RA patients from a high-prevalence anemia region.

Findings

CRP positivity was the strongest independent predictor of elevated ESR in RA patients.

Anemia was not independently associated with elevated ESR after adjusting for covariates.

Normocytic anemia was more common than microcytic anemia among anemic RA patients.

Abstract

Background: In regions such as North India, where anemia is prevalent, interpretation of the erythrocyte sedimentation rate (ESR) in rheumatoid arthritis (RA) may be challenging. We evaluated the independent associations of inflammation, autoantibody status, and anemia with ESR elevation and examined morphologic anemia patterns in this cohort.

Methods: We conducted a retrospective cross-sectional analysis of 152 RA patients attending a tertiary care center. Multivariate logistic regression identified independent predictors of elevated ESR and of anemia after adjustment for covariates. Seropositivity was defined by rheumatoid factor (RF) or anti-cyclic citrullinated peptide (anti-CCP) positivity. Among anemic patients, anemia was classified morphologically as microcytic or normocytic based on mean corpuscular volume (MCV), and inflammatory markers were compared across groups. Missing laboratory data were addressed using multiple imputation by chained equations (MICE).

Results: The cohort was predominantly female (133/152, 87.5%), and seropositive RA accounted for 75.7% (115/152) of cases. In the ESR model, C-reactive protein (CRP) positivity was the strongest independent predictor (adjusted odds ratio [aOR] 7.81, p<0.001), whereas anemia was not independently associated after adjustment (aOR 1.45, p=0.305). In a separate model predicting anemia, seropositive RA remained independently associated (aOR 2.12, p=0.024). Among anemic patients (n=89), 87 had available morphologic data; of these, 47 (54%) were normocytic and 40 (46%) microcytic. The normocytic group demonstrated significantly higher ESR and CRP values than other groups (p<0.001).

Conclusion: ESR elevation was independently associated with CRP-defined inflammatory activity after multivariate adjustment, whereas anemia did not demonstrate an independent association. These findings suggest that ESR retains clinical relevance in reflecting inflammatory burden when interpreted in conjunction with complementary laboratory parameters.

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