Background/Purpose: Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) have been demonstrated to correlate with disease activity and predict treatment response in rheumatic diseases including rheumatoid arthritis and SLE. A reliable and readily accessible biomarker that fulfils these roles has not been identified in polymyalgia rheumatica (PMR). This study evaluated the relationship between NLR and PLR, and disease activity and glucocorticoid resistance in PMR.    

Methods: Data for disease activity (as measured by the PMR-Activity Score [PMR-AS]), prednisolone dose and full blood count was obtained from  the Melbourne Predictors of Relapse in PMR (MPR-PMR) study: a prospective observational cohort comprising 37 patients (35 steroid naïve) with newly diagnosed PMR (2012 EULAR/ACR Classification Criteria) treated with a standardised weaning course of prednisolone (British Society of Rheumatology Guideline) for the duration of follow-up (46 weeks) or until the addition of a steroid-sparing agent was indicated. Prior ethics approval was received from Austin Health Research Ethics Committee and the trial registered with the Australian and New Zealand Clinical Trials Registry (trial identification ACTRN1261400696695). Glucocorticoid resistance was defined as non-response to initial prednisolone dose (15mg/day) or initial response followed by flare (as defined by PMR-AS ≥9.35 or D≥6.6) upon weaning prednisolone to 5mg/day. Univariable linear regression analysis of the relationship between PMR-AS (baseline and mean) and NLR and PLR was performed, with comparison of glucocorticoid-resistant patients to glucocorticoid-responders undertaken using logistic regression on baseline NLR. All statistical analysis was performed using R version 3.5.0.      

Results: Complete data was available for 33/37 patients (89.2%). Mean age was 69.2±7.53 years, 54% were male and 97% Caucasian. Median ESR was 46 (29 – 65) and CRP 40.2 (19 – 64.4) at diagnosis, whilst median PMR-AS was high at 68.7 (49.7 – 98). A statistically significant relationship was identified between PMR-AS and both NLR (p = 0.025) and PLR (p = 0.005) at baseline. PLR correlated with mean PMR-AS during follow-up (p = 0.033), whilst there was a trend towards significance in the relationship between NLR and mean PMR-AS (p = 0.054). In evaluating treatment response, baseline NLR was found to predict glucocorticoid resistance (p= 0.042).

Figure 1: Relationship between PMR-AS and NLR and PLR.   

Conclusion: Baseline NLR can predict glucocorticoid resistance in newly diagnosed patients with PMR. Both NLR and PLR may also be useful biomarkers of disease activity in PMR.