Article Text

FRI0142 Aggressive dmard therapy elevates hdl-cholesterol and lowers the atherogenic index in the taser study
  1. J. Robertson1,
  2. J. Dale2,
  3. N. Sattar3,
  4. D. Porter2
  1. 1Institute of Infection, Immunity & Inflammation, UNIVERSITY OF GLASGOW
  2. 2Dept. of Rheumatology, Gartnavel General Hospital
  3. 3Institute of Cardiovascular & Medical Sciences, UNIVERSITY OF GLASGOW, Glasgow, United Kingdom


Background In patients with RA elevations in total, HDL and LDL cholesterol, with variable changes in TC to HDL-c ratio, have been reported after biologic drugs therapy. In contrast, lipidaemic data for conventional DMARDS is relatively scant. The Targeting Synovitis in Early Rheumatoid Arthritis (TaSER) study (NCT00920478) is an ongoing RCT in early RA comparing a standard DAS28-driven DMARD escalation strategy with one driven by musculoskeletal ultrasound (MSUS). All patients were treated in a stepwise fashion with DMARDS and/or etanerceptas dictated by a standardised escalation protocol.

Objectives For this presentation we analysed the relationship between changes in lipid profile and disease activity in the context of an intensive “treat-to-target” strategy.

Methods Newly diagnosed patients with RA were randomised between standard (DAS28) and MSUS-assisted assessment groups, with 3-monthly assessments of DAS and CRP. Non-fasting lipid profiles were obtained at baseline and after the 18-month treatment period in 41 patients who were not taking cholesterol-lowering agents, 7 of whom progressed to etanercept treatment. We analysed (a) the changes in lipid profile after 18 months of anti-inflammatory treatment; and (b) the correlation between lipids and measures of inflammation. Data were analysed in Minitab v15 and SPSS. Changes in mean measures of inflammation and lipids were analysed using paired t-test, with non-parametric data log transformed prior to analysis. Correlations between the lipid and inflammatory parameters were analysed using Pearson’s coefficient and Spearman’s rank coefficient depending on normality of data.

Results Statistically significant falls in mean DAS (4.42 v 1.66, p < 0.001) and CRP (47mg/l v 11mg/l, p <0.001) were seen after treatment. Triglycerides and the TC/HDL-c ratio also fell, with a rise in HDL-c and a numerical but not statistical rise in TC (Table 1). Results were similar after excluding the 7 patients receiving etanercept.

Significant correlations were seen between baseline DAS v TC and LDL-c (r = -0.32, p = 0.04 for both measurements); baseline CRP v TC (r = -0.56, p<0.001) and LDL-c (r = -0.57, p < 0.001); and change in CRP v TC (r = -0.38, p=0.01) and HDL-c (r = -0.39, p=0.01). After excluding patients receiving etanercept, the correlations involving baseline and change CRP above remained significant.

Conclusions Aggressive disease control using conventional DMARDS in this RA cohort resulted in a fall in serum triglycerides and the atherogenic index, driven predominantly by an increase in serum HDL-c of around 15%; this compares with documented increases in HDL-c of around 7% in meta-analyses of anti-TNF treatment. The reduction in CRP from baseline to 18 months correlated with the rise in total and HDL-cholesterol. Given the importance of TC to HDL-c ratio in CVD risk prediction these results add to the paradigm that lipid profiles are potentially favourably modified upon inflammation suppression.

Disclosure of Interest None Declared

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