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The inflammatory protein calprotectin (MRP8/14) has been identified as a promising biomarker of treatment response in rheumatoid arthritis (RA). Our aim was to test MRP8/14 as a biomarker of response to TNF-inhibitors in the largest RA cohort to date and to compare with CRP.
Serum MRP8/14 was measured in 470 RA patients about to commence treatment with adalimumab (n=196) or etanercept (n=274). Additionally, MRP8/14 was measured in the 3-month sera of 179 adalimumab treated patients. Response was determined using EULAR response criteria calculated using the traditional 4-component (4C) DAS28-CRP and alternate validated versions using 3- (3C) and 2-components (2C), CDAI improvement criteria and change in individual outcome measures. Logistic/linear regression models were fitted for response outcome.
In the 3C and 2C models, RA patients were 1.92(CI:1.04-3.54) and 2.03(1.09-3.78) times more likely to be classified as EULAR responders if they had high (75th quartile) pre-treatment levels of MRP8/14 compared to low (25th quartile). No significant associations were observed for the 4C model. When only using CRP as a predictor, in the 3C and 2C analyses, patients above the 75th quartile were 3.79(CI:1.81-7.93) and 3.58(CI:1.74-7.35) times more likely to be EULAR responders and addition of MRP8/14 did not significantly improve model fit (p-value=0.62 and 0.80, respectively). No significant associations were observed in the 4C analysis. Exclusion of CRP from the outcome measure (CDAI), did not result in any significant associations with MRP8/14 (OR 1.00(CI:0.99-1.01); suggesting the associations were due to the correlation with CRP and that there is no additional utility of MRP8/14 beyond use of CRP in RA patients starting TNFi therapy.
Beyond correlation with CRP, we found no evidence to suggest MRP8/14 explains additional variability in response to TNFi in RA patients over and above CRP alone.
|Journal||Annals of Rheumatic Diseases|
|Publication status||Accepted/In press - 12 Jan 2023|
- Rheumatoid arthritis
- TNF inhibitors
- treatment response
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- 2 Active
NIHR Manchester Biomedical Research Centre
Bruce, I., Lord, G., Lennon, R., Black, G., Wedge, D., Morris, A., Hussell, T., Sharrocks, A., Stivaros, S., Buch, M., Gough, J., Kostarelos, K., Thistlethwaite, F., Kadler, K., Barton, A., Hyrich, K., Mcbeth, J., O'Neill, T., Vestbo, J., Simpson, A., Singh, S., Smith, J., Felton, T., Murray, C., Griffiths, C., Cullum, N., Rhodes, L., Warren, R., Paus, R., Dumville, J., Viros Usandizaga, A., Keavney, B., Tomaszewski, M., Allan, S., Body, R., Cartwright, E., Heagerty, A., Kalra, P., Miller, C., Rutter, M., Smith, C., Trafford, A., Evans, D., Crosbie, E., Crosbie, P., Harvie, M., Howell, S., Renehan, A., Dive, C., Blackhall, F., Landers, D., Krebs, M., Cook, N., Clarke, R., Taylor, S., Jorgensen, C., Lorigan, P., Jayson, G., Valle, J., Mccabe, M., Armstrong, A., Freitas, A., Illidge, T., Choudhury, A., Hoskin, P., West, C., Van Herk, M., Faivre-Finn, C., Bristow, R., Kirkby, K., Birtle, A., Mackay, R., Radford, J., Linton, K., Higham, C., Munro, K., Plack, C., Arden Armitage, C., Bruce, I., Moore, D., Saunders, G., Stone, M., Haddock, G., Lewis, S., Elliott, R., Green, J., Lovell, K., Morrison, A., Shaw, J., Bucci, S., Ainsworth, J., Webb, R., Newman, W., Banka, S., Clayton-Smith, J., Payne, K., Moldovan, R., Wynn, R. & Jones, S.
1/12/22 → 30/11/27
Centre for Epidemiology Versus Arthritis.
Dixon, W., Bruce, I., Felson, D., Hyrich, K., Lunt, M., Mcbeth, J., Mcdonagh, J., O'Neill, T., Sergeant, J., Verstappen, S. & Serafimova, I.
1/08/18 → 14/03/24