Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose
Short-term efficacy of tumour necrosis factor-alpha inhibitor (TNFi) therapy in patients with psoriatic arthritis (PsA) is well documented. In observational studies, effectiveness has mainly been explored in the short term (1-3 years) and predictors of improved short-term drug-survival include male gender, concomitant methotrexate (MTX) use, etanercept (ETN) use and high CRP. The aim of this analysis was to identify predictors of long-term (5 years) persistent treatment with TNFi in patients with PsA.
Methods
We included PsA patients registered with the British Society for Rheumatology Biologics Register starting a TNFi (recruited 2002-2006). Demographics, disease activity (joint counts, patient reported outcomes and inflammatory markers), disability, comorbidities and previous/current treatments were recorded at baseline. Follow-up (biannual for 3 years and then annually) includes changes in treatment, disease activity and adverse events. We identified patients who had continued their initial treatment for 5 years (allowing pauses < 90 days). Univariate logistic regression was used to identify factors associated with 5 years persitent therapy – covariates included age, disease duration, gender, number of previously used non-biologic DMARDs, comorbidity, TNFi-type, co-medication, steroid use, disease activity score (DAS) 28, erythrocyte sedimentation rate (ESR), patient global assessment, tender and swollen joints, current smoking and Health Assessment Questionnaire (HAQ). Age, gender and variables with p-value < 0.25 were included in a multivariate model and a backward section was performed to fit the final model.
Results
We included 666 patients starting TNFi (table). At 5 years, 312 (46.8%) patients were still on their initial treatment. Gender, disease duration, TNFi-type, comorbidity, tender joints, current smoking and HAQ were relevant predictors in univariate analysis (p<0.25). Concomitant MTX was not a predictor, neither in the whole cohort or when stratified by TNFi-type, but only 14 patients received infliximab (IFX) as monotherapy. Male gender, absence of baseline comorbidity and use of ETN or adalimumab (ADA) rather than IFX were independently associated with persistent treatment at 5 years (Table). HAQ, disease duration, tender joint count and current smoking were not significant predictors in the multivariate model.
Conclusion
Among this severe cohort of patients with PsA who initiated a TNFi prior to 2007, almost 50 percent were still on their initial treatment at 5 years. The only patient characteristics predicting this were gender and baseline comorbidity status which limits applicability to clinical practice. Concomitant MTX was not a significant predictor of long-term treatment persistence, suggesting an absence of a beneficiary effect across all TNFi therapies, opposed to that seen in rheumatoid arthritis.
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Table Baseline variables and logistic regression predicting continued treatment at 5 years |
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|
Baseline |
Univariate analysis |
Final multivariate model |
|
|
|
|
OR (95% CI)e |
OR (95% CI)e |
p-value |
|
Females (n(%)) |
352 (52.9) |
0.54 (0.40-0.74) |
0.55 (0.40-0.75) |
<0.001 |
|
Age (years) |
45.83 (11.05) a |
1.01 (0.99-1.02) |
1.01 (1.00-1.03) |
0.052 |
|
Disease duration (years) |
12.71 (8.75) a |
1.02 (1.00-1.04) |
– |
– |
|
Previously used DMARDs |
3 (2-4) b |
0.92 (0.74-1.14) |
– |
– |
|
TNFi (n(%)) Etanercept |
365 (54.8) |
REF |
REF |
REF |
|
Infiximab |
196 (29.4) |
0.52 (0.37-0.75) |
0.55 (0.38-0.78) |
0.001 |
|
Adalimumab |
105 (15.8) |
0.87 (0.53-1.34) |
0.89 (0.57-1.39) |
0.622 |
|
Current smoker (n(%)) |
111 (21.0) |
0.62 (0.41-0.95) |
– |
– |
|
Comorbidityc (n(%)) |
366 (54.9) |
0.62 (0.46-0.85) |
0.60 (0.44-0.84) |
0.002 |
|
Co-medication (n(%)) None |
190 (28.5) |
REF |
– |
– |
|
MTXd |
396 (59.5) |
0.87 (0.61-1.23) |
– |
– |
|
Other |
80 (12.0) |
0.70 (0.41-1.19) |
– |
– |
|
Baseline steroid use (n(%)) |
156 (23.4) |
0.84 (0.59-1.21) |
– |
– |
|
Global (0-100) |
70.97 (20.99) a |
1.00 (0.99-1.01) |
– |
– |
|
DAS 28 |
6.05 (1.19) a |
0.98 (0.85-1.11) |
– |
– |
|
Tender joints (28 joint-count) |
13 (7-19) b |
0.98 (0.96-1.00) |
– |
– |
|
Swollen joints (28 joint-count) |
8 (4-12) b |
1.00 (0.98-1.03) |
– |
– |
|
ESR (mm/hr) |
33 (18-57) b |
1.00 (1.00-1.01) |
– |
– |
|
HAQ (0-3) |
1.88 (1.38-2.25)b |
0.72 (0.57-0.92) |
– |
– |
|
Reason for discontinuation |
|
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Inefficacy (n(%)) |
125 (35.3) |
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Adverse events (n(%)) |
102 (28.8) |
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Other/missing (n(%)) |
127 (35.9) |
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OR=Odds ratio amean (standard deviation) bmedian (inter-quartile range) c≥1 of (previous or current) hypertension, angina, MI , stroke, epilepsy, asthma, chronic obstructive airway disease, peptic ulcer disease, liver disease, renal disease, tuberculosis, demyelinating disease, diabetes, depression, cancer dalone or in combination with other DMARD eper unit increase (in continuous variables) |
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Disclosure:
K. M. Fagerli,
None;
K. D. Watson,
None;
J. Packham,
None;
D. P. Symmons,
None;
K. L. Hyrich,
Pfizer Inc,
9,
Abbott Immunology Pharmaceuticals,
9;
On behalf of the BSRBR,
Pfizer Inc, Abbvie, UCB, Merck, Roche,
2.
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