1212 - Mortality and Cause of Death In Young Rheumatoid Arthritis Patients Treated with Anti-TNF Therapy: Results From the British Society for Rheumatology Biologics Register

Monday, November 7, 2011: 9:00 AM-6:00 PM
Hall F2 - Poster Hall (McCormick Place West)
Malack Alachkar, Kath D. Watson, Kimme L. Hyrich and Deborah PM Symmons, Arthritis Research UK Epidemiology Unit, University of Manchester, Manchester, United Kingdom
Presentation Number: 1212

Background/Purpose: Rheumatoid arthritis (RA) is associated with increased mortality, with cardiovascular disease (CVD) being the leading cause of mortality and premature death. Any deaths observed in young RA patients are likely premature and possibly related to the underlying RA. In this study, we examined the cause of death in young RA patients aged 50 years or less who were treated with anti-TNF therapy. 

Method: The patients were selected from the British Society for Rheumatology Biologics Register (BSRBR), a UK national prospective cohort study to monitor the long-term safety of biologic therapy. The analysis included subjects with RA aged 50 years or less at registration with the BSRBR. Patients were followed either from the start of anti-TNF (adalimumab, etanercept or infliximab) therapy or from registration into the non-biologic disease modifying antirheumatic drug (nbDMARD) comparison cohort until 10/31/2009 or death, whichever came first. All patients were flagged with the UK national death register who provided copies of death certificates. We used student’s t or chi-square (χ2) tests to compare the baseline demographic characteristics and comorbidites between the two cohorts. Mortality rate per 1000 patient-years of observation (pyrs) with 95% confidence interval (95% CI) was estimated in each group and the two rates were compared. However, it was not possible to do baseline adjustment in the analysis because the numbers of death were too small.

Result: In total, 4883 young RA patients were recruited to this study; 4089 anti-TNF (21380 pyrs) and 794 nbDMARD (3206 pyrs) treated patients. Compared to the nbDMARD treated patients, anti-TNF treated patients were younger at RA onset, had longer RA duration and higher disease activity, and were more likely to be rheumatoid factor (RF) positive and to be receiving steroids (Table). Subjects in the biologic group were more likely to have hypertension (15% vs. 10.5%, p=0.003) but less likely to have chronic obstructive pulmonary disease (1.8% vs. 3.7%, p=0.0009) and a history of asthma (10% vs. 14%, p=0.0017).

During the time of observation, 36 patients died in the anti-TNF cohort compared to 3 patients in the nbDMARD cohort (Table).

Table: Patient baseline characteristics, number of deaths and mortality rate.

Number of Patients

nbDMARD cohort


Anti-TNF cohort 


Patient-years of observation 



Age at onset of RA years, mean (SD)

35.4 (8.9)*

30.7 (9.4)*

Age at registration years, mean (SD)

41.8 (7)

41.2 (7.3)

Disease duration years, mean (SD)

6.7 (6.1)*

15 (8)*

Female %



Steroid use, no (%)

64 (15.8)*

2042 (66.9)*

RF status positive, no (%)

429 (54.2)*

2472 (61.4)*

Baseline DAS28 mean (SD)

5.1 (1.1)*

6.4 (0.8)*

Baseline HAQ mean (SD)

1.5 (0.6)*

2.1 (0.5)*

Number of deaths



Mortality rate /1000 pyrs (95% CI)

0.94** (0.19-2.7)

1.68** (1.2-2.3)    

*p value <0.001, **p value = 0.32

Causes of death in the anti-TNF group were infection (n=11), malignant neoplasms (n=7), CVD (n=6), interstitial lung disease (ILD) (n=4) and other (n=8). The causes of the death in the nbDMARD group were malignant neoplasm (n=1), CVD (n=1) and an intestinal vascular event (n=1).

Conclusion: There was no significant difference in mortality rate in this young cohort between those treated with anti-TNF and nbDMARD therapy. It is possible that the deaths due to infection and ILD may be attributable to the underlying RA or its treatment. RA may also have contributed to the CVD deaths.

Keywords: anti-TNF therapy, morbidity and mortality and rheumatoid arthritis (RA)

Disclosure: M. Alachkar, None; K. D. Watson, None; K. L. Hyrich, None; D. P. Symmons, None.