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Abstract Number: 2038

Respiratory Cause Mortality Was Significantly Predicted By Incident Rheumatoid Arthritis (RA) and Higher Pre-RA Levels (0.50+ SD) of Soluble Interleukin-2 Receptor Alpha (sIL-2Rá): Results of a 21-Year Community-Based Cohort Survival Analysis

Alfonse T. Masi1, Azeem Rehman1, Huaping Wang1 and Jean Aldag2, 1Medicine, University of Illinois College of Medicine at Peoria, Peoria, IL, 2Medicine, University of Illinois College of Medicince at Peoria, retired, Peoria, IL

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Biomarkers, Epidemiologic methods, morbidity and mortality, respiratory disease and rheumatoid arthritis (RA)

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Session Information

Session Title: Epidemiology and Public Health (ACR): Rheumatoid Arthritis Pathogenesis and Treatment

Session Type: Abstract Submissions (ACR)

Background/Purpose: Interstitial lung disease (ILD) mortality is reported to be increased in RA (Bongartz T et al. A&R 2010; 62: 1583-91). However, non-malignant respiratory mortality has not been reported in population-based RA and CN subjects.  This study aimed to analyze predictors of non-malignant respiratory cause mortality in a community-based cohort of incident RA vs non-RA control (CN) subjects as well as the relation of higher baseline levels of immunological biomarkers.   

Methods: Total incident cases (n = 54) had onset of ACR-positive RA, 3 to 20 (mean 12) years, after cohort entry (n = 21,061 adults) in 1974. Cases were matched at entry with 203 CN by age, gender, and race (all Caucasian). All subjects (n=257) had baseline data on: demographic, cigarette smoking, and inflammatory or cytokine biomarkers (n = 7) tested on stored (-70˚C) sera. A total of 113 deaths were identified from 1992 to 2013, and 100 of them had completed death certificates retrieved. Two investigators independently determined underlying causes of death from the completed certificate codes, without knowledge of RA vs CN status. The few differences in interpretation were also “blindly” resolved. Multiple imputation and aggregate methods were used to enter values for a minority of randomly missing test results on the analyzed biomarkers: acute serum amyloid A (ASAA); C-reactive protein (CRP);  IL-1β; IL-1ra; TNFα; sTNF-R1, and sIL-2Rα. Biomarker values were normalized using z-scores within sexes to adjust for any dimorphic differences.  Critical limits of biomarker levels were searched to identify associations with total mortality, e.g., 0.50+SE for sIL-2Rα. Non-malignant respiratory diseases included ICD-9 codes, 460-519, and ICD-10 codes, J00-J99.  Cox regression models were used to estimate hazard ratios (HRs) for respiratory causes of death vs remaining subjects, adjusting for covariates.   

Results: Non-malignant respiratory deaths occurred in 8 (14.8%) of 54 RA vs 5 (2.5%) of 203 CN, p = 0.001 by Fisher’s exact test. The HR for respiratory deaths was 14.3 (95% CI 3.07-66.82), p = 0.001, in RA vs CN, after adjusting for cohort entry age, cigarette smoking, years of education, and the 7 immunological biomarkers.  Respiratory death was independently predicted by: RA vs CN; entry age, and higher levels (0.50+SE) of sIL-2Rα, as shown in the below Cox survival model, adjusted for 9 additional covariates.

Conclusion: Respiratory deaths were significantly (p = 0.001) greater in incident RA (14.8%) than CN (2.5%), with an HR of 14.3 (3.07-66.82), and higher sIL-2Rα levels significantly (p = 0.001) predicted respiratory cause mortality, which deserve further investigation.    

Variables in the Model

HR (95% CI)

P values

CN vs RA (CN=0, RA=1)

14.32 (3.07-66.82)

0.001

Cohort Entry Age (yrs)

1.29 (1.13-1.46)

0.000

sIL-2Rα (0.50+ SD), no = 0, yes = 1

37.65 (4.68-302.90)

0.001

Degree of Smoking  (7-scale)

1.01 (0.65-1.59)

0.960

Sex (F= 0, M = 1)

2.71 (0.57-12.90)

0.211

Completed Education  (yrs)

0.95 (0.72-1.24)

0.690

ASAA  (0.0+ SD), no = 0, yes = 1

1.05 (0.25-4.48)

0.948

CRP (0.0+ SD), no = 0, yes = 1

0.42 (0.11-1.65)

0.214

IL-1β (continuous)

2.27 (0.77-6.71)

0.139

IL-1ra (continuous)

 

1.61 (0.51-5.12)

0.416

TNFα (continuous)

0.57 (0.22-1.47)

0.243

sTNF- R1 (0.0+ SD), no = 0, yes = 1

1.21 (0.32-4.63)

0.782

                                                                               


Disclosure:

A. T. Masi,
None;

A. Rehman,
None;

H. Wang,
None;

J. Aldag,
None.

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