Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


The Relationship between Disease Status in Wegener's Granulomatosis with the Development of Subclinical Atherosclerosis.

Hajj-Ali5,  Rula, Silverstein2,  Roy, Joseph1,  Douglas, Imrey2,  Peter, Hoffman4,  Gary S., Zhang2,  Li, Langford3,  Carol A.

Cleevland Clinic
Cleveland Clinic
Cleveland Clinic Foundation, Cleveland, OH
Cleveland Clinic Foundation, Pepper Pike, OH
Cleveland Clinic, Cleveland, OH

Background:

A role for inflammation in the development of accelerated atherosclerosis in patients with chronic inflammatory disease has been proposed. However, the pathophysiology of this process is not fully understood. The objective of this study was to asses the relationship between inflammatory disease in Wegener's granulomatosis (WG) with the development of subclinical atherosclerosis.

Methods:

Eligible consenting adult patients who met the 1990 ACR classification criteria for WG were enrolled from the Cleveland Clinic Center for Vasculitis Care and Research. Exclusion criteria included history of coronary heart disease, heart failure, stroke, peripheral vascular diseases, acute or chronic infection within the past 3 months, NSAID or aspirin use within a week of MP and platelet studies, or diagnosis of chronic inflammatory disease, an autoimmune disease, or thrombophilia. Disease status was measured by BVAS-WG, VDI, disease duration and numbers of relapses (from onset of disease diagnosis until enrollment in the current study). Classic atherosclerotic risk factors and other co-morbidities were recorded in addition to platelet aggregation responses and circulating microparticle (MP) levels. All patients underwent ultrasound of the carotid arteries to assess intima media thickness (IMT) as an outcome for subclinical atherosclerosis.

Results:

45 WG patients were included. In univariate analyses, systolic and diastolic blood pressure, creatinine, and age at onset of disease were significantly associated with a higher IMT with rho values of 0.37, 0.38, 0.35 and 0.54 respectively (p < 0.02 for all), determined by Spearman rank correlation (Table 1).

Table 1. Spearman rank correlation between IMT and patient characteristics

OutcomeVariableNrho95%CIP value
IMTBMI440.19(-0.12, 0.49)0.23
IMTSystolic blood pressure450.37(0.09, 0.66)0.012
IMTDiastolic blood pressure450.38(0.09, 0.66)0.011
IMTCreatinine450.35(0.06, 0.64)0.019
IMTHDL45-0.21(-0.51, 0.10)0.18
IMTLDL45-0.19(-0.50, 0.11)0.2
IMTFBG450.12(-0.18, 0.43)0.42
IMTAge at onset of disease450.54(0.28, 0.80)<0.001
IMTDisease Duration450.23(-0.07, 0.53)0.13
IMTAzathioprine Duration45-0.24(-0.53, 0.06)0.12
IMTMethotrexate Duration450.11(-0.20, 0.41)0.48
IMTCyclophosphamide Duration45-0.13(-0.43, 0.18)0.41
IMTCumulative Dose of cyclophosphamide45-0.15(-0.45, 0.16)0.34
IMTTotal MP counts45-0.18(-0.48, 0.12)0.23
IMTAnnexin counts45-0.2(-0.50, 0.10)0.18
IMTCD_14 MP counts45-0.04(-0.34, 0.27)0.81
IMTCD_16 MP counts45-0.12(-0.42, 0.19)0.45
IMTCD_18 MP counts450(-0.31, 0.31)0.99
IMTCD_41 MP counts45-0.16(-0.47, 0.14)0.29
IMTCD_105 MP counts45-0.21(-0.51, 0.09)0.16
IMTCD_144 MP counts450(-0.31, 0.31)0.99
IMTCD_235 MP counts43-0.05(-0.37, 0.26)0.73
IMTPlatelet aggregation400.24(-0.08, 0.56)0.14

When all variables were considered in a multiple regression model that included the total number of disease relapses, and after adjusting for the other significant factors, higher relapse number, older age at onset of disease, and higher diastolic blood pressure were found to be associated with higher IMT as shown in Table 2.

Table 2. Multiple regression model for assessing the association between IMT and sum of Flares

OutcomeParameterEstimate (%95 CI)P value
IMTFlare sum0.0119 (0.0001, 0.0236)0.003
 Age at onset of disease0.005 (0.003, 0.008)<0.001
 Diastolic blood pressure0.0033 (0.0003, 0.0064)0.031

Conclusion:

This is the first study that addresses disease status as it relates to atherosclerosis in WG. Our data suggests that total number of disease relapses, but not disease duration, is a more important risk factor for atherosclerosis and implies that the cumulative inflammatory events contributes to the development of atherosclerosis.

To cite this abstract, please use the following information:
Hajj-Ali, Rula, Silverstein, Roy, Joseph, Douglas, Imrey, Peter, Hoffman, Gary S., Zhang, Li, et al; The Relationship between Disease Status in Wegener's Granulomatosis with the Development of Subclinical Atherosclerosis. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :2049
DOI: 10.1002/art.29814

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