ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 1946

Antineutrophil Cytoplasmic Antibody (ANCA) Type and Body Mass Index in ANCA-Associated Vasculitis (AAV)

Zachary Wallace1, Na Lu2, Eli Miloslavsky3, Ulrich Specks4, Gary S. Hoffman5, Cees G.M. Kallenberg6, Carol A. Langford7, Peter A. Merkel8, Paul A. Monach9, Philip Seo10, Robert F. Spiera11, Eugene William St.Clair12, Paul Bruntetta13, Hyon K. Choi14 and John H. Stone15, 1Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Boston, MA, 2Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 3Division of Rheumatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 4Mayo Clinic, Rochester, MN, 5Rheumatology, Cleveland Clinic, Cleveland, OH, 6Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands, 7Rheumatic and Immunologic Diseases, Cleveland Clinic, Cleveland, OH, 8Division of Rheumatology, Univ of Pennsylvania; Perelman School of Med, Philadelphia, PA, 9Rheumatology, Boston University School of Medicine, Boston, MA, 10Medicine, Johns Hopkins University, Baltimore, MD, 11Hospital for Special Surgery, Cornell, New York, NY, 12Rheumatology and Immunology, Duke University, Durham, NC, 13Genentech, Inc., South San Francisco, CA, 14Rheumatology, Allergy and Immunology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 15Massachusetts General Hospital Rheumatology Unit, Harvard Medical School, Boston, MA

Meeting: 2016 ACR/ARHP Annual Meeting

Date of first publication: September 28, 2016

Keywords:

Session Information

Date: Monday, November 14, 2016

Title: Vasculitis - Poster II: ANCA-Associated Vasculitis

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Antineutrophil Cytoplasmic Antibody (ANCA) Type and Body Mass Index in ANCA-Associated Vasculitis (AAV)

Background/Purpose: Phenotypic, genetic, and treatment differences distinguish PR3- and MPO-ANCA+ ANCA-associated vasculitis (AAV) patients and suggest that these serotypes represent distinct conditions which might have different risk factors.  Being overweight or obese is a risk factor in some autoimmune conditions (e.g., rheumatoid arthritis)  but differences in body mass index (BMI) between the PR3- and MPO-ANCA+ AAV subtypes have not been investigated.  Such differences could suggest novel genetic or environmental risk factors and have implications for treatment response, as in psoriatic arthritis, and the risk of cardiovascular disease which is a common cause of death in AAV.  We evaluated whether BMI differences exist between patients with PR3-ANCA+ and MPO-ANCA+ AAV.

Methods: We analyzed AAV patients from the Rituximab in ANCA-Associated Vasculitis (RAVE) trial.  In univariate analyses, we compared the BMI of PR3- and MPO-ANCA+ AAV patients at enrollment; in a multivariate linear regression, we adjusted for age, gender, glucocorticoids prior to enrollment, relapsing disease at baseline, and baseline disease activity.  We used an analysis of response profile to evaluate trends in BMI, adjusted for the above confounders as well as glucocorticoid exposure and flares during the trial. 

Results: The majority of patients in RAVE (N=197, Table 1) were PR3+ (131, 67%).  PR3-ANCA+ patients had a higher baseline BMI (29.6±6.6 vs. 27.2 ± 5.3; P=0.01) and were more often obese (42% vs. 24%, P=0.04).  When analyzing only those with a new diagnosis at enrollment (N=96), PR3-ANCA+ patients still had a significantly higher BMI (29.2 ± 6.2 vs. 26.8 ± 4.9, P=0.04).  In multivariate regression analyses, these differences (PR3-ANCA+ BMI 2.1 kg/m2 (±1.1) higher than MPO-ANCA+ patients) remained (P=0.047).  To address the potential impact of disease duration on BMI, we investigated the temporal trend in BMI between AAV subtypes over the course of the trial (18 months) and found a constant difference in BMI (Figure 1; P=0.3).   

Conclusion: PR3-ANCA+ patients have a significantly higher BMI than MPO-ANCA+ patients, even after adjustment for important potential confounders. Several possibilities may explain findings.  First, an elevated BMI may predispose to PR3-ANCA+ AAV.  Second, the activity of hormones associated with metabolism (e.g., leptin) may differ in AAV subtypes.  Third, BMI differences could be related to variations in shared genetic risk factors.  Table 1: RAVE Trial Cohort

Variable

PR3-ANCA+

MPO-ANCA+

P-Value
Number (N, %) 131 (66.5%) 66 (33.5%)  
Age 49.6 (±14.8) 59 (±15) <0.001
Male (N, %) 75 (57.3%) 24 (36.4%) 0.007
Baseline BVAS-WG 8.3 (±3.2) 8.5 (±3.1) 0.8
New Diagnosis at Enrollment 50 (38.2%) 46 (70%) <0.0001
Disease Category
Granulomatosis with polyangiitis (N, %) 127 (97%) 20 (30%) <0.0001
Microscopic polyangiitis (N, %) 4 (3%) 44 (66.7%)
Indeterminant (N, %) 0 (0%) 2 (3%)
Weight and BMI
Baseline weight (kg) 89.3 (±22.0) 77.2 (±16.0) <0.0001
Baseline BMI  (kg/m2) 29.6 (±6.6) 27.2 (± 5.3) <0.0001
Obese (N, %) 55 (42%) 16 (24%) 0.04
Glucocorticoid Dosing
GC prior to baseline (mg) 1263 (±1492) 1130 (±1408) 0.6
GC over the course of study (mg) 4838.2 (±2001) 4817.7 (±3433.1) 0.96

  Figure 1: Change in BMI During the RAVE Trial, Analysis of Response Profile

Disclosure: Z. Wallace, None; N. Lu, None; E. Miloslavsky, None; U. Specks, Genentech, 5; G. S. Hoffman, None; C. G. M. Kallenberg, None; C. A. Langford, Genentech and Biogen IDEC Inc., 2,GlaxoSmithKline, 2,Bristol-Myers Squibb, 2; P. A. Merkel, Chemocentryx, 5,Chemocentryx, 9; P. A. Monach, Genentech and Biogen IDEC Inc., 2,Bristol-Myers Squibb, 2,MedScape, 5,GlaxoSmithKline, 2,Vasculitis Foundation Board of Directors, 6,Editorial Board of Arthritis and Rheumatology, 6; P. Seo, None; R. F. Spiera, Chemocentryx, 9; E. W. St.Clair, Eli Lilly and Company, 2,Bristol-Myers Squibb, 5,Biogen Idec, 2; P. Bruntetta, Genentech, Inc., 3; H. K. Choi, None; J. H. Stone, Genentech/Roche, 2,Xencor, 2,Xencor, 5,Genentech/Roche, 5.

To cite this abstract in AMA style:

Wallace Z, Lu N, Miloslavsky E, Specks U, Hoffman GS, Kallenberg CGM, Langford CA, Merkel PA, Monach PA, Seo P, Spiera RF, St.Clair EW, Bruntetta P, Choi HK, Stone JH. Antineutrophil Cytoplasmic Antibody (ANCA) Type and Body Mass Index in ANCA-Associated Vasculitis (AAV) [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/antineutrophil-cytoplasmic-antibody-anca-type-and-body-mass-index-in-anca-associated-vasculitis-aav/. Accessed .

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