Abstract

Objective: To compare anti-malondialdehyde–acetaldehyde (MAA) antibody concentrations between rheumatoid arthritis (RA) patients and healthy and rheumatic disease controls. Methods: Anti-MAA antibody (IgA, IgM, IgG) was measured using ELISA and banked serum from patients with RA (n = 284), osteoarthritis (OA, n = 330), spondyloarthropathy (SpA, n = 50), and systemic lupus erythematosus (SLE, n = 88) as well as healthy controls (n = 82). Anti-MAA antibody concentrations and the frequency of positivity were compared across groups. Multivariable linear regression analysis limited to RA and OA patients (due to sample size and data availability) was used to identify factors associated with anti-MAA antibody concentrations. Results: Although RA patients demonstrated among the highest circulating concentrations across isotypes, only IgA anti-MAA antibody was significantly higher than all other groups (p ≤ 0.02). Proportions (7% to 74%) of OA and SLE (less so for SpA) samples were positive for anti-MAA antibody, limiting the discriminatory capacity of anti-MAA antibody in RA (positive in 18% to 80%). In analyses limited to those with RA or OA, factors associated with higher anti-MAA antibody concentrations included RA case status, younger age (IgM), male sex (IgG), African American race (IgA, IgG) and current smoking (IgA). C-reactive protein levels and comorbidities were not associated with anti-MAA antibody concentrations. Conclusion: With the possible exception of the IgA isotype, serum anti-MAA antibodies measured with currently available assays do not appear to adequately discriminate RA from other rheumatic conditions. With the identification of specific proteins that are MAA-modified in diseased tissues and requisite assay refinement, anti-MAA antibody holds potential promise as a biomarker in RA.

Original languageEnglish (US)
Pages (from-to)113-118
Number of pages6
JournalInternational Immunopharmacology
Volume56
DOIs
StatePublished - Mar 1 2018

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Anti-Idiotypic Antibodies
Rheumatoid Arthritis
Antibodies
Immunoglobulin A
Immunoglobulin G
Immunoglobulin M
Spondylarthropathies
Rheumatic Diseases
Serum
Osteoarthritis
African Americans
Systemic Lupus Erythematosus
C-Reactive Protein
Sample Size
Comorbidity
Linear Models
Biomarkers
Smoking
Enzyme-Linked Immunosorbent Assay
Regression Analysis

Keywords

  • Malondialdehyde–acetaldehyde
  • Oxidative stress
  • Rheumatoid arthritis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pharmacology

Cite this

@article{bc93da961af1405f90249f8c1ff48f82,
title = "Malondialdehyde–acetaldehyde antibody concentrations in rheumatoid arthritis and other rheumatic conditions",
abstract = "Objective: To compare anti-malondialdehyde–acetaldehyde (MAA) antibody concentrations between rheumatoid arthritis (RA) patients and healthy and rheumatic disease controls. Methods: Anti-MAA antibody (IgA, IgM, IgG) was measured using ELISA and banked serum from patients with RA (n = 284), osteoarthritis (OA, n = 330), spondyloarthropathy (SpA, n = 50), and systemic lupus erythematosus (SLE, n = 88) as well as healthy controls (n = 82). Anti-MAA antibody concentrations and the frequency of positivity were compared across groups. Multivariable linear regression analysis limited to RA and OA patients (due to sample size and data availability) was used to identify factors associated with anti-MAA antibody concentrations. Results: Although RA patients demonstrated among the highest circulating concentrations across isotypes, only IgA anti-MAA antibody was significantly higher than all other groups (p ≤ 0.02). Proportions (7{\%} to 74{\%}) of OA and SLE (less so for SpA) samples were positive for anti-MAA antibody, limiting the discriminatory capacity of anti-MAA antibody in RA (positive in 18{\%} to 80{\%}). In analyses limited to those with RA or OA, factors associated with higher anti-MAA antibody concentrations included RA case status, younger age (IgM), male sex (IgG), African American race (IgA, IgG) and current smoking (IgA). C-reactive protein levels and comorbidities were not associated with anti-MAA antibody concentrations. Conclusion: With the possible exception of the IgA isotype, serum anti-MAA antibodies measured with currently available assays do not appear to adequately discriminate RA from other rheumatic conditions. With the identification of specific proteins that are MAA-modified in diseased tissues and requisite assay refinement, anti-MAA antibody holds potential promise as a biomarker in RA.",
keywords = "Malondialdehyde–acetaldehyde, Oxidative stress, Rheumatoid arthritis",
author = "Mikuls, {Ted R} and Duryee, {Michael J.} and Bryant England and Anderson, {Daniel R} and Hearth-Holmes, {Michelene P} and Kaihong Su and Michaud, {Kaleb D} and Payne, {Jeffrey B} and Harlan Sayles and Carlos Hunter and McGowan, {Jacob D.} and Klassen, {Lynell Warren} and Thiele, {Geoffrey Milton}",
year = "2018",
month = "3",
day = "1",
doi = "10.1016/j.intimp.2018.01.022",
language = "English (US)",
volume = "56",
pages = "113--118",
journal = "International Immunopharmacology",
issn = "1567-5769",
publisher = "Elsevier",

}

TY - JOUR

T1 - Malondialdehyde–acetaldehyde antibody concentrations in rheumatoid arthritis and other rheumatic conditions

AU - Mikuls, Ted R

AU - Duryee, Michael J.

AU - England, Bryant

AU - Anderson, Daniel R

AU - Hearth-Holmes, Michelene P

AU - Su, Kaihong

AU - Michaud, Kaleb D

AU - Payne, Jeffrey B

AU - Sayles, Harlan

AU - Hunter, Carlos

AU - McGowan, Jacob D.

AU - Klassen, Lynell Warren

AU - Thiele, Geoffrey Milton

PY - 2018/3/1

Y1 - 2018/3/1

N2 - Objective: To compare anti-malondialdehyde–acetaldehyde (MAA) antibody concentrations between rheumatoid arthritis (RA) patients and healthy and rheumatic disease controls. Methods: Anti-MAA antibody (IgA, IgM, IgG) was measured using ELISA and banked serum from patients with RA (n = 284), osteoarthritis (OA, n = 330), spondyloarthropathy (SpA, n = 50), and systemic lupus erythematosus (SLE, n = 88) as well as healthy controls (n = 82). Anti-MAA antibody concentrations and the frequency of positivity were compared across groups. Multivariable linear regression analysis limited to RA and OA patients (due to sample size and data availability) was used to identify factors associated with anti-MAA antibody concentrations. Results: Although RA patients demonstrated among the highest circulating concentrations across isotypes, only IgA anti-MAA antibody was significantly higher than all other groups (p ≤ 0.02). Proportions (7% to 74%) of OA and SLE (less so for SpA) samples were positive for anti-MAA antibody, limiting the discriminatory capacity of anti-MAA antibody in RA (positive in 18% to 80%). In analyses limited to those with RA or OA, factors associated with higher anti-MAA antibody concentrations included RA case status, younger age (IgM), male sex (IgG), African American race (IgA, IgG) and current smoking (IgA). C-reactive protein levels and comorbidities were not associated with anti-MAA antibody concentrations. Conclusion: With the possible exception of the IgA isotype, serum anti-MAA antibodies measured with currently available assays do not appear to adequately discriminate RA from other rheumatic conditions. With the identification of specific proteins that are MAA-modified in diseased tissues and requisite assay refinement, anti-MAA antibody holds potential promise as a biomarker in RA.

AB - Objective: To compare anti-malondialdehyde–acetaldehyde (MAA) antibody concentrations between rheumatoid arthritis (RA) patients and healthy and rheumatic disease controls. Methods: Anti-MAA antibody (IgA, IgM, IgG) was measured using ELISA and banked serum from patients with RA (n = 284), osteoarthritis (OA, n = 330), spondyloarthropathy (SpA, n = 50), and systemic lupus erythematosus (SLE, n = 88) as well as healthy controls (n = 82). Anti-MAA antibody concentrations and the frequency of positivity were compared across groups. Multivariable linear regression analysis limited to RA and OA patients (due to sample size and data availability) was used to identify factors associated with anti-MAA antibody concentrations. Results: Although RA patients demonstrated among the highest circulating concentrations across isotypes, only IgA anti-MAA antibody was significantly higher than all other groups (p ≤ 0.02). Proportions (7% to 74%) of OA and SLE (less so for SpA) samples were positive for anti-MAA antibody, limiting the discriminatory capacity of anti-MAA antibody in RA (positive in 18% to 80%). In analyses limited to those with RA or OA, factors associated with higher anti-MAA antibody concentrations included RA case status, younger age (IgM), male sex (IgG), African American race (IgA, IgG) and current smoking (IgA). C-reactive protein levels and comorbidities were not associated with anti-MAA antibody concentrations. Conclusion: With the possible exception of the IgA isotype, serum anti-MAA antibodies measured with currently available assays do not appear to adequately discriminate RA from other rheumatic conditions. With the identification of specific proteins that are MAA-modified in diseased tissues and requisite assay refinement, anti-MAA antibody holds potential promise as a biomarker in RA.

KW - Malondialdehyde–acetaldehyde

KW - Oxidative stress

KW - Rheumatoid arthritis

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U2 - 10.1016/j.intimp.2018.01.022

DO - 10.1016/j.intimp.2018.01.022

M3 - Article

VL - 56

SP - 113

EP - 118

JO - International Immunopharmacology

JF - International Immunopharmacology

SN - 1567-5769

ER -