Clinical and pathologic differences in interstitial lung disease based on antisynthetase antibody type

C. Johnson, G. R. Connors, J. Oaks, S. Han, A. Truong, B. Richardson, Noah Lechtzin, A. L. Mammen, Livia A Casciola Rosen, Lisa Christopher-Stine, Sonye Danoff

Research output: Contribution to journalArticle

Abstract

Background Interstitial lung disease (ILD) is a common extramuscular manifestation of the idiopathic inflammatory myopathies (IIMs), dermatomyositis (DM) and polymyositis (PM). Patients with antisynthetase antibodies (ASA) demonstrate some or all of the features of the antisynthetase syndrome including IIM and ILD. It has been hypothesized that the clinical expression of antisynthetase syndrome varies between specific ASAs. Objective We sought to determine whether the myositis-associated ILD (MA-ILD) phenotype differs based on the presence of ASAs and by ASA subtype. Methods A cross-sectional and longitudinal analysis of consecutive patients enrolled at the Johns Hopkins Myositis Center with ILD in the setting of clinically diagnosed autoimmune myositis was conducted. Results Seventy-seven subjects were included; 36 were ASA negative, 28 were anti-Jo1 positive, and 13 were non-Jo1 ASA positive (5 anti-PL-12, 4 anti-PL-7, 2 anti-EJ, and 2 anti-OJ). Non-Jo1 ASA positive participants were more likely to be African-American than Caucasian as compared to both the anti-Jo1 positive (p = 0.01) and ASA negative groups (p <0.01). ASA negative participants had better mean forced vital capacity percent predicted (FVC%) and total computed tomography scores over time compared to those with anti-Jo1 after controlling for potential confounders. Conclusions ASA status was significantly different by race. Those with anti-Jo1 antibodies had worse lung function and CT scores over time compared to those without detectable antisynthetase antibodies. Further prospective study in a larger cohort is needed to determine whether these apparent antibody-specific differences in demographics and manifestations of disease translate into meaningful disparities in clinical outcomes.

Original languageEnglish (US)
Pages (from-to)1542-1548
Number of pages7
JournalRespiratory Medicine
Volume108
Issue number10
DOIs
StatePublished - Oct 1 2014

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Interstitial Lung Diseases
Myositis
Antibodies
Polymyositis
Dermatomyositis
Vital Capacity
African Americans
Anti-Idiotypic Antibodies
Cross-Sectional Studies
Tomography
Demography
Prospective Studies
Phenotype
Lung

Keywords

  • Dermatomyositis
  • IL
  • Polymyositis Antisynthetase syndrome

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Medicine(all)

Cite this

Clinical and pathologic differences in interstitial lung disease based on antisynthetase antibody type. / Johnson, C.; Connors, G. R.; Oaks, J.; Han, S.; Truong, A.; Richardson, B.; Lechtzin, Noah; Mammen, A. L.; Casciola Rosen, Livia A; Christopher-Stine, Lisa; Danoff, Sonye.

In: Respiratory Medicine, Vol. 108, No. 10, 01.10.2014, p. 1542-1548.

Research output: Contribution to journalArticle

Johnson, C. ; Connors, G. R. ; Oaks, J. ; Han, S. ; Truong, A. ; Richardson, B. ; Lechtzin, Noah ; Mammen, A. L. ; Casciola Rosen, Livia A ; Christopher-Stine, Lisa ; Danoff, Sonye. / Clinical and pathologic differences in interstitial lung disease based on antisynthetase antibody type. In: Respiratory Medicine. 2014 ; Vol. 108, No. 10. pp. 1542-1548.
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abstract = "Background Interstitial lung disease (ILD) is a common extramuscular manifestation of the idiopathic inflammatory myopathies (IIMs), dermatomyositis (DM) and polymyositis (PM). Patients with antisynthetase antibodies (ASA) demonstrate some or all of the features of the antisynthetase syndrome including IIM and ILD. It has been hypothesized that the clinical expression of antisynthetase syndrome varies between specific ASAs. Objective We sought to determine whether the myositis-associated ILD (MA-ILD) phenotype differs based on the presence of ASAs and by ASA subtype. Methods A cross-sectional and longitudinal analysis of consecutive patients enrolled at the Johns Hopkins Myositis Center with ILD in the setting of clinically diagnosed autoimmune myositis was conducted. Results Seventy-seven subjects were included; 36 were ASA negative, 28 were anti-Jo1 positive, and 13 were non-Jo1 ASA positive (5 anti-PL-12, 4 anti-PL-7, 2 anti-EJ, and 2 anti-OJ). Non-Jo1 ASA positive participants were more likely to be African-American than Caucasian as compared to both the anti-Jo1 positive (p = 0.01) and ASA negative groups (p <0.01). ASA negative participants had better mean forced vital capacity percent predicted (FVC{\%}) and total computed tomography scores over time compared to those with anti-Jo1 after controlling for potential confounders. Conclusions ASA status was significantly different by race. Those with anti-Jo1 antibodies had worse lung function and CT scores over time compared to those without detectable antisynthetase antibodies. Further prospective study in a larger cohort is needed to determine whether these apparent antibody-specific differences in demographics and manifestations of disease translate into meaningful disparities in clinical outcomes.",
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T1 - Clinical and pathologic differences in interstitial lung disease based on antisynthetase antibody type

AU - Johnson, C.

AU - Connors, G. R.

AU - Oaks, J.

AU - Han, S.

AU - Truong, A.

AU - Richardson, B.

AU - Lechtzin, Noah

AU - Mammen, A. L.

AU - Casciola Rosen, Livia A

AU - Christopher-Stine, Lisa

AU - Danoff, Sonye

PY - 2014/10/1

Y1 - 2014/10/1

N2 - Background Interstitial lung disease (ILD) is a common extramuscular manifestation of the idiopathic inflammatory myopathies (IIMs), dermatomyositis (DM) and polymyositis (PM). Patients with antisynthetase antibodies (ASA) demonstrate some or all of the features of the antisynthetase syndrome including IIM and ILD. It has been hypothesized that the clinical expression of antisynthetase syndrome varies between specific ASAs. Objective We sought to determine whether the myositis-associated ILD (MA-ILD) phenotype differs based on the presence of ASAs and by ASA subtype. Methods A cross-sectional and longitudinal analysis of consecutive patients enrolled at the Johns Hopkins Myositis Center with ILD in the setting of clinically diagnosed autoimmune myositis was conducted. Results Seventy-seven subjects were included; 36 were ASA negative, 28 were anti-Jo1 positive, and 13 were non-Jo1 ASA positive (5 anti-PL-12, 4 anti-PL-7, 2 anti-EJ, and 2 anti-OJ). Non-Jo1 ASA positive participants were more likely to be African-American than Caucasian as compared to both the anti-Jo1 positive (p = 0.01) and ASA negative groups (p <0.01). ASA negative participants had better mean forced vital capacity percent predicted (FVC%) and total computed tomography scores over time compared to those with anti-Jo1 after controlling for potential confounders. Conclusions ASA status was significantly different by race. Those with anti-Jo1 antibodies had worse lung function and CT scores over time compared to those without detectable antisynthetase antibodies. Further prospective study in a larger cohort is needed to determine whether these apparent antibody-specific differences in demographics and manifestations of disease translate into meaningful disparities in clinical outcomes.

AB - Background Interstitial lung disease (ILD) is a common extramuscular manifestation of the idiopathic inflammatory myopathies (IIMs), dermatomyositis (DM) and polymyositis (PM). Patients with antisynthetase antibodies (ASA) demonstrate some or all of the features of the antisynthetase syndrome including IIM and ILD. It has been hypothesized that the clinical expression of antisynthetase syndrome varies between specific ASAs. Objective We sought to determine whether the myositis-associated ILD (MA-ILD) phenotype differs based on the presence of ASAs and by ASA subtype. Methods A cross-sectional and longitudinal analysis of consecutive patients enrolled at the Johns Hopkins Myositis Center with ILD in the setting of clinically diagnosed autoimmune myositis was conducted. Results Seventy-seven subjects were included; 36 were ASA negative, 28 were anti-Jo1 positive, and 13 were non-Jo1 ASA positive (5 anti-PL-12, 4 anti-PL-7, 2 anti-EJ, and 2 anti-OJ). Non-Jo1 ASA positive participants were more likely to be African-American than Caucasian as compared to both the anti-Jo1 positive (p = 0.01) and ASA negative groups (p <0.01). ASA negative participants had better mean forced vital capacity percent predicted (FVC%) and total computed tomography scores over time compared to those with anti-Jo1 after controlling for potential confounders. Conclusions ASA status was significantly different by race. Those with anti-Jo1 antibodies had worse lung function and CT scores over time compared to those without detectable antisynthetase antibodies. Further prospective study in a larger cohort is needed to determine whether these apparent antibody-specific differences in demographics and manifestations of disease translate into meaningful disparities in clinical outcomes.

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