Association of HLA-C3 and smoking with vasculitis in patients with rheumatoid arthritis

Carl Turesson, Daniel J Schaid, Cornelia M. Weyand, Lennart T. Jacobsson, Jörg J. Goronzy, Ingemar F. Petersson, Sonja A. Dechant, Britt Marie Nyähll-Wåhlin, Lennart Truedsson, Gunnar Sturfelt, Eric Lawrence Matteson

Research output: Contribution to journalArticle

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Abstract

Objective. To compare HLA-C genotypes and smoking habits in patients with vasculitis or other severe extraarticular manifestations of rheumatoid arthritis (ExRA) with those in RA patients without extraarticular disease. Methods. Patients were recruited from a large research database of patients with RA at the Mayo Clinic, from 2 Swedish cohorts of prevalent RA cases, and from a regional Swedish early RA cohort. Patients with severe ExRA (n = 159) and control patients with RA but no history of ExRA (non-ExRA controls) (n = 178) were matched for duration of RA and for clinical center. Data on smoking at RA onset, rheumatoid factor (RF) status, and antinuclear antibodies (ANAs) were extracted from the medical records. Polymerase chain reaction-based HLA-C genotyping was performed using a sequence-specific primer kit. Results. The distribution of HLA-C alleles was significantly different between patients with RA-associated vasculitis and non-ExRA controls (P = 0.014). This was mainly due to a positive association of the HLA-C3 allele with vasculitis (allele frequency 0.411 in vasculitis patients versus 0.199 in non-ExRA controls; P < 0.001) and a decreased frequency of HLA-C7 (0.122 and 0.243, respectively; P = 0.018). The association between HLA-C3 and vasculitis was not due to linkage disequilibrium with HLA-DRB1. Smoking (P = 0.001), RF posithity (P < 0.0001), and presence of ANAs (P < 0.0001) were all associated with ExRA. HLA-C3 and smoking were both significant predictors of vasculitis in a multivariate model. Conclusion. Vasculitis in RA is associated with HLA-C3. Smoking is an independent predictor of vasculitis and other types of severe ExRA. Our results suggest that these variables are among the genetic and environmental factors that contribute significantly to the pathomechanisms of systemic RA.

Original languageEnglish (US)
Pages (from-to)2776-2783
Number of pages8
JournalArthritis and Rheumatism
Volume54
Issue number9
DOIs
StatePublished - Sep 2006

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Vasculitis
Rheumatoid Arthritis
Smoking
HLA-C Antigens
Rheumatoid Factor
Antinuclear Antibodies
Alleles
HLA-DRB1 Chains
Linkage Disequilibrium
Gene Frequency
Habits
Medical Records
Genotype
Databases
Polymerase Chain Reaction
Research

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

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Association of HLA-C3 and smoking with vasculitis in patients with rheumatoid arthritis. / Turesson, Carl; Schaid, Daniel J; Weyand, Cornelia M.; Jacobsson, Lennart T.; Goronzy, Jörg J.; Petersson, Ingemar F.; Dechant, Sonja A.; Nyähll-Wåhlin, Britt Marie; Truedsson, Lennart; Sturfelt, Gunnar; Matteson, Eric Lawrence.

In: Arthritis and Rheumatism, Vol. 54, No. 9, 09.2006, p. 2776-2783.

Research output: Contribution to journalArticle

Turesson, C, Schaid, DJ, Weyand, CM, Jacobsson, LT, Goronzy, JJ, Petersson, IF, Dechant, SA, Nyähll-Wåhlin, BM, Truedsson, L, Sturfelt, G & Matteson, EL 2006, 'Association of HLA-C3 and smoking with vasculitis in patients with rheumatoid arthritis', Arthritis and Rheumatism, vol. 54, no. 9, pp. 2776-2783. https://doi.org/10.1002/art.22057
Turesson, Carl ; Schaid, Daniel J ; Weyand, Cornelia M. ; Jacobsson, Lennart T. ; Goronzy, Jörg J. ; Petersson, Ingemar F. ; Dechant, Sonja A. ; Nyähll-Wåhlin, Britt Marie ; Truedsson, Lennart ; Sturfelt, Gunnar ; Matteson, Eric Lawrence. / Association of HLA-C3 and smoking with vasculitis in patients with rheumatoid arthritis. In: Arthritis and Rheumatism. 2006 ; Vol. 54, No. 9. pp. 2776-2783.
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abstract = "Objective. To compare HLA-C genotypes and smoking habits in patients with vasculitis or other severe extraarticular manifestations of rheumatoid arthritis (ExRA) with those in RA patients without extraarticular disease. Methods. Patients were recruited from a large research database of patients with RA at the Mayo Clinic, from 2 Swedish cohorts of prevalent RA cases, and from a regional Swedish early RA cohort. Patients with severe ExRA (n = 159) and control patients with RA but no history of ExRA (non-ExRA controls) (n = 178) were matched for duration of RA and for clinical center. Data on smoking at RA onset, rheumatoid factor (RF) status, and antinuclear antibodies (ANAs) were extracted from the medical records. Polymerase chain reaction-based HLA-C genotyping was performed using a sequence-specific primer kit. Results. The distribution of HLA-C alleles was significantly different between patients with RA-associated vasculitis and non-ExRA controls (P = 0.014). This was mainly due to a positive association of the HLA-C3 allele with vasculitis (allele frequency 0.411 in vasculitis patients versus 0.199 in non-ExRA controls; P < 0.001) and a decreased frequency of HLA-C7 (0.122 and 0.243, respectively; P = 0.018). The association between HLA-C3 and vasculitis was not due to linkage disequilibrium with HLA-DRB1. Smoking (P = 0.001), RF posithity (P < 0.0001), and presence of ANAs (P < 0.0001) were all associated with ExRA. HLA-C3 and smoking were both significant predictors of vasculitis in a multivariate model. Conclusion. Vasculitis in RA is associated with HLA-C3. Smoking is an independent predictor of vasculitis and other types of severe ExRA. Our results suggest that these variables are among the genetic and environmental factors that contribute significantly to the pathomechanisms of systemic RA.",
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T1 - Association of HLA-C3 and smoking with vasculitis in patients with rheumatoid arthritis

AU - Turesson, Carl

AU - Schaid, Daniel J

AU - Weyand, Cornelia M.

AU - Jacobsson, Lennart T.

AU - Goronzy, Jörg J.

AU - Petersson, Ingemar F.

AU - Dechant, Sonja A.

AU - Nyähll-Wåhlin, Britt Marie

AU - Truedsson, Lennart

AU - Sturfelt, Gunnar

AU - Matteson, Eric Lawrence

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N2 - Objective. To compare HLA-C genotypes and smoking habits in patients with vasculitis or other severe extraarticular manifestations of rheumatoid arthritis (ExRA) with those in RA patients without extraarticular disease. Methods. Patients were recruited from a large research database of patients with RA at the Mayo Clinic, from 2 Swedish cohorts of prevalent RA cases, and from a regional Swedish early RA cohort. Patients with severe ExRA (n = 159) and control patients with RA but no history of ExRA (non-ExRA controls) (n = 178) were matched for duration of RA and for clinical center. Data on smoking at RA onset, rheumatoid factor (RF) status, and antinuclear antibodies (ANAs) were extracted from the medical records. Polymerase chain reaction-based HLA-C genotyping was performed using a sequence-specific primer kit. Results. The distribution of HLA-C alleles was significantly different between patients with RA-associated vasculitis and non-ExRA controls (P = 0.014). This was mainly due to a positive association of the HLA-C3 allele with vasculitis (allele frequency 0.411 in vasculitis patients versus 0.199 in non-ExRA controls; P < 0.001) and a decreased frequency of HLA-C7 (0.122 and 0.243, respectively; P = 0.018). The association between HLA-C3 and vasculitis was not due to linkage disequilibrium with HLA-DRB1. Smoking (P = 0.001), RF posithity (P < 0.0001), and presence of ANAs (P < 0.0001) were all associated with ExRA. HLA-C3 and smoking were both significant predictors of vasculitis in a multivariate model. Conclusion. Vasculitis in RA is associated with HLA-C3. Smoking is an independent predictor of vasculitis and other types of severe ExRA. Our results suggest that these variables are among the genetic and environmental factors that contribute significantly to the pathomechanisms of systemic RA.

AB - Objective. To compare HLA-C genotypes and smoking habits in patients with vasculitis or other severe extraarticular manifestations of rheumatoid arthritis (ExRA) with those in RA patients without extraarticular disease. Methods. Patients were recruited from a large research database of patients with RA at the Mayo Clinic, from 2 Swedish cohorts of prevalent RA cases, and from a regional Swedish early RA cohort. Patients with severe ExRA (n = 159) and control patients with RA but no history of ExRA (non-ExRA controls) (n = 178) were matched for duration of RA and for clinical center. Data on smoking at RA onset, rheumatoid factor (RF) status, and antinuclear antibodies (ANAs) were extracted from the medical records. Polymerase chain reaction-based HLA-C genotyping was performed using a sequence-specific primer kit. Results. The distribution of HLA-C alleles was significantly different between patients with RA-associated vasculitis and non-ExRA controls (P = 0.014). This was mainly due to a positive association of the HLA-C3 allele with vasculitis (allele frequency 0.411 in vasculitis patients versus 0.199 in non-ExRA controls; P < 0.001) and a decreased frequency of HLA-C7 (0.122 and 0.243, respectively; P = 0.018). The association between HLA-C3 and vasculitis was not due to linkage disequilibrium with HLA-DRB1. Smoking (P = 0.001), RF posithity (P < 0.0001), and presence of ANAs (P < 0.0001) were all associated with ExRA. HLA-C3 and smoking were both significant predictors of vasculitis in a multivariate model. Conclusion. Vasculitis in RA is associated with HLA-C3. Smoking is an independent predictor of vasculitis and other types of severe ExRA. Our results suggest that these variables are among the genetic and environmental factors that contribute significantly to the pathomechanisms of systemic RA.

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