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Aetiopathogenesis

 

Smoking and systemic sclerosis: influence on microangiopathy and expression of anti-topoisomerase I antibodies in a monocentric cohort

1, 2, 3, 4

 

  1. Department of Rheumatology, Leiden University Medical Centre, Leiden, The Netherlands; Rheumatology Unit, Azienda Policlinico of Modena, University of Modena and Reggio Emilia, Modena; and Medicine and Rheumatology Unit, IRCCS Istituto Ortopedico Rizzoli, Bologna, Italy. jacopo.ciaffi91@gmail.com; j.ciaffi@lumc.nl
  2. Department of Rheumatology, Leiden University Medical Centre, Leiden, The Netherlands.
  3. Department of Rheumatology, Leiden University Medical Centre, Leiden, The Netherlands.
  4. Department of Rheumatology, Leiden University Medical Centre, Leiden, The Netherlands.

CER12854
2020 Vol.38, N°3 ,Suppl.125
PI 0025, PF 0028
Aetiopathogenesis

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PMID: 32242801 [PubMed]

Received: 10/10/2019
Accepted : 11/03/2020
In Press: 25/03/2020
Published: 25/08/2020

Abstract

OBJECTIVES:
To investigate whether systemic sclerosis (SSc) patients exposed to active tobacco smoke exhibit a different autoantibody profile or are at higher risk for severe microangiopathy compared to never-smokers, and to assess differences between men and women.
METHODS:
We performed an exploratory observational study in a cohort of SSc patients fulfilling the 2013 ACR/EULAR classification criteria. According to the smoking habit, patients were categorised as ever-smokers or never-smokers. Microvascular damage was assessed at baseline using nailfold videocapillaroscopy. The presence of SSc-specific autoantibodies was investigated.
RESULTS:
The studied population was composed of 361 patients (279 women, 82 men). Of these, 208 (58%) were ever-smokers and 153 (42%) were never-smokers. Anti-centromere, anti-topoisomerase I (ATA) and anti-RNA polymerase III antibodies were found, respectively, in 90 (43%), 41 (20%), and 11 (5%) ever-smokers, and in 66 (43%), 40 (26%) and 5 (3%) never-smokers (all p>0.05). Scleroderma patterns early, active and late were present respectively in 12%, 44% and 21% of ever-smokers, and in 9%, 48%, and 29% of never-smokers (all p>0.05). In multivariable logistic regression, being a never-smoker was significantly associated with ATA positivity (OR 1.77, 95% CI 1.04-2.99, p= 0.034). In the gender-based sub-cohorts, 36 (27%) female patients who never smoked were ATA positive, compared to 16 (11%) ever-smoking women (p<0.001).
CONCLUSIONS:
We observed a significant association between smoking history and positivity of ATA and we outlined the idea of a different effect of smoking on autoantibody expression between men and women.

Rheumatology Article