Smoking and spondyloarthritis: a bad connection

Wendling, Daniel; Prati, Clément

doi:10.1007/s00296-015-3368-0

Cited by 4 publications

(3 citation statements)

References 21 publications

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“…And so, there is a complicated association between smoking and spondyloarthropathy [12]. Although some findings are suggesting increased severity of the disease with smoking [13,14], the mechanism is still unclear [15].…”

Section: Discussionmentioning

confidence: 99%

Relationship between smoking, clinical, inflammatory, and radiographic parameters in patients with ankylosing spondylitis

Farouk

Abdel-Rahman

Hassan

2021

Egypt Rheumatol Rehabil

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Background Ankylosing spondylitis (AS) is an autoimmune multisystemic disease that attacks the spine, sacroiliacs, and often causes asymmetrical peripheral oligoarthritis. It results from the interaction between the genetic factors mainly Human Leukocyte Antigen B27 (HLA B27) and environmental factors. Current smoking has been reported to be a major risk factor for the incidence and progression of ankylosing spondylitis. So, we aim to explore the relationship between smoking and each of the clinical, inflammatory markers, functional limitation, and radiographic progression in ankylosing spondylitis patients. Results Fifty ankylosing spondylitis patients were included in this study. Comparisons of clinical data, radiographic, and inflammatory markers among smokers and nonsmokers revealed that AS current smokers showed a statistically significant decrease in chest expansion, increase in the occiput to wall distance (p < 0.001**), higher inflammatory marker, higher disease activity indices (Ankylosing Spondylitis Disease Activity Score, Bath Ankylosing Spondylitis Disease Activity Index), higher Bath Ankylosing Spondylitis functional index, and modified Stoke Ankylosing Spondylitis Spine Score than nonsmokers (P < 0.001**). The smoking index was positively correlated with BASFI, ASDAS, (mSASSS) (r = 0.584, p = 0.005*) and negatively correlated with chest expansion. Conclusions Current smoking in ankylosing spondylitis patients is associated with higher disease activity, inflammatory markers, functional disability, and radiological progression. This may add to the disease burden and thus interferes with the personal daily activities, physical mobility, life quality, and the response to TNFi therapy. So, stopping smoking is a mandatory step in controlling the disease activity and having favorable outcome.

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Section: Discussionmentioning

confidence: 99%

Relationship between smoking, clinical, inflammatory, and radiographic parameters in patients with ankylosing spondylitis

Farouk

Abdel-Rahman

Hassan

2021

Egypt Rheumatol Rehabil

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“…For example, sirtuin (SIRT1) is an enzyme in the cell nucleus that deacetylates transcription factors to control epigenetic gene silencing (22). It modulates IL-23/Th 17 pathway, sclerostin/Wnt pathways, and autophagy, which are implicated in SpA (23). Endothelial cells from human umbilical vein exposed to cigarette smoke extracts showed decreased SIRT1 levels, highlighting the possible role of cigarette smoke-mediated oxidative stress in endothelial dysfunction (24).…”

Section: Pathophysiologymentioning

confidence: 99%

The impact of nicotine smoking on spondyloarthritis and rheumatoid arthritis

El Hasbani,

E Nassar,

Elsayed Ali

et al. 2024

Reumatismo

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Objective. Nicotine has major side effects on human health through numerous mechanisms, one of which is the alteration of the immune system and its genetic components. Such alteration can be a predisposing factor for autoimmune diseases such as spondyloarthritis (SpA) and rheumatoid arthritis (RA). This review aims to shed light on the effects of nicotine smoking on the pathophysiology, clinical presentation, and management of SpA and RA. Methods. This review looked into the studies, excluding case reports and series, which were cited by PubMed/MEDLINE. Results. Patients with established autoimmune conditions may have a different underlying pathophysiology and disease course when exposed to nicotine through cigarette smoking. Through the involvement of several cytokines, endothelial dysfunction, and epigenetic mechanisms, the severity of SpA is more prominent in smokers. The global health status, pain, and fatigue are worse in SpA patients. The evidence on the effect of nicotine smoking on the treatment of SpA is still limited. Nicotine can contribute to RA via the disruption of cellular regulatory activity, inflammatory responses, morphological, physiological, biochemical, and enzymatic responses. As such, smokers with RA have higher disease activity and are more likely to be seropositive through the citrullination of peptides. In addition, these patients are at risk of achieving a suboptimal response to tumor necrosis factor inhibitors. Conclusions. Cigarette smoking can substantially affect the pathophysiology and clinical presentation of patients with SpA and RA. The impact of nicotine on the management of these diseases still needs to be further studied.

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“…Overall, for both radiographic and non-radiographic axial SpA, the same predictors of good response were identified: male sex, young age, short disease duration, high initial Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), presence of HLA-B27, high initial CRP, and sacroiliac inflammation on MRI. Some factors were found to be associated with poor response to anti-TNF therapy in axial SpA: smoking [11], increased BMI, and obesity [12]. Of interest, these two factors had the same impact in ankylosing spondylitis (axial disease) and psoriatic arthritis (peripheral disease).…”

Section: Value Of Observational Studies and Cohortsmentioning

confidence: 99%