Soluble intercellular adhesion molecule 1 in spondylarthropathies

Wendling, Daniel; Racadot, E; Augé, B.; Toussirot, Éric

doi:10.1007/bf01451047

Cited by 21 publications

(12 citation statements)

References 11 publications

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“…As with RA and SLE, the available data are discordant. Wendling et al [68] demonstrated that mildly elevated ICAM-1 levels correlated with markers of disease activity ( i.e ., erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), disease severity score) in patients with spondyloarthropathies. Moreover, markedly elevated ICAM-1 levels (>400) were found only in patients with disease.…”

Section: Clinical Findings Of Major Chronic Inflammatory Diseases mentioning

confidence: 99%

Endothelial Dysfunction in Chronic Inflammatory Diseases

Steyers

Miller

2014

IJMS

381

299

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Chronic inflammatory diseases are associated with accelerated atherosclerosis and increased risk of cardiovascular diseases (CVD). As the pathogenesis of atherosclerosis is increasingly recognized as an inflammatory process, similarities between atherosclerosis and systemic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel diseases, lupus, psoriasis, spondyloarthritis and others have become a topic of interest. Endothelial dysfunction represents a key step in the initiation and maintenance of atherosclerosis and may serve as a marker for future risk of cardiovascular events. Patients with chronic inflammatory diseases manifest endothelial dysfunction, often early in the course of the disease. Therefore, mechanisms linking systemic inflammatory diseases and atherosclerosis may be best understood at the level of the endothelium. Multiple factors, including circulating inflammatory cytokines, TNF-α (tumor necrosis factor-α), reactive oxygen species, oxidized LDL (low density lipoprotein), autoantibodies and traditional risk factors directly and indirectly activate endothelial cells, leading to impaired vascular relaxation, increased leukocyte adhesion, increased endothelial permeability and generation of a pro-thrombotic state. Pharmacologic agents directed against TNF-α-mediated inflammation may decrease the risk of endothelial dysfunction and cardiovascular disease in these patients. Understanding the precise mechanisms driving endothelial dysfunction in patients with systemic inflammatory diseases may help elucidate the pathogenesis of atherosclerosis in the general population.

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Section: Clinical Findings Of Major Chronic Inflammatory Diseases mentioning

confidence: 99%

Endothelial Dysfunction in Chronic Inflammatory Diseases

Steyers

Miller

2014

IJMS

381

299

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“…In addition, the expression of a variety of proinflammatory cytokines, as well as markers of bone metabolism, are increased in the sacroiliac joints and entheses of patients with AS. Elevated serum levels of inflammatory markers (including tumour necrosis factor (TNF)α, interleukin (IL-) 6,1 vascular endothelial growth factor (VEGF),2 Intercellular adhesion molecule-1 (ICAM-1))3 and markers of bone metabolism (bone alkaline phosphatase (BAP) and osteocalcin) have previously been shown to be associated with active AS 4…”

mentioning

confidence: 99%

“…In addition, serum matrix metalloproteinase -3 (MMP-3) levels have been shown to correlate with disease activity as assessed by the Bath ankylosing spondylitis disease activity index (BASDAI) score5 and to be an independent predictor of structural damage6 in patients with AS. Patients with spondyloarthropathies also have elevated levels of ICAM-1, which has been shown to correlate with IL-6 and CRP levels 3. IL-6 has been shown to be elevated in the serum of AS patients and to decrease following treatment with infliximab 7.…”

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confidence: 99%

Serum markers associated with clinical improvement in patients with ankylosing spondylitis treated with golimumab

Wagner¹,

Visvanathan

Braun

et al. 2011

Ann Rheum Dis

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ObjectiveIdentify serum biomarkers modulated by golimumab treatment and associated with clinical response in patients with ankylosing spondylitis (AS).MethodsSera were collected at weeks 0, 4 and 14 from 100 patients with active AS in the GO–RAISE study. Patients were randomly assigned subcutaneous injections of placebo, golimumab 50 mg, or golimumab 100 mg every 4 weeks. Samples were tested for select inflammatory, bone and cartilage markers, and protein profiling was also performed.ResultsGolimumab treatment resulted in significant decreases in several serum proteins at weeks 4 and 14 compared with placebo. Patients who achieved clinical response at week 14, as assessed by a ≥20% improvement in the Assessment in SpondyloArthitis international Society response criteria (ASAS 20), demonstrated a distinct biomarker profile with lower levels of acute phase reactants and inflammatory biomarkers compared with patients who did not. Notably, combinations of two or three biomarkers assessed at baseline were predictive of various clinical outcomes (ASAS 20, Bath ankylosing spondylitis disease activity index 50 or Bath ankylosing spondylitis functional index) using a logistic regression analysis, and the overall predictive values for these combined biomarkers were greater than observed for C-reactive protein (CRP) alone.ConclusionGolimumab modulated acute phase reactants and inflammatory markers in patients with active AS. Specific combinations of biomarkers at baseline demonstrated a stronger prediction for clinical efficacy than CRP alone. These data provide insights into the mechanism of golimumab on inflammatory processes driving AS pathology, and may have utility in managing the treatment of patients with AS.

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“…Finally, several other options may arise via extrapolation of the therapeutic advances achieved in CIBD. For instance, integrin antagonists are being evaluated as potential treatments for CIBD [22,23] and adhesion molecules may be involved in SpA [24,25]. It might be worth assessing the impact of these new agents on the rheumatic manifestations.…”

Section: Perspectives For Management and Treatmentmentioning

confidence: 99%