Nejvíce citovaný článek - PubMed ID 21618078
No effect of physiotherapy on the serum levels of adipocytokines in patients with ankylosing spondylitis
The purpose of this cross-sectional study was to assess the visfatin levels in patients with axial spondyloarthritis (axSpA) and to investigate the association between visfatin, disease activity and radiographic spinal damage. Serum visfatin levels were determined by enzyme-linked immunosorbent assay in 64 patients with axSpA (46 with radiographic axSpA (r-axSpA) and 18 with non-radiographic axSpA (nr-axSpA)) and 61 age-/sex-matched healthy individuals. Patients with r-axSpA were further divided into two subsets based on radiographic spinal damage using modified Stoke Ankylosing Spondylitis Spine Score (mSASSS = 0 and mSASSS ≥ 1). The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) was used to assess disease activity. C-reactive protein (CRP) levels and human leukocyte antigen (HLA)-B27 were determined. Visfatin levels were significantly higher in patients with axSpA and in the subgroup of patients with r-axSpA than in healthy individuals (p = 0.010 and p = 0.005, respectively), with no difference between patients with r-axSpA and with nr-axSpA. In general, disease activity was high (mean BASDAI 5.01) and was moderately correlated with visfatin levels (r = 0.585; p = 0.011) in patients with nr-axSpA. Visfatin levels correlated with mSASSS (r = 0.281; p = 0.026) and were significantly higher in axSpA patients with mSASSS ≥ 1 than in those with mSASSS = 0 (p = 0.025). Our study showed that circulating visfatin levels are elevated in axSpA patients, may be associated with disease activity in early phase of the disease and with the degree of radiographic spinal involvement.
- Klíčová slova
- Axial spondyloarthritis, Disease activity, Radiographic damage, Visfatin,
- MeSH
- bederní obratle diagnostické zobrazování MeSH
- cytokiny krev MeSH
- dospělí MeSH
- krční obratle diagnostické zobrazování MeSH
- lidé středního věku MeSH
- lidé MeSH
- magnetická rezonanční tomografie MeSH
- nikotinamidfosforibosyltransferasa krev MeSH
- páteř diagnostické zobrazování MeSH
- průřezové studie MeSH
- sakroiliakální kloub diagnostické zobrazování MeSH
- spondylartropatie krev diagnostické zobrazování patofyziologie MeSH
- studie případů a kontrol MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- cytokiny MeSH
- nicotinamide phosphoribosyltransferase, human MeSH Prohlížeč
- nikotinamidfosforibosyltransferasa MeSH
Both immune and non-immune mechanisms are involved in muscle damage and dysfunction occurring in idiopathic inflammatory myopathies (IIMs). Crosstalk among inflammatory cells, muscle and endothelial cells is essential in the pathogenesis of IIMs. Resistin, originally described as an adipokine linking obesity and insulin resistance in rodents, has been shown a pro-inflammatory molecule in humans. Besides its direct effect on production of several inflammatory mediators, resistin influences chemotaxis, migration, proliferation, cell survival, endothelial dysfunction and metabolism--all aspects implicated in the pathogenesis of IIMs. Up-regulation of resistin in muscle tissue and elevated serum resistin levels have been recently demonstrated in patients with IIMs. In addition, serum levels of resistin reflected global disease activity, including extramuscular organ involvement, in patients with this disease. However, there are currently not sufficient data to distinguish the features of resistin that cause injury of muscle tissue from those that promote muscle regeneration and repair. The aim of this review is therefore to summarize current knowledge about potential implication of resistin in idiopathic inflammatory myopathies.
- MeSH
- biologické markery metabolismus MeSH
- cévní endotel metabolismus patologie MeSH
- chemotaxe fyziologie MeSH
- cytokiny metabolismus MeSH
- endoteliální buňky metabolismus patologie MeSH
- lidé MeSH
- myozitida krev etiologie patologie MeSH
- pohyb buněk fyziologie MeSH
- proliferace buněk MeSH
- resistin fyziologie MeSH
- upregulace MeSH
- viabilita buněk fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- biologické markery MeSH
- cytokiny MeSH
- resistin MeSH
- RETN protein, human MeSH Prohlížeč