Disease relevance of Spondylarthropathies

• Ankylosing spondylitis and seronegative spondylarthropathies such as Reiter's syndrome and reactive arthritis are strongly associated with HLA-B27 [1].
• Psoriatic arthritis, undifferentiated arthritis, and spondylarthropathy patients also displayed anti-GPI antibodies at similar frequencies (12-25%) [2].
• These 2 cases, together with the recently reported case of PG and B27-positive psoriatic spondylarthropathy, suggest that PG may also occur in association with forms of seronegative SpA that are different from primary ankylosing spondylitis (AS) and AS associated with inflammatory bowel disease [3].
• Microbial spondylitis, degenerative disc disease, and destructive spondylarthropathy of calcium pyrophosphate dihydrate deposition disease were each, in turn, ruled out [4].
• Immunomodulatory effects of etanercept on peripheral joint synovitis in the spondylarthropathies [5].

High impact information on Spondylarthropathies

• BACKGROUND & AIMS: It has been suggested that subclinical intestinal inflammation plays a pathogenic role in the spondylarthropathy of ankylosing spondylitis (AS) [6].
• B27-restricted CTLs with specificity for arthritogenic bacteria or autoantigens provide a missing link in the pathogenesis of the HLA-B27-associated spondylarthropathies [1].
• Tumor necrosis factor alpha blockade treatment down-modulates the increased systemic and local expression of Toll-like receptor 2 and Toll-like receptor 4 in spondylarthropathy [7].
• METHODS: Thirty-four patients with spondylarthropathy (SpA) and 59 patients with rheumatoid arthritis (RA) were treated with infliximab for 2 years [8].
• OBJECTIVE: Because different tumor necrosis factor alpha (TNFalpha) blockers may have distinct immunomodulatory effects on specific disease manifestations, the present study was carried out to investigate the immunomodulating effects of etanercept on peripheral synovitis in the spondylarthropathies (SpA) [5].

Chemical compound and disease context of Spondylarthropathies

• Sulfasalazine in the treatment of spondylarthropathy. A randomized, multicenter, double-blind, placebo-controlled study [9].
• The efficacy of thalidomide in severe refractory seronegative spondylarthropathy: comment on the letter by Breban et al [10].
• The median values of the complex and of both enzyme activities were higher in patients with rheumatoid arthritis than in patients with spondylarthropathy; however, the difference was statistically significant only for the cysteine proteinase activity measured with Z-Arg-Arg-AMC substrate [11].
• CONCLUSION: The results of our study indicate that the periarticular injection of methylprednisolone may be effective in the treatment of clinical sacroiliitis in patients with seronegative spondylarthropathy [12].
• Progress in the treatment of juvenile rheumatoid arthritis (JRA) and the spondylarthropathies has lagged behind, however, although methotrexate does appear to be promising in the short-term treatment of JRA [13].

Biological context of Spondylarthropathies

• At a mean disease duration of 33 weeks, 98 patients (46%) met the American College of Rheumatology (ACR) criteria for rheumatoid arthritis (RA), 38 (18%) met the European Spondylarthropathy Study Group criteria for spondylarthropathy (SpA), and 75 (36%) were classified as having undifferentiated arthropathy (UA) [14].
• Autosomal dominant spondylarthropathy due to a type II procollagen gene (COL2A1) point mutation [15].
• RESULTS: Patients with RA expressed an increased humoral immunity to biglycan, while patients with seronegative spondylarthropathies displayed elevated decorin-specific synovial antibody levels compared with OA patients [16].
• Reactive arthritis and enteropathic arthritis are observed in the elderly more rarely.The effects of aging on drug metabolism and pharmacokinetics, together with the existence of co-morbidities and polypharmacy, are responsible for difficulties in the therapeutic management of late-onset ankylosing spondylitis or spondylarthropathies [17].
• As the marker D2S160 has been characterized as a candidate locus for Ankylosing Spondylitis (AS) after a genome-wide scan, and since this locus is located approximately 0.3 cM telomeric to the IL-1 gene cluster, we hypothesized that these cytokines might be good candidates for Spondylarthropathies (SpA) [18].

Anatomical context of Spondylarthropathies

• OBJECTIVE: Tumor necrosis factor alpha (TNFalpha) has been detected in sacroiliac joint biopsy specimens from patients with spondylarthropathy [19].
• METHODS: PBL from 55 HLA-B27+ patients with ankylosing spondylitis (AS), 28 HLA-B27+ patients with other spondylarthropathies, 7 rheumatoid arthritis patients, and 30 HLA-B27+ and 22 HLA-B27- healthy controls were tested in lymphocyte proliferation assays with 4 synthetic peptides derived from the HLA-B*2705 molecule [20].
• We examined the response of normal T cells to dendritic cells isolated from the synovial fluid (SF) of patients with either rheumatoid arthritis (RA) or seronegative spondylarthropathies (rheumatoid variants) and to dendritic cells from normal and RA peripheral blood (PB) in the allogeneic mixed leukocyte reaction [21].
• The presence of paf, its precursor lyso paf, and lipo-paf has been determined in blood and synovial fluid from 13 patients with rheumatoid arthritis (RA), 11 with spondylarthropathies, eight with other inflammatory rheumatisms, 13 with chondrocalcinosis, 15 with osteoarthritis, and also in blood from nine healthy subjects [22].
• Beta 2 microglobulin-related amyloidosis causing atlantoaxial spondylarthropathy with spinal-cord compression in haemodialysis patients: detection by MRI [23].

Gene context of Spondylarthropathies

• RESULTS: Of 175 patients evaluated at baseline, 85 had rheumatoid arthritis (RA), 39 had seronegative spondylarthropathy, 38 had undifferentiated arthritis, and 13 had self-limiting arthritis [24].
• Some patients with spondylarthropathy also manifested increased serum levels of IL-10 [25].
• High serum vascular endothelial growth factor correlates with disease activity of spondylarthropathies [26].
• Serum levels of interleukin 1-beta, tumor necrosis factor-alpha, soluble interleukin 2 receptor and soluble CD8 in seronegative spondylarthropathies [27].
• Experimental immunity to the G1 domain of the proteoglycan versican induces spondylitis and sacroiliitis, of a kind seen in human spondylarthropathies [28].

Analytical, diagnostic and therapeutic context of Spondylarthropathies

• We conclude that progressive ankylosis is a systemic disease with many clinical and radiographic similarities to human spondylarthropathies, and it may represent a useful animal model for the study of the human diseases [29].
• Antigliadin antibodies (AGA) and antireticulin antibodies (ARA) were determined in two groups of RA patients and in a control group of patients with spondylarthropathies [30].
• A causal relationship between beta-2 microglobulin and hemodialysis spondylarthropathy has yet to be definitely established [31].
• HLA B27 and respiratory involvement in axial spondylarthropathies. A retrospective study in 107 male patients [32].
• A meta-analysis comparing treatment termination because of toxicity among RA, inflammatory bowel disease and seronegative spondylarthropathy patients was conducted [33].

References