Etiological factors and underlying conditions in patients with leucocytoclastic vasculitis.

This study concerns a retrospective analysis of 63 consecutive patients presenting with leukocytoclastic vasculitis at the Departments of Dermatology or Rheumatology of the University Hospital Ghent (Belgium) (period 1988-1993). The diagnosis of leukocytoclastic vasculitis was confirmed by histopathology in all cases. All patients were screened for underlying causes, including drugs, infection, systemic autoimmune disease or neoplasia. In 34 patients, an etiological factor was identified: drugs (5 patients), infection (6 patients), drugs or infection (4 patients), systemic autoimmune disease (10 patients), Henoch Shönlein (6 patients), neoplasia (2 patients) and cryoglobulinemia (1 patient). In the group of patients with leukocytoclastic vasculitis in the context of systemic autoimmune disease, 4 patients suffered from systemic lupus erythematosus, 2 from Wegener's disease, 2 from Behçet's disease, 1 from polyarteritis nodosa and 1 from rheumatoid arthritis. In the remaining 29 patients, no cause for the vasculitis could be identified.

Influence of interferon-gamma on isolated chondrocytes from human articular cartilage. Dose dependent inhibition of cell proliferation and proteoglycan synthesis.

The effect of human recombinant interferon-gamma (IFN-gamma) on cultured human cartilage cells was studied by 2 variables: cell proliferation and proteoglycan synthesis. Cell proliferation was determined from 3H-thymidine incorporation rates in monolayer cultured chondrocytes. Proteoglycan synthesis was determined from 35S incorporation rates in monolayers and in chondrocytes cultured in agarose gel. IFN-gamma concentrations used in these experiments ranged from 10(-6) micrograms/ml (0.025 U/ml) to 10(-2) micrograms/ml (250 U/ml). The lowest concentrations are comparable with the synovial fluid levels in inflamed joints of patients with rheumatoid arthritis. At these concentrations, IFN-gamma was found to induce a dose dependent decrease of cell proliferation and of proteoglycan synthesis in monolayer cultured human chondrocytes. The decrease of proteoglycan synthesis was ascribed both to an inhibition of the proteoglycan protein core production and to a downregulation of the glycosaminoglycan chain elongation.

Gut inflammation in psoriatic arthritis: a prospective ileocolonoscopic study.

OBJECTIVE: Some forms of psoriatic arthritis (PsA) are classified as spondylarthropathy, and subclinical gut inflammation is found in spondylarthropathies. Our study was designed to determine if inflammatory gut lesions were also present in PsA, and if the prevalence of subclinical gut involvement was different in the subgroups of this disease. The relationship with HLA subtypes was also determined. METHODS: Ileocolonoscopy was performed on 64 patients with PsA (37 men, 27 women). RESULTS: Inflammatory gut lesions were found in 10 of the 64 patients (16%): in 3 of the 15 patients (20%) with oligoarthritis and in 7 of the 23 patients (30%) with axial involvement. None of the 26 patients with polyarthritis showed these lesions. The prevalence of HLA-B27, Bw62, and B17 was significantly raised in our total group of patients with PsA. HLA-B27 and Bw62 were significantly more prevalent in patients with gut inflammation, 60 and 50%, respectively. CONCLUSION: Gut inflammation is only present in PsA subgroups that belong to the spondylarthropathy concept. This suggests that the gut plays a role in the pathogenesis of locomotor inflammation in these subgroups. The prevalence of gut inflammation in psoriatic spondylarthropathy is significantly lower than in nonpsoriatic spondylarthropathies. Consequently, not only the gut but also the skin may be a portal of entry for causative antigens in PsA.

The evolution of spondyloarthropathies in relation to gut histology. III. Relation between gut and joint.

OBJECTIVE: To study prospectively the clinical evolution of different forms of spondyloarthropathy (SpA) in relation to the evolution of gut histology in consecutive ileocolonoscopic biopsy specimens. METHODS: Ileocolonoscopy was performed in 49 patients with SpA (34 men, 15 women). They also underwent clinical, laboratory, and radiological examinations. Two to 9 years later, a 2nd and sometimes a 3rd or 4th ileocolonoscopy was performed, and the other examinations were repeated. RESULTS: At first ileocolonoscopy, 34 patients (69%) showed inflammatory gut lesions. At the 2nd ileocolonoscopy, 16 patients (32%) were in clinical remission; none were found to have inflammatory gut lesions. Of the 33 patients with persistent locomotor inflammation, 14 had persistent inflammatory gut lesions, predominantly the chronic type. Of these 14 patients, 6 had developed inflammatory bowel disease (IBD). None of the 15 patients with an initially normal gut histology had gut inflammation at 2nd examination. Of the 9 with initially acute lesions, 3 developed chronic lesions (1 Crohn's disease). Initial chronic lesions in 25 patients persisted in 9, of whom 5 had developed IBD. Seven of the 19 patients with non-SpA ankylosing spondylitis (non-AS-SpA) developed ankylosing spondylitis (AS); all had initially presented inflammatory gut lesions, which persisted at 2nd examination. In the 11 patients with more than 2 consecutive ileocolonoscopies, clinical remission was always associated with normal gut histology, and flares of the joint disease were related temporally to the reappearance of gut inflammation. CONCLUSION: This study demonstrates the close relationship between gut and locomotor inflammation in SpA. Clinical remission was always associated with normal gut histology, whereas active locomotor inflammation was usually associated with the presence of gut inflammation. Absence of gut inflammation in the SpA is a good prognostic indicator, since gut inflammation or IBD never develops in these patients. Evolution of non-AS-SpA to full blown AS or of uncomplicated SpA to a form of IBD was always associated with gut inflammation at disease onset.