Objective. Understanding of the molecular pathophysiology of spondylarthritis (SpA) remains largely elusive. This is related both to the complexity of the disease (axial versus peripheral disease, inflammation versus tissue remodeling) and to the difficulty in obtaining samples from primary disease sites. This study was undertaken to explore a gene expression approach for identifying novel candidate mediators of SpA.Methods. Sacroiliac joint fluid aspirates from 3 SpA patients with active sacroiliitis were studied by microarray analysis. The expression of selected candidate molecules in peripheral synovitis was confirmed by reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay.Results. Microarray analysis identified 4 sacroiliitis gene clusters, containing a total of 47 messenger RNA (mRNA) transcripts. Two clusters contained genes expressed in all sacroiliitis samples, corresponding to both known and unsuspected candidate mediators of SpA pathology. These included proinflammatory molecules as well as molecules involved in tissue remodeling, such as transforming growth factor 2. Of the novel candidate genes selected for confirmation, interleukin-7 (IL-7) mRNA expression was higher in SpA peripheral synovial fluid and synovial tissue samples than in osteoarthritis samples, and similar to expression in rheumatoid arthritis (RA) samples. At the protein level, synovial fluid IL-7 levels were even higher in SpA than in RA, despite lower levels of tumor necrosis factor ␣ and IL-1.Conclusion. In the present study, both known and unsuspected candidate mediators of SpA pathogenesis were identified, including IL-7. The specific overexpression of IL-7 at sites of peripheral synovitis in SpA suggests that further functional investigations of the role of this cytokine in SpA pathogenesis are warranted.
We report the case of a young white woman in whom cerebrovascular moyamoya disease, which was associated with nonarteriosclerotic peripheral artery disease of the subclavian, iliac, and femoropopliteal arteries, was diagnosed by means of angiography. During 8 years of follow-up, the peripheral artery disease progressed, without any signs characteristic of systemic inflammation or vasculitis, leading to severe calf and arm claudication. Despite the absence of histologic confirmation, this observation strongly suggests that peripheral artery involvement may be a feature of moyamoya disease. To our knowledge, this is the first report of an association of classical cerebrovascular moyamoya disease with peripheral artery disease.
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