Angiogenesis is the formation of new capillaries from pre-existing vasculature, which plays a critical role in the pathogenesis of several inflammatory autoimmune diseases such as rheumatoid arthritis (RA), spondyloarthropathies, psoriasis, systemic lupus erythematosus, systemic sclerosis and atherosclerosis. In RA, excessive migration of circulating leukocytes into the inflamed joint necessitates formation of new blood vessels to provide nutrients and oxygen to the hypertrophic joint. The dominance of the pro-angiogenic factors over the endogenous angiostatic mediators triggers angiogenesis. In this review article, we highlight the underlying mechanisms by which cells present in the RA synovial tissue are modulated to secrete pro-angiogenic factors. We focus on the significance of pro-angiogenic factors such as growth factors, hypoxia inducible factors, cytokines, chemokines, matrix metalloproteinase and adhesion molecules on RA pathogenesis. As pro-angiogenic factors are primarily produced from RA synovial tissue macrophages and fibroblasts, we emphasize the key role of RA synovial tissue lining layer in maintaining synovitis through neovascularization. Lastly, we summarize the specific approaches utilized to target angiogenesis. We conclude that the formation of new blood vessels plays an indispensable role in RA progression. However since the function of several pro-angiogenic mediators is cross regulated, discovering novel approaches to target multiple cascades or selecting an upstream cascade that impairs the activity of a number of pro-angiogenic factors may provide a promising strategy for RA therapy.

BackgroundSarcoidosis is a chronic multisystem disease of unknown etiology characterized by noncaseating granulomas that most often involves the lungs, but frequently has extrapulmonary manifestations, which might be difficult to treat in individual patients.ObjectiveTo review different disease manifestations, focusing on extrapulmonary organ systems, and to provide treatment options for refractory cases.Materials and methodsWe performed a literature search using Medline and Google Scholar for individual or combined keywords of “sarcoidosis, extrapulmonary, treatment, kidney, neurosarcoidosis, cardiovascular, gastrointestinal, transplantation, musculoskeletal, rheumatology, arthritis, and skin”. Peer-reviewed articles, including review articles, clinical trials, observational trials, and case reports that were published in English were included. References from retrieved articles were also manually searched for relevant articles.Results and conclusionIsolated involvement of a single organ or organ system is rare in sarcoidosis, and thus all patients must be thoroughly evaluated for additional disease manifestations. Cardiac sarcoidosis and neurosarcoidosis may be life-threatening. Clinicians need to assess patients comprehensively using clinical, laboratory, imaging, and histopathological data to recommend competently the best and least toxic treatment option for the individual patient.

Introduction. Osteoarthritis, a degenerative joint disease, is a key cause of disability around the world and an ever-growing public health concern. Intra-articular hyaluronic acid viscosupplementation is used as a conservative option for osteoarthritis knee pain relief (McArthur et al., 2012; Hootman and Helmick, 2006; Huang el al., 2011). In general, the literature has shown an excellent safety profile for this treatment modality (McArthur et al., 2012; Clegg et al., 2013; Hammesfahr et al., 2003; Neustadt et al., 2005; Cohen et al., 2008; Neustadt, 2003; Jüni et al., 2007; Peterson and Hodler, 2011). Case Presentation. In this report, we describe a case of a woman who had received multiple sodium hyaluronate injections and developed severe necrotizing fasciitis near the injection site. Conclusion. We recommend that clear guidelines for clean technique be put in place for use with sodium hyaluronate injections and consideration of full sterile technique in immunosuppressed patients.

Tumor necrosis factor α (TNF α) inhibitors are commonly used for treatment of aggressive rheumatoid arthritis and other rheumatic diseases. Etanercept is one of the medications approved for treatment of rheumatoid arthritis. Though many studies have documented the safety and efficacy of these medications, evidence for adverse effects is emerging including cancer, infections, and cardiovascular disease. There have been studies showing that these medications induce autoantibody production, including antinuclear antibodies and anti-dsDNA antibodies. Limited data exists, however, regarding induction of antiphospholipid antibodies (APLs) by TNF α inhibitors, including anticardiolipin antibodies (ACLs), lupus anticoagulant (LAC), and anti-β 2-glycoprotein I (anti-β 2 GPI), or an association between antibody development and clinical manifestations. In this case series, we describe five patients who developed venous thromboembolism (VTE) and APLs while receiving etanercept therapy. All five of our patients met the criteria for diagnosis of APS after receiving etanercept. Our case series supports the association between etanercept, APLs, and VTE. We believe that testing for APLs prior to initiation of anti-TNF therapy is reasonable, given this relationship and the risks associated with VTE.

Intravenous immunoglobulin (IVIG) is a therapeutic preparation of pooled polyspecific IgG used effectively in immune thrombocytopenic purpura (ITP), autoimmune diseases, and inflammatory diseases. We present a case of a 67-year-old male who presented with diffuse petechiae and was diagnosed with immune thrombocytopenic purpura with platelet count less than 10,000 per milliliter. Treatment was initiated with IVIG. When the third dose of IVIG was being administered he developed hypertensive urgency and non-ST segment elevation myocardial infarction. He was deemed not to be a candidate for cardiac catheterization and was treated conservatively. IVIG can cause major thrombotic adverse events such as deep vein thrombosis, myocardial infarction and stroke, which are attributed to thrombosis and hyperviscocity. Decreasing the dosage of IVIG, administration of anticoagulants are proposed treatments for such events. We propose that patients receiving high-dose IVIG with previous coronary artery disease require meticulous cardiac monitoring. Further research is needed to determine the true adverse effects of high-dose IVIG and prophylaxis regimens to decrease the risk.