105,380 research outputs found
Autoimmunity vs autoinflammation in Behcet's disease: do we oversimplify a complex disorder?
No full textBehcet's disease (BD) is a systemic inflammatory disorder with a diverse spectrum of clinical manifestations including mucocutaneous, ocular, vascular, gastrointestinal, musculoskeletal and central nervous system involvement [1]. A complex genetic background leading to a pro-inflammatory, innate-immune-system-derived activation perpetuated by adaptive immune responses against enviromental and auto-antigens is accepted to be the hallmark of BD [2]. This review aims to make an in-depth critical analysis of current data for recent controversies on the role of innate immune system vs autoimmunity in BD [3-5]
Excess cardiovascular risk in inflammatory rheumatic diseases: Pathophysiology and targeted therapy
No full textThe article reviews the evidence and extent of the excess cardiovascular risk in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and ankylosing spondylitis. RA entails nearly twice as high a standardized mortality ratio and is considered an equivalent of type 2 diabetes with regard to cardiovascular risk. The associated excess cardiovascular risk can only partly be explained by traditional risk factors, and the underlying inflammation is crucially involved in the pathogenesis. Data obtained from patients with early RA suggest that serum triglycerides, a proxy of disease activity as markers of systemic inflammation, impaired function of apolipoprotein A-I and HDL particles, and mediating hypertension are determinants of the excess cardiovascular risk. These changes seem to be preceded by a lowering of total cholesterol and are followed in the course of the disease by immune processes typically illustrated by positivity of rheumatoid factor. Evidence is available to postulate the notion that reduced plasma lipoprotein-associated phospholipaseA2 mass or activity, mediated by diminished hydrolysis of VLDL triglycerides and of Lp(a) phospholipids, may induce reduction or altered composition of HDL particles and apoA-I dysfunction which, along with elevated plasma triglycerides, initiate and contribute to chronic inflammation. Lifestyle modification, traditional non-steroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors, low-dose corticosteroids, statins, tumor-necrosis-α inhibitors and, particularly, the immunosuppressive methotrexate, all have potential beneficial effects in eliciting a reduction in disease activity and cardiovascular risk. Adherence to the recent EULAR recommendations is a key in the prevention and management of cardiovascular risk among patients with rheumatic diseases. © 2012 Bentham Science Publishers
Serious infections under treatment with TNF-alpha antagonists compared to traditional DMARDs in patients with rheumatoid arthritis
No full textBiological treatments aiming to neutralize TNF-alpha (tumour necrosis factor alpha) (infliximab, adalimumab and etanercept) are increasingly used to treat rheumatoid arthritis (RA). Although increased frequency has not been observed in randomized clinical trials with TNF-alpha antagonist agents, postmarketing surveillance suggests that infections might be serious consequences of these therapies. Our aim was to compare infections in patients with RA under treatment with disease-modifying antirheumatic drugs (DMARDs) and TNF-alpha antagonists in a university outpatient rheumatology clinic in Turkey. A total of 130 RA patients treated with DMARDs and 48 treated with TNF-alpha antagonists were analysed for the incidence of infections. Patients taking TNF-alpha antagonists were also reviewed for infections before these therapies. The incidence of serious infections was 7/100 patient-years before TNF-alpha antagonists and 8.6/100 patient-years in DMARDs group. The incidence rose to 17/100 patient-years during therapy with TNF-alpha antagonists. In patients with RA on routine follow-up, treatment with TNF-alpha antagonists seems to carry an increased risk of infections compared to traditional DMARDs
Effects of interferon-alpha treatment on serum IL-6, IL-8, TNF-alpha and soluble TNF-alpha receptors in Behcet's disease
No full text
Pathogenesis of Behçet's Syndrome: Genetic, Environmental and Immunological Factors
No full textBehçet's syndrome (BS) is a rare systemic vasculitis, characterized by a wide range of different clinical involvements and unpredictable phases of recurrence and remission. BS can be described as a multifactorial disease with an incompletely known etiopathogenesis; in fact, though presenting some peculiar features, such as its typical geographic distribution and the strong association with the well-known genetic predisposing factor HLA-B*51, the cause behind the onset and progression of the disease remains currently not fully understood. Besides genetic HLA and non-HLA predisposing associations and epigenetic influence, environmental factors also play an important role in the pathogenesis of the disease, and among these, infectious agents (both bacterial and viral) and specific microbiome alterations are considered of particular relevance in BS pathogenesis. BS has been included for decades among autoimmune diseases, in light of evidence showing T- and B-cell aberrant responses. However, because of recurrent mucocutaneous lesions and episodes of inflammation without antigen-specific T-cell or autoantibody responses, BS has also been classified among autoinflammatory disorders. Nevertheless, differently from autoinflammatory diseases, BS mildly responds to therapies targeting IL-1, its onset is not usually in childhood, and has high neutrophilic vasculitic involvement. Finally, given the association with HLA class I alleles, similar to spondyloarthropathies, the concept of BS as a major histocompatibility complex (MHC) I -opathy has been introduced. Understanding the complex etiopathogenesis of BS is essential to identify modifiable risk factors of BS occurrence or exacerbation and to develop targeted therapies. This review summarizes current evidence on the main genetic, environmental and immunological factors contributing to BS development
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