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Systemic Inflammatory Diseases (systemic + inflammatory_disease)
Selected AbstractsCellular microparticles: new players in the field of vascular disease?EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2004M. Diamant Abstract Microparticles are small membrane vesicles that are released from cells upon activation or during apoptosis. Cellular microparticles in body fluids constitute a heterogeneous population, differing in cellular origin, numbers, size, antigenic composition and functional properties. Microparticles support coagulation by exposure of negatively charged phospholipids and sometimes tissue factor, the initiator of coagulation in vivo. Microparticles may transfer bioactive molecules to other cells or microparticles, thereby stimulating cells to produce cytokines, cell-adhesion molecules, growth factors and tissue factor, and modulate endothelial functions. Microparticles derived from various cells, most notably platelets but also leucocytes, lymphocytes, erythrocytes and endothelial cells, are present in the circulation of healthy subjects. Rare hereditary syndromes with disturbances in membrane vesiculation leading to a decreased numbers of microparticles clinically present with a bleeding tendency. In contrast, elevated numbers of microparticles are encountered in patients with a great variety of diseases with vascular involvement and hypercoagulability, including disseminated intravascular coagulation, acute coronary syndromes, peripheral arterial disease, diabetes mellitus and systemic inflammatory disease. Finally, microparticles are a major component of human atherosclerotic plaques. In view of their functional properties, cell-derived microparticles may be an important intermediate in the cascade of cellular and plasmatic dysfunctions underlying the process of atherogenesis. [source] Orbital blood flow velocities in patients with rheumatoid arthritisJOURNAL OF CLINICAL ULTRASOUND, Issue 7 2007Besir Erdogmus MD Abstract Purpose. To assess orbital blood flow changes in patients with rheumatoid arthritis using Doppler sonography. Patients and Methods. The study comprised 35 patients who were diagnosed with RA and were treated at the Department of Physical Therapy and Rehabilitation at Duzce Medical School. A control group consisted of 35 healthy volunteers. Color Doppler imaging was used to measure peak systolic velocity (PSV) and end diastolic velocity (EDV), from which the resistance index (RI) was calculated in the ophthalmic artery (OA), central retinal artery (CRA), and posterior ciliary arteries (PCAs). Results. In the OA, PSV, EDV, and RI were, respectively, 36.7 ± 0.6 cm/sec, 9.7 ± 0.2 cm/sec, and 0.73 in the control group versus 34.7 ± 3.0 cm/sec, 9.1 ± 1.1 cm/sec, and 0.74 in the patient group. In the CRA, they were, respectively, 11.8 ± 1.7 cm/sec, 3.6 ± 0.7 cm/sec, and 0.66 in the control group versus 11.1 ± 1.7 cm/sec, 3.4 ± 0.7 cm/sec, and 0.68 in the patient group. In the PCAs, they were, respectively, 13.2 ± 1.2 cm/sec, 4.7 ± 0.6 cm/sec, and 0.65 in the control group versus 12.4 ± 1.2 cm/sec, 4.2 ± 0.6 cm/sec, and 0.66 in the PCAs. PSV, EDV, and RI of the PCAs and OA and RI of the CRA were significantly different between patients and controls, whereas there was no difference in the serum levels of glucose, triglyceride, low-density lipoprotein cholesterol, and total cholesterol. In the patient group, there was a significant correlation between orbital blood flow and duration of disease. Conclusion. Ocular blood flow appears to be slightly lower in RA patients than in healthy controls, suggesting that RA is a systemic inflammatory disease that may also involve ocular vessels. © 2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2007 [source] Transcription of proteinase 3 and related myelopoiesis genes in peripheral blood mononuclear cells of patients with active Wegener's granulomatosisARTHRITIS & RHEUMATISM, Issue 6 2010Chris Cheadle Objective Wegener's granulomatosis (WG) is a systemic inflammatory disease that is associated with substantial morbidity. The aim of this study was to understand the biology underlying WG and to discover markers of disease activity that would be useful for prognosis and treatment guidance. Methods Gene expression profiling was performed using total RNA from peripheral blood mononuclear cells (PBMCs) and granulocyte fractions from 41 patients with WG and 23 healthy control subjects. Gene set enrichment analysis (GSEA) was performed to search for candidate WG-associated molecular pathways and disease activity biomarkers. Principal components analysis was used to visualize relationships between subgroups of WG patients and controls. Longitudinal changes in proteinase 3 (PR3) gene expression were evaluated using reverse transcription,polymerase chain reaction, and clinical outcomes, including remission status and disease activity, were determined using the Birmingham Vasculitis Activity Score for WG (BVAS-WG). Results Eighty-six genes in WG PBMCs and 40 in WG polymorphonuclear neutrophils (PMNs) were significantly up-regulated relative to controls. Genes up-regulated in WG PBMCs were involved in myeloid differentiation, and these included the WG autoantigen PR3. The coordinated regulation of myeloid differentiation genes was confirmed by GSEA. The median expression values of the 86 up-regulated genes in WG PBMCs were associated with disease activity (P = 1.3 × 10,4), and WG patients with low-level expression of the WG signature genes showed expression profiles that were only modestly different from that in healthy controls (P = 0.07). PR3 transcription was significantly up-regulated in WG PBMCs (P = 1.3 × 10,5, false discovery rate [FDR] 0.002), but not in WG PMNs (P = 0.03, FDR 0.28), and a preliminary longitudinal analysis showed that the fold change in PR3 RNA levels in WG PBMCs corresponded to changes in the BVAS-WG score over time. Conclusion Transcription of PR3 and related myeloid differentiation genes in PBMCs may represent novel markers of disease activity in WG. [source] Biologic therapy in the management of extraintestinal manifestations of inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 11 2007Arthur Barrie MD Abstract The inflammatory bowel diseases (IBD), notably Crohn's disease (CD) and ulcerative colitis (UC), are systemic inflammatory diseases primarily involving the gastrointestinal tract. Twenty percent to 40% of patients with IBD develop extraintestinal inflammation and symptoms, known as extraintestinal manifestations (EIMs).1,7 The most common EIMs affect the joints, skin, eyes, and biliary tract. The EIMs associated with IBD bear a negative impact on patients with UC and CD. Thus, the successful treatment of EIMs is essential for improving the quality of life of IBD patients. For most EIMs, their resolution often parallels that of the active IBD in both timing and therapy required. However, some EIM such as axial arthritis, pyoderma gangrenosum, uveitis, and primary sclerosing cholangitis run a clinical course independent of IBD disease activity. The advent of biologic response modifiers, e.g., tumor necrosis factor-, (TNF) inhibitors, has improved the treatment of IBD and its associated EIMs. This article reviews the therapeutic experiences of the 2 most widely used anti-TNF neutralizing antibodies, infliximab and adalimumab, for immune-mediated EIM of IBD. (Inflamm Bowel Dis 2007) [source] The pathology and pathogenesis of retinal vasculitisNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2003E. H. Hughes Retinal vasculitis is a rare, but potentially blinding intraocular inflammatory condition with diverse aetiology. Although commonly idiopathic, it has a strong association with systemic inflammatory diseases known to involve other areas of the central nervous system, most notably Behcet's disease, sarcoidosis, systemic lupus erythematosis and multiple sclerosis. This article describes the clinicopathologic features of retinal vasculitis and its visually damaging sequelae, reviewing available human histopathologic studies and work with experimental models to discuss the pathogenesis and immunopathology. Evidence indicates that noninfective retinal vasculitis is an autoimmune condition that may be induced by antecedent infection with microbes cross,reacting with putative autoantigens, influenced by genetic susceptibility of both HLA associations and cytokine polymorphisms. The growing understanding of the cellular mechanisms involved in the effector immune response is already providing a rationale for more specific therapeutic approaches. [source] Autoinflammatory syndromes with a dermatological perspectiveTHE JOURNAL OF DERMATOLOGY, Issue 9 2007Nobuo KANAZAWA ABSTRACT The term autoinflammatory syndromes describes a distinct group of systemic inflammatory diseases apparently different from infectious, autoimmune, allergic and immunodeficient ones. Originally, it was almost synonymous with clinically defined hereditary periodic fever syndromes, including familial Mediterranean fever, hyper immunoglobulin D syndrome with periodic fever and tumor necrosis factor receptor-associated periodic syndrome. Similar but distinct periodic fever syndromes accompanied by urticarial rash, familial cold autoinflammatory syndrome, Muckle,Wells syndrome and chronic infantile neurological cutaneous articular syndrome, have all been reportedly associated with CIAS1 mutations and are collectively called cryopyrin-associated periodic syndromes. Consequently, the concept of autoinflammatory syndromes has been spread to contain other systemic inflammatory diseases: rare hereditary diseases with or without periodic fevers, such as pyogenic sterile arthritis, pyoderma gangrenosum and acne syndrome, Blau syndrome and chronic recurrent multifocal osteomyelitis, and the more common collagen disease-like diseases, such as Behcet's disease, Crohn's disease, sarcoidosis and psoriatic arthritis. These diseases are all caused by or associated with mutations of genes regulating innate immunity and have common clinical features accompanied with activation of neutrophils and/or monocytes/macrophages. In this review, major autoinflammatory syndromes are summarized and the pathophysiology of related skin disorders is discussed in association with dysregulated innate immune signaling. [source] Inflammation assessment after selective laser trabeculoplasty (SLT) treatmentACTA OPHTHALMOLOGICA, Issue 2009M AYALA Purpose Glaucoma is a progressive neuropathy, reducing intraocular pressure (IOP) seems to be the only treatment to stop progression in glaucoma. There are several methods to reduce IOP: medical treatment, laser and surgery. Selective Laser Trabeculoplasty (SLT) is a new treatment alternative. SLT selectively targets the pigmented cells of the trabecular meshwork without causing thermal or collateral damage to the surroundings structures. The aim of the present study was to assess inflammation after SLT treatment. Methods 40 patients (80 eyes) were included in the study. Inclusion criteria: Glaucoma (POAG, pigmentary and pseudoexfoliative glaucoma)/ OHT patients that will be treated with SLT in just one eye, both with and without eye-drops. Exclusion criteria: patients suffering from ocular or systemic inflammatory diseases or treated with cortisone or immunosuppressive drugs. Inflammation was measured in 2 different ways: 1) clinically with a slit lamp and classified 0-4; 2) with a "Laser flare meter (Kowa FM 500)". Measurements were done before, 2 hours after, 1 week and 1 month after SLT treatement, both eyes were evaluated. IOP was also checked in the same way. SLT treatment was performed in 90° with the SLT Solo Ellex laser. Results inflammation before and after SLT showed no significant difference measured both clinically with slit lamp and objectively with the laser flare meter. No inflammation was found in the untreated eyes. No IOP peaks after SLT treatment were found. Conclusion SLT treatment seems not to induce inflammation in the anterior chamber when 90° were treated. SLT treatment might be considered as a first choice treatment against high intraocular pressure. [source] Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitisCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009J. W. Cohen Tervaert Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible. [source] | ||||||||||