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Danila, Maria; Louis Bridges, S.
doi: 10.1007/s11926-008-0070-1pmid: 19007531
Systemic necrotizing vasculitis is rare but can have serious sequelae. Despite recent advances in cellular and molecular immunology and genetics, the causes of vasculitic syndromes remain largely undefined. Although mechanisms of blood vessel damage in systemic necrotizing vasculitis are complex, recent studies have provided significant insights.
doi: 10.1007/s11926-008-0071-0pmid: 19007532
Systemic vasculitides were initially reported as acute, progressive, severe, and life-threatening diseases. The introduction of glucocorticoids and cyclophosphamide for the treatment of vasculitis improved survival dramatically, but morbidity has remained high. Damage develops as a consequence of recurrent or persistent active vasculitis or its treatment. It is defined as the accumulation of nonhealing scars that are unlikely to respond to immunosuppressive therapy. Damage assessment is essential in systemic vasculitis because it may facilitate patient stratification in clinical trials and possibly in clinical practice. Moreover, it may avoid unnecessary use of immunosuppressive therapy. The Vasculitis Damage Index, developed and validated in 1997, has been very useful in solving many matters in systemic vasculitis and is currently the only validated damage-assessment tool available. However, the vasculitis community has recognized that there is a growing need to improve the evaluation of damage in vasculitis. The development of a Combined Damage Assessment index, which would permit a more appropriate and standardized approach to disease assessment applicable to systemic vasculitis, has been proposed.
Ramos-Casals, Manuel; Brito-Zerón, Pilar; Cuadrado, Maria-Jose; Khamashta, Munther
doi: 10.1007/s11926-008-0072-zpmid: 19007533
Tumor necrosis factor (TNF)-targeted therapies are increasingly used for a rapidly expanding number of rheumatic and autoimmune diseases. With this use and longer follow-up periods of treatment, there are a growing number of reports of the development of autoimmune processes related to these new therapeutic agents. We have analyzed the clinical characteristics, outcomes, and patterns of association with the different anti-TNF agents used in all reports of vasculitis developed after TNF-targeted therapy. A total of 132 cases, identified up to July 2008, are included and analyzed in this review.
doi: 10.1007/s11926-008-0074-xpmid: 19007535
Churg-Strauss syndrome (CSS) is a rare necrotizing small-vessel vasculitis associated with eosinophil-rich granulomatous inflammation of tissues and vessels and is also associated with asthma and eosinophilia. Epidemiologic studies continue to show that CSS is the rarest of the necrotizing small-vessel vasculitides. However, it is not possible to know with any certainty if there has been an increase in incidence. There has been an attempt to divide the patients with CSS into an antineutrophil cytoplasmic antibody-positive and cytoplasmic antibody-negative group. The former group has an increased frequency of renal involvement, parenchymal pulmonary disease, constitutional symptoms, and peripheral and central nervous system involvement, whereas the latter group has more frequent cardiac disease. The role of eosinophils and antineutrophil cytoplasmic antibodies remains poorly defined but provocative. Leukotriene receptor antagonists do not appear to induce CSS but facilitate the tapering of glucocorticoids, which unmasks the condition. Glucocorticoids and cyclophosphamide remain the foundation of treatment for vasculitis, but there are other promising and less toxic alternatives on the horizon.
doi: 10.1007/s11926-008-0076-8pmid: 19007537
Although fibromyalgia (FM) syndrome is defined by chronic widespread pain and tenderness, additional symptoms, including disabling fatigue and dizziness, are often reported by patients with this chronic illness. Although nonrestorative sleep may play an important role for chronic fatigue in FM, other mechanisms, including dysfunction of the autonomic nervous system (ANS), need to be considered. Many important biological functions, such as heart rate, blood pressure, respirations, and bowel function, are tightly regulated by the ANS. However, dysfunction of the ANS is common in FM and often becomes quite apparent after positional changes from supine to upright. Although such positional changes sometimes result in syncope, they are more often associated with palpitations and dizziness. Head-up tilt table testing can be used to evaluate autonomic dysfunction and is frequently helpful for the work-up of FM complaints, including fatigue, dizziness, and palpitations. One of the most common events experienced by FM patients during tilt table testing is postural orthostatic tachycardia syndrome, which is defined as a heart rate increase of more than 30 beats per minute after more than 3 minutes of standing upright.
doi: 10.1007/s11926-008-0077-7pmid: 19007538
Various peripheral and spinal mechanisms have been hypothesized to contribute to pain amplification and chronicity. However, the role of the brain in chronic pain states remains to be fully elucidated. Functional brain imaging techniques, such as positron emission tomography and functional magnetic resonance imaging, have frequently been used to investigate brain activity during acute/experimental pain perception, which has helped to establish the notion of the human pain network. In the context of chronic pain, the assessment of brain chemistry (by way of spectroscopy) and brain morphology is of growing interest, and there is a quickly expanding body of evidence that persons with chronic pain conditions, including chronic low back pain, chronic tension-type headache, and fibromyalgia, display changes in global and regional brain morphology. It has been suggested that prolonged nociceptive input to the brain might induce functional and morphologic maladaptive processes that in turn further exacerbate the experience of chronic pain. Alternatively, morphologic changes might predispose toward vulnerability to develop a chronic pain state. The purpose of this review is to examine current literature regarding altered brain morphology in patients with various chronic pain states, summarize these findings, and evaluate their implications for our understanding of the pathophysiology of chronic pain.
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