Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

Abstract

SummaryPremature 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.

Translational Mini-Review Series on Immunology of Vascular Disease: Mechanisms of vascular inflammation and remodelling in systemic vasculitis

“…Danger signals generated after sterile ischaemia-reperfusion injury also cause exocytosis of Weibel-Palade bodies, with release of von Willebrand factor and IL-8 in the circulation [21]. As discussed below and elsewhere in this series [22,23], TLR-2 and possibly other innate receptors involved in the inflammatory response to danger, may be important [10,24]. Inflammation elicited in response to vessel injury is required for the repair of the vessel wall, with eventual healing [10].…”

A Case Series Study to Assess Body Mass Index in Patients’ with ANCA Associated Vasculitis

“…However one may hypothesize that perhaps just like how Petermann Smits et al, recently reported an increased prevalence of metabolic syndrome in patients with AAV and how it may have an impact on the clinical course of AAV and correlation with elevated CRP levels [35]; obesity or the presence of increased leptin levels may play a role in pre-disposing patients to AAV and place them at a higher risk for more severe disease. Activation of the immune system in AAV is thought to increase the risk of acceleration of atherosclerosis and increase risk for cardiovascular events in patients with metabolic syndrome [36]. Thus it may be postulated that the presence of increased visceral adipose tissue may be responsible for making this population vulnerable to AAV.…”

Progress and Clinical Applications in Proteomics

“…One of the more than 50 proteins identified was peroxiredoxin2 (Prx2), an anti-oxidative enzyme. Oxidative stress is known to cause inflammation such as vasculitis [70,71]. In an animal model, it has been shown that the oxidation status of Prx reflected oxidative stress in the vasculature and correlated to the extent of lesion formation [72].…”