Satta R, Biondi G
Department of Surgical, Microsurgical and Medical Sciences, Dermatology University of Sassari, Sassari, Italy -
G Ital Dermatol Venereol. 2015 Apr;150(2):211-20.
Vasculitis usually presents without a well-known underline cause (idiopathic vasculitis), nevertheless, it is sometimes possible to find out one or more causative agents (secondary vasculitis). Nowadays, thanks to the increasing amount of precise diagnostic tools, a piece of idiopathic vasculitis is reclassified as associated with probable etiology, which can be set off by several factors, such as infections. Infections are considered to be the most common cause of secondary vasculitis. Virtually, every infectious agent can trigger a vasculitis by different mechanisms which can be divided in two main categories: direct and indirect. In the former, infectious agents destroy directly the vascular wall leading, eventually, to a subsequent inflammatory response. In the latter, indirect form, they stimulate an immune response against blood vessels. Different infectious agents are able to directly damage the vascular wall. Among these, it is possible to recognize Staphylococcus spp, Streptococcus spp, Salmonella spp, Treponema spp, Rickettsia spp, Cytomegalovirus, Herpes Simplex Virus 1 and 2, and many others which have a peculiar tropism for endothelial cells. Conversely, another group of microbial agents, such as Mycobacterium tuberculosis, Mycobacterium leprae, Hepatits B Virus, Human Immunodeficiency Virus and others, trigger vasculitis in the indirect way. This is due to the fact that they can share epitopes with the host or modify self-antigens, thus leading to a cross-self reaction of the immune system. These mechanism, in turn, leads to immunological responses classified as type I-IV by Gell-Coombs. Nevertheless, it is difficult to strictly separate the direct and indirect forms, because most infectious agents can cause vasculitis in both ways (mixed forms). This paper will analyze the link between infectious agents and vasculitis, focusing on direct and indirect secondary vasculitis, and on a group of probable infection-related idiopathic vasculitis, and finally on a group of idiopathic vasculitis with microbiological triggers. Furthermore, a diagnostic and therapeutic approach to vasculitis when an underline infection has been suspected is suggested.
血管炎通常在没有已知潜在病因(特发性血管炎)的情况下出现,不过,有时也能找出一种或多种致病因素(继发性血管炎)。如今,得益于越来越多精确的诊断工具,一部分特发性血管炎被重新归类为与可能的病因相关,这些病因可能由多种因素引发,比如感染。感染被认为是继发性血管炎最常见的病因。实际上,每种感染因子都能通过不同机制引发血管炎,这些机制可分为两大类:直接机制和间接机制。在前一种直接机制中,感染因子直接破坏血管壁,最终引发后续的炎症反应。在后一种间接机制中,它们刺激针对血管的免疫反应。不同的感染因子能够直接损伤血管壁。其中,可以识别出葡萄球菌属、链球菌属、沙门氏菌属、密螺旋体属、立克次体属、巨细胞病毒、单纯疱疹病毒1型和2型等,还有许多其他对内皮细胞有特殊嗜性的病原体。相反,另一组微生物因子,如结核分枝杆菌、麻风分枝杆菌、乙型肝炎病毒、人类免疫缺陷病毒等,则以间接方式引发血管炎。这是因为它们可以与宿主共享表位或修饰自身抗原,从而导致免疫系统的交叉自身反应。这些机制进而导致被盖尔-库姆斯分类为I-IV型的免疫反应。然而,很难严格区分直接和间接形式,因为大多数感染因子都能通过两种方式引发血管炎(混合形式)。本文将分析感染因子与血管炎之间的联系,重点关注直接和间接继发性血管炎、一组可能与感染相关的特发性血管炎,以及最后一组有微生物触发因素的特发性血管炎。此外,还提出了在怀疑有潜在感染时对血管炎的诊断和治疗方法。