Brancato L, Itescu S, Skovron M L, Solomon G, Winchester R
Department of Rheumatology, Hospital for Joint Diseases, New York, NY 10003.
Rheumatol Int. 1989;9(3-5):137-41. doi: 10.1007/BF00271870.
Arthrocutaneous disorders including Reiter's syndrome, psoriasiform rashes, and other forms of chronic arthritis and enthesopathy, such as psoriatic arthritis, occur with an increased prevalence in the setting of HIV infection. Herein we describe the spectrum and prevalence of musculoskeletal and allied skin disorders as they occur in the setting of HIV infection. The role of genetic susceptibility in the development of these disorders is addressed. Based on the frequency of infectious agents capable of triggering reactive arthritis and the presence of HLA-B27 in 71% of these individuals, it is suggested that the disorder strongly resembles Reiter's syndrome as it occurs in the not HIV-infected group. Preliminary evidence indicates an enhanced penetrance for susceptibility among HLA-B27 individuals. In contrast, among HIV-infected patients with psoriasiform lesions there was no statistically significant association (P less than 0.05) between the presence of psoriasiform rash and the HLA alleles Cw6, B7, B17, Bw16, or Bw57 when compared with HIV-infected controls. These findings suggest that among HIV-infected individuals the development of Reiter's syndrome involves an immune recognition event primarily dependent upon HLA-B27 molecules in which an unknown antigen in the context of HLA-B27 is presented to CD8 lineage suppressor/cytotoxic cells. In contrast, the pathogenesis of psoriasiform lesions in HIV patients, despite their similarity to certain lesions in Reiter's syndrome, proceeds by distinct pathways that do not involve events influenced by specific polymorphic class I molecules.
包括赖特综合征、银屑病样皮疹以及其他形式的慢性关节炎和附着点病(如银屑病关节炎)在内的关节皮肤疾病,在HIV感染患者中发病率增加。在此,我们描述了HIV感染患者中肌肉骨骼及相关皮肤疾病的范围和发病率,并探讨了遗传易感性在这些疾病发生过程中的作用。鉴于能够引发反应性关节炎的感染因子的出现频率以及这些个体中71%存在HLA - B27,提示该疾病与未感染HIV人群中发生的赖特综合征极为相似。初步证据表明HLA - B27个体的易感性外显率增加。相比之下,在患有银屑病样皮损的HIV感染患者中,与HIV感染对照组相比,银屑病样皮疹的出现与HLA等位基因Cw6、B7、B17、Bw16或Bw57之间无统计学显著关联(P小于0.05)。这些发现表明,在HIV感染个体中,赖特综合征的发生涉及主要依赖HLA - B27分子的免疫识别事件,即HLA - B27背景下的未知抗原呈递给CD8谱系抑制/细胞毒性细胞。相比之下,HIV患者中银屑病样皮损的发病机制,尽管与赖特综合征中的某些皮损相似,但通过不涉及受特定多态性I类分子影响的事件的不同途径进行。