These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Aspects of the spectrum, prevalence and disease susceptibility determinants of Reiter's syndrome and related disorders associated with HIV infection.
    Author: Brancato L, Itescu S, Skovron ML, Solomon G, Winchester R.
    Journal: Rheumatol Int; 1989; 9(3-5):137-41. PubMed ID: 2532780.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]