No abstract

Twenty-six percent of 53 systemic lupus erythematosus sera had high levels of IgM antibody to human T-lymphotropic virus Type I, significantly more than the 5% of normal controls. Neither IgG antibodies to Type I virus nor IgM or IgG antibodies to Type II virus were increased in lupus. Further analysis using competition immunoassay and Western blot techniques also suggested that the IgM Type I antibodies in lupus sera were directed against viral antigens but did not completely exclude a nonviral reaction. Other studies also have not found IgG antibodies to the Type I virus but have not tested for IgM antibodies. Our study suggests that human T-lymphotropic virus Type I or a related virus may be involved in the pathogenesis of some cases of systemic lupus erythematosus.

Because patients with diabetes mellitus are at increased risk for vascular disease, we suspected that they might have increased circulating platelet aggregates. Therefore, we determined the platelet aggregate ratio of 30 diabetic patients (15 diagnosed before 30 years of age and classified as juvenile-onset and 15 diagnosed after 30 years of age and classified as adult-onset) and 30¹ controls. The mean platelet aggregate ratio of the juvenile-onset diabetics was 0.75 and of their controls was 0.91 (p < 0.02) confirming our hypothesis in this subgroup. However, the mean platelet aggregate ratio of the adult-onset diabetics was not lower than that of their controls.

The clinical similarities of the spondylarthropathies and their frequent association with both HLA B27 and microbial infections suggest common pathogenetic mechanisms. The latter may include deposition of immune complexes containing bacterial antigens. or cross-reactivity of such antigens with host target tissue or responding cell antigens. Enteric bacteria, chlamydia and mycoplasma are all candidate etiologic agents, but proof is difficult because they are often found as normal flora, although only genetically susceptible individuals may acquire disease, and many patients have been treated with antibiotics before they can be studied. Nonetheless, a role for endogenous bacteria in reactive arthritis at least seems certain, and should stimulate further investigation into similar pathogenetic mechanisms in other chronic arthritides.