[Anti-lipoprotein autoantibodies with hypolipidemia in infectious rheumatism]

Presence of anti-lipoprotein activity, a new serological finding in inflammatory rheumatoid disease, has been established in sera and synovial fluids of 20 patients, among which were 6 cases of ankylosing spondylitis. In 18 of the patients, sera were negative for rheumatoid factor. Anti-lipoprotein activity can best be demonstrated by the hemagglutination technique. The binding activity is directed against autologous as well as homologous, however not against heterologous HDL and LDL. It has no specificity for Ag factors. Anti-LDL activity can also be demonstrated by means of double-diffusion tests, whereas no agar-precipitation has been noticeable using HDL as the antigen. Lipoprotein binding-activities were shown to be localized in the Fab fragments of IgG and, in 2 of the cases, also in IgA. We therefore assume that the underlying mechanism of the antilipoprotein activity is auto-immunization, despite of the fact that neither activation of complement nor a stoichiometric character of the binding reaction could be ascertained. Because hemagglutination and immunoprecipitation tests, respectively, were postive with apo-HDL und apo-LDL too, we consider the apo-protein to carry the antigenic site of the reaction. Sera with anti-lipoprotein autoantibodies from patients with chronic rheumatoid disease also presented another pecularity, i.e., a significant decrease of total lipids, cholesterol, and other components of the lipid spectrum. In patients with paraproteinemia, a similar combination of lipoprotein-binding activity and hypolipidemia or hypocholesterolemia was discussed in a previous paper. Regarding the pathogenesis of hypolipidemia or hypocholesterolemia in our patients with rheumatoid disorders, results of LDL turnover studies were indicative for an increase of the lipoprotein catabolism in the presence of anti-lipoprotein autoantibodies, together with a shift of the intra-extravascular distribution toward the intravascular pool. We assume the increased lipoprotein catabolism in these cases to be due to a trapping of lipoproteins by autoantibodies, and to accelerated degradation of these immune complexes. From a practical point of view, it may be of clinical importance that this new serological finding has been observed mainly in patients with chronic rheumatoid disease lacking a rheumatoid serum factor, and was frequently found in patients with ankylosing spondylitis (6 out of the 20 cases). As a screening method, we recommend systematic determinations of the total lipids and of serum cholesterol in all patients with inflammatory rheumatoid disease. In cases with low levels of total lipids and cholesterol, respectively, it may be useful to search for anti-lipoprotein autoantibodies using the hemagglutination method. Results are reported from some preliminary experiments on animals elicitation of an arthritis by means of intra-articular injections of autologous apo-HDL and apo-LDL, and demonstration of autoantibodies against HDL and LDL).