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We studied a group of 80 unselected patients with systemic lupus erythematosus (SLE). Twenty six (32.5%) of them were considered in clinical activity using criteria based on clinical features and laboratory abnormalities. Using an isotype specific enzyme linked immunosorbent assay (ELISA) for anticardiolipin antibodies we found IgG anticardiolipin in 28/80 (35%) and IgM anticardiolipin in 20/80 (25%) patients. Antibodies to native DNA by immunofluorescence were found in 11/80 (14%) patients, whereas antibodies to denatured DNA by ELISA were found in 51/80 (64%) patients. There was an association between disease activity and the presence of anticardiolipin and anti-DNA antibodies particularly of the IgG isotype. We also found an association between anticardiolipin and anti-DNA suggesting a cross reaction between these antibodies, but we are not able to exclude the possibility of a simple coincidental phenomenon due to polyclonal synthesis of immunoglobulin observed during periods of disease activity.

Isoniazid (INH) is one among many drugs capable of inducing autoantibodies and, in some cases, a lupus-like syndrome (LE). A longitudinal study was performed in 24 tuberculosis patients treated with INH to detect antibodies (A-AH) to total histones and fractions. Antinuclear antibodies were observed in two patients after treatment. Higher frequency of IgM-AH was also observed. IgM-AH binding to all fractions were observed in those serum samples exhibiting stronger ELISA reactivity. Conversely, binding to only H1 occurred when lower IgM-AH activity was tested. Correlations with clinical expressions of LE were not observed in the present study.

A haemolytic assay was used to test the complement fixation ability of 16 serum samples with high concentrations of anti-cardiolipin antibodies. Fourteen patients had clinical complications usually associated with these antibodies--namely, recurrent abortions, thrombosis, or thrombocytopenia. Complement fixation by anticardiolipin antibodies was shown in only four of these patients and was not directly related to the antibody concentration. Because anticardiolipin antibodies in most of these patients did not activate the complement pathway it is unlikely that the complement cascade has an important role in the clinical complications associated with these antibodies.

IgG or IgM anticardiolipin antibodies were present in the sera of 67% of 33 patients with Hansen 's disease, in 53 % of 30 patients with tuberculosis and in 50% of 16 patients with endocarditis. Despite the high frequency of these antibodies, no patient had a history of thrombosis or abortion. Antidenatured DNA antibodies were tested in patients with tuberculosis and patients with Hansen 's disease. Only in the latter group did we observe a statistically significant association between anticardiolipin and antidenatured DNA antibodies. Anticardiolipin binding activity, however, could not be inhibited by preincubation of sera with a variable concentration of denatured DNA. These data suggest that: a) Anticardiolipin antibodies in infectious diseases do not necessarily participate in the pathogenesis of thrombotic or obstetric complications; b) Anti-denatured DNA and anticardiolipin antibodies in the population studied do not have a crossreaction.