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The lupus anticoagulant was found in the plasma of 31 of 60 patients with systemic lupus erythematosus and other connective tissue disorders

Two-dimensional echocardiographic studies were prospectively performed in 93 patients with systemic lupus erythematosus (SLE) to discover the incidence and spectrum of cardiac abnormalities and to relate these findings to the presence of high levels of anticardiolipin antibodies. Assessment of the intracardiac anatomy was also performed in an additional 12 patients who had increased anticardiolipin antibody levels but did not have SLE. Fifty patients (54%) with SLE had cardiac abnormalities, and 43 patients (46%) had normal hearts. Three categories of cardiac abnormalities were identified -valvular lesions, ranging from vegetations to valvular thickening, were found in 28%, pericardial effusion or thickening was found in 20%, and regional or global left ventricular dysfunction was found in 5%. High levels of anticardiolipin antibodies were detected in 50 patients (54%) with SLE. Of those, only 11 (22%) had an entirely normal heart, whereas the remaining 39 (78%) had at least one cardiac abnormality (valvular lesions in 20, pericardial effusion in 15, and myocardial dysfunction in five patients). In patients with SLE, the presence of abnormal intracardiac anatomy was strongly associated with increased levels of anticardiolipin antibodies (p<0.0001). The overall sensitivity and specificity of high levels of anticardiolipin antibodies in the prediction of cardiac abnormalities was 78% and 74%, respectively, with a positive predictive accuracy of 78% and a negative predictive accuracy of 74%. Eight of the 12 patients (67%) who had increased anticardiolipin antibodies but whose disease did not fulfill the American Rheumatism Association classification criteria for SLE had cardiac abnormalities similar to those in patients with SLE compared with only four (33%) who had normal hearts (p<0.001). High levels of anticardiolipin antibodies are strongly associated (p<0.0001) with cardiac abnormalities, not only in SLE but also in other lupuslike syndromes. (Circulation 1990;82:369-375) T he heart is a major target for disease in patients with systemic lupus erythematosus (SLE

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Objectives: To investigate IgG, IgM, and IgA, antiphospholipid antibodies (aPL), against cardiolipin (aCL), b 2 -glycoprotein I (anti-b 2 GPI), and prothrombin (anti-PT), in black South African patients with infectious disease. Unlike patients with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS), raised levels of aPL in infectious diseases are not usually associated with thrombotic complications. Patients and methods: Serum samples from 272 patients with a variety of infectious diseases (100 HIV positive, 112 leprosy, 25 syphilis, 25 malaria, and 10 HCV patients) were studied and compared with autoantibody levels in 100 normal controls. All three aPL were measured using commercial enzyme linked immunosorbent assay (ELISA) kits. Results: Raised levels of all thee aPL were found in all patient groups studied: aCL in 7%, anti-b 2 GPI in 6%, and aPT in 43% of 100 HIV patients, in 29%, 89%, and 21% of 112 patients with leprosy, in 8%, 8%, and 28% of 25 patients with syphilis, in 12%, 8%, and 28% of 25 patients with malaria, and in 20%, 30%, and 30% of 10 HCV patients studied, respectively. Conclusions: The prevalence of aCL and anti-b 2 GPI in black South African HIV positive patients, or those with syphilis, malaria, or hepatitis C virus is lower than reported for mixed race or white populations. aPT were the most prevalent aPL detected in these patient groups, except in patients with leprosy, for whom anti-b 2 GPI was the most prevalent, and where the spectrum of aPL was similar to that seen in patients with SLE and APS.

Objective. To assess the phospholipid specificity and immunoglobulin isotype of antiphospholipid (aPL) antibodies in patients with acute parvovirus B19 infection.Methods. Specificity of aPL and isotype distribution in the negatively charged phospholipids, cardiolipin and phosphatidyl serine, and in the neutral phospholipid, phosphatidyl ethanolamine, were measured in the sera of patients with acute parvovirus B19 infections (n = 12), in those with other acute viral infections (n = lo), and in those with syphilis (n = 15) by enzymelinked immunosorbent assays. The dependence of anticardiolipin (aCL) binding on the presence of p2-glycoprotein I (p2-GPI) as a binding cofactor was assessed in these same groups, and was compared with sera from systemic lupus erythematosus (SLE) patients (n = 11) with raised aCL antibody reactivity.Results. Antibodies against any of the 3 phospholipids were found in all 3 groups of patients with infections (B19 in 11 of 12 patients, other viral infections in 8 of 10 patients, and syphilis in 14 of 15 patients). B19 patients' sera contained predominantly IgG antibodies against the negatively charged phospholipids, cardiolipin and phosphatidyl serine, and differed in their specificity and isotype distribution from those found in the other 2 patient groups. B19-associated aCL increased their binding to antigen in the presence of &GPI as a binding cofactor, similar to aCL found in Conclusion. The results show the remarkable similarity in specificity of aPL antibodies between B19-infected patients and SLE patients, and raise the question of whether parvovirus infection may be a trigger for the development of aPL antibodies in autoimmune diseases.Human infection with parvovirus B19, a small, single-stranded DNA virus, is associated with a variety of clinical manifestations, including rash, arthralgia, thrombocytopenia, leukopenia, fetal wastage, hypocomplementemia, autoimmune hemolytic anemia, and vasculitis (1-3). In addition, infection can be associated with elevated levels of autoantibodies to nuclear components (antinuclear antibodies [ANA]), doublestranded DNA (dsDNA), lymphocyte antigens, neutrophi1 cytoplasmic antigens, and cardiolipin (1-4).The prevalence and specificities of anticardiolipin antibodies (aCL) in B19 infection are not known. Raised levels of antiphospholipid antibodies (aPL) or aCL have been reported in a variety of other infections, including chicken pox, hepatitis A, infectious mononucleosis, rubella, adenovirus, mumps, and human immunodeficiency virus (HIV) (5), and are also well recognized in syphilitic infections (6). In light of the similarity of some of the clinical features presented by parvovirus B19 infection with those of autoimmune connective tissue diseases, we were interested in determining if the aCL antibodies observed in B19 infection were similar to those found in systemic lupus erythematosus (SLE) and whether similar antibodies were found in patients with acute viral infections other than parvovirus B19. One distinguishing feature of aCL found in au...

The objectives of this study were to estimate the prevalence of IgA anticardiolipin antibodies (aCL) and anti-beta(2)-glycoprotein 1 antibodies (abeta(2)-GP1) in a large number of patients with systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (PAPS) and to examine possible associations between the clinical manifestations of the APS and the levels of IgA aCL and abeta(2)-GP1. We also assessed the operative characteristics of IgA aCL and abeta(2)-GP1. We retrospectively studied 130 patients with SLE and 35 patients with PAPS. In all patients we measured IgG, IgM, and IgA aCL and abeta(2)-GP1 and recorded any of the clinical manifestations of the APS. IgA aCL were positive in 8.5% of patients with SLE and in 40% of patients with PAPS. Positive IgA abeta(2)-GP1 were found in 17.7% of patients with SLE and in 25.7% of patients with PAPS. IgA aCL were associated with a history of venous thrombosis, thrombocytopenia, and recurrent fetal loss. In contrast, we could not establish significant associations between IgA abeta(2)-GP1 and any of the clinical manifestations of the APS. Measurement of the IgA in addition to IgG and IgM aCL hardly changed the operative characteristics of aCL testing, while measurement of the IgA in addition to IgG and IgM abeta(2)-GP1 increased sensitivity but with a greater loss in specificity. IgA aCL is significantly associated with more than one of the clinical manifestations of the APS in contrast to the IgA abeta(2)-GP1. Routine measurement of the IgA isotype of both aCL and abeta(2)-GP1 does not improve the operative characteristics of aCL and abeta(2)-GP1 and therefore is not recommended at present.

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