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Anti-cardiolipin antibodies in infectious diseases and in APS can be distinguished with respect to their dependence on cofactors: whereas ACA from patients with infectious diseases recognize the pure phospholipid as antigen, binding of ACA from patients with APS requires β2-glycoprotein I as a cofactor. For this reason, ACA ELISAs need β2-glycoprotein I to be incorporated into the assay. ‘Lupus anticoagulant' (LA) describes a phenomenon related to the presence of antiphospholipid antibodies, defined by the measurement of antibody dependent coagulation inhibition in vitro.^1,5,7,8,9ACA/LA are considered to be of significant diagnostic relevance, as a correlation has been found between these antibodies and a tendency towards thromboses, resulting in an increased incidence of thromboses, thrombocytopenia, livedo reticularis, habitual abortion and neurological manifestations in ACA/LA-positive patients. Raised ACA/LA may also be found in patients with cerebrovascular insufficiency or myocardial infarction. aPL may play a direct role in the pathogenesis of APS.^1,3,10,11,12,13The EliA Cardiolipin IgM Test permits the determination of IgM antibodies directed against the Cardiolipin antigen as described in the directions for use.The EliA Cardiolipin IgM Wells are coated with bovine cardiolipin antigen. If present in the patient's specimen, antibodies to cardiolipin bind to their specific antigen and are detected by the assay.Specimen Collection, Handling and Preparation:The procedure can be performed with serum or plasma specimens. Lipemic, hemolyzed or microbially contaminated samples may give poor results and should not be used.Sample Dilution:Samples must be diluted with EliA Sample Diluent. A 1:10 dilution of the samples is required for the EliA Cardiolipin Test. Samples can be diluted manually, but instrument dilution is recommended.Expected Values:The expected value in the normal population is negative. However, low percentages (up to 5%) of apparently healthy, asymptomatic individuals have been reported to be positive for ACA. Their proportion may increase with age.^4 Anti-cardiolipin antibodies are characteristic for the antiphospholipid syndrome (primary or secondary) and occur with a prevalence of 30-40% in SLE patients.^13 Clinical manifestations can be thromboses, recurrent abortions and other features, such as thrombocytopenia, livedo reticularis or neurological disorders.^1,3,10,11Cardiolipin antibodies show the following prevalences in APS:
• Primary APS - Cardiolipin IgG 81%, IgM 40%, IgA 24%
• Secondary APS - Cardiolipin IgG 85%, IgM 65%, IgA 10%Expected values may vary depending on the population tested.Measuring Range:No hook effects could be observed for concentrations up to 10 fold above the measuring ranges.Only values above the Detection Limit can be regarded as valid results. The upper limit of the reported results can vary due to a lot-specific conversion from μg/l to MPL-U/ml. Results above the upper limit are reported as “above”.Please note that due to differing binding characteristics of the antibodies in patient samples, not all sera can be diluted linearly within the measuring range.1. Boey ML, Colaco CB, Gharavi AE, et al. (1983) Thrombosis in systemic lupus erythematosus: striking association with the presence of circulating lupus anticoagulant. Br Med J 287, 1021-10233. Gromnica-Ihle E, Schössler W (2000) Antiphospholipid Syndrome. Int Arch Allergy Immunol 123, 67-764. Petri M (2000) Epidemiology of the Antiphospholipid Antibody Syndrome. J Autoimm 15, 145-1515. Roubey RAS (1999) Immunology of the Antiphospholipid Syndrome: Antibodies, Antigens, and Autoimmune Response. Thromb Haemost 82, 656-6617. Galli M, Comfurius P, Maassen C, et al. (1990) Anticardiolipin antibodies (ACA) directed not to cardiolipin but to a plasma cofactor. Lancet 335, 1544-15478. Matsuura E, Igarashi Y, Yasuda T, et al. (1994) Anticardiolipin Antibodies Recognize #-Glycoprotein I Structure Altered by Interacting with an Oxygen Modified Solid Phase Surface. J Exp Med 179, 457-4629. Koike T, Ichikawa K, Atsumi T, et al. (2000) #-glycoprotein I - anti-#-glycoprotein I Interaction. J Autoimm 15, 97-10010. Harris EN, Asherson RA, Gharavi AE, et al. (1985) Thrombocytopenia in SLE and related autoimmune disorders: Association with anticardiolipin antibody. Br J Haematol 59, 227-23011. Harris EN, Chan JKH, Asherson RA, et al. (1986) Thrombosis, recurrent fetal loss, and thrombocytopenia. Arch Intern Med 146, 2153-215612. Bili A, Moss AJ, Francis CW, et al. (2000) Anticardiolipin Antibodies and Recurrent Coronary Events - A Prospective Study of 1150 Patients. Circulation 102, 1258-1263.13. Khamashta M, Hughes GRV (1996) Phospholipid Autoantibodies - Cardiolipin. In: Peter JB, Shoenfeld Y (eds), Autoantibodies, pp 624-629, Elsevier, Amsterdam
