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Anti-Cardiolipin IgG/IgM ELISA

  • Bio-Type Serum/Plasma
  • Method ELISA
  • CE Y
  • # of Tests 96 wells
  • Range Refer to User Manual
  • Sensitivity Refer to User Manual
  • Sample Volume 10 uL
  • Incubation Time(s) 30 / 15 / 15 / 5 min
  • Storage Conditions 2° C - 8° C
  • SKU:  EIA3587
  • Category: Autoimmune Diseases
  • $389.00
Approximate Lead Time 1 - 2 Weeks
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Anti-Cardiolipin IgG / IgM ELISA is a test system for the quantitative measurement of IgG and IgM class autoantibodies against cardiolipin in human serum or plasma. This product is intended for professional in vitro diagnostic use only. Highly purified cardiolipin is coated on microwells saturated with beta-2-glycoprotein I. The determination is based on an indirect enzyme linked immune reaction with the following steps: Specific antibodies in the patient sample bind to the antigen coated on the surface of the reaction wells. After incubation, a washing step removes unbound and unspecifically bound serum or plasma components. Subsequently added enzyme conjugate binds to the immobilized antibody-antigen-complexes. After incubation, a second washing step removes unbound enzyme conjugate. After addition of substrate solution the bound enzyme conjugate hydrolyses the substrate forming a blue coloured product. Addition of an acid stops the reaction generating a yellow end-product. The intensity of the yellow colour correlates with the concentration of the antibody-antigen-complex and can be measuredphotometrically at 450 nm. Anti-phospholipid syndrome (APS, Hughes Syndrome) is a systemic autoimmune disease that causes thromboses, recurrent miscarriage, and intrauterine foetal death. Clinical symptoms are accompanied by the occurrence of specific autoantibodies that are detectable in the blood of patients with APS.  These antibodies bind to phospholipids like cardiolipin, or phospholipid-binding proteins like beta-2-glycoprotein I. The clinical symptoms of APS alone are not sufficiently specific to make a definitive diagnosis. Laboratory tests thus play an important role in the diagnosis of the disease. The Scientific and Standardization Committee of the International Society on Thrombosis and Hemostasis defined clinical criteria and diagnostically relevant laboratory parameters in the Sapporo Criteria for the classification of anti-phospholipid syndrome, published in 1999. These were revised and updated in 2006 and 2012. They include the following laboratory parameters: 1. Detection of lupus anticoagulant (LA) in the plasmatwice in the space of twelve weeks, according to the guidelines of theInternational Society on Thrombosis and Hemostasis. 2. Elevated anti-cardiolipin titre (IgG and/or IgM) inthe blood. The values must be determined on two occasions at least  twelve weeks  apart  using standardized  ELISA  tests for  beta-2-glycoprotein  I dependent  cardiolipin antibodies. 3. Elevated beta-2-glycoprotein I antibody titre (IgGand/or IgM). The values must be determined on two occasions at least twelveweeks apart. Detection is performed by means of a standardized ELISA test. The diagnosis of APS is considered as confirmed whenat least one clinical and one of the laboratory criteria are fulfilled.In primary APS autoantibodies against phospholipidsappear independently, while in secondary APS phospholipid antibodies aredetected in conjunction with other autoimmune diseases, such as lupuserythematosus, rheumatoid arthritis, or Sjögren’s syndrome. Phospholipidantibodies are detectable in only 1-5 % of healthy individuals, but they arefound in 16-35 % of lupus patients.The presence of anti-cardiolipin antibodies insystemic lupus erythematosus (SLE) can be related to the development ofthrombosis and thrombocytopenia. In gynaecology they are supposed to causeintrauterine death or recurrent abortion. Furthermore, anti-cardiolipinantibodies have been detected in neurological disorders like cerebrovascularinsufficiency, cerebral ischemia, epilepsy or chorea.Anti-cardiolipin autoantibodies occur in theimmunoglobulin classes IgG, IgM or IgA. The determination of IgM antibodies isa valuable indicator in the diagnosis of beginning autoimmune diseases, whereasIgG antibodies are present in progressive stages of manifested autoimmunedisorders. The determination of IgA antibodies seems to have a greaterimportance in the African-Caribbean population.Quantitative measurement of anti-cardiolipinantibodies, especially IgG, shows high specificity in therapy-monitoring ofsecondary APS related to SLE.Clinical indications for determination ofanti-cardiolipin antibodies are: SLE, thrombosis, thrombocytopenia, cerebralischemia, chorea, epilepsy, recurrent abortion, intrauterine death.The discovery that anti-phospholipid antibodiesrecognize plasma proteins that are associated with phospholipids rather thanbinding to the phospholipids themselves has been a major advance in APSresearch. Several reports indicate that beta-2-glycoprotein I antibodies areclinically relevant. Recent studies suggest the presence of a dominant epitopeon the first domain of beta-2-glycoprotein I. In contrast to antibodiesrecognizing other domains of beta-2-glycoprotein I, anti-domain I antibodiesare found to be highly associated with clinical symptoms.Anti-cardiolipin and anti-beta-2-glycoprotein Iantibodies are independent risk factors for the occurrence of vascularthrombosis and pregnancy loss. However, patients testing positive for multipleantibody specificities generally have a more severe disease and higher recurrencerates despite treatment.Besides the standardized laboratory assays fordetection of anti-cardiolipin antibodies, antibodies directed tobeta-2-gycoprotein I and LA, defined in the classification criteria, severalother autoantibodies have shown to be relevant to APS. Among them areantibodies against negatively-charged phospholipids, like phosphatidyl serine,phosphatidyl inositol and phosphatidic acid (PA). These antigens can improvethe clinical sensitivity in patient samples with suspected APS but they willnot replace the determination of autoantibodies against cardiolipin orbeta-2-glycoprotein I.Autoantibodies that bind to proteins of thecoagulation cascade or complexes of these proteins with phospholipids have alsobeen proposed to be relevant for APS. As an example, a test foranti-prothrombin antibodies in conjunction with other parameters may be a goodrisk marker for thrombosis. Antibodies to Annexin V may also be detectablewithin the clinical framework of APS with otherwise negative phospholipidantibody results.