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      Elevated IgA and IgM anticardiolipin antibodies in acute Kawasaki disease.

      Radiology
      Acute Disease, Antibodies, Anticardiolipin, blood, immunology, Biological Markers, Child, Child Welfare, Child, Preschool, Female, Humans, Immunoglobulin A, Immunoglobulin G, Immunoglobulin M, Infant, Infant Welfare, Male, Mucocutaneous Lymph Node Syndrome

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          Abstract

          There is marked activation of the endothelium and immune system in Kawasaki disease. Anticardiolipin antibodies (aCL) can cause activation of the endothelium. We measured aCL levels in acute Kawasaki disease patients and compared them to other febrile patients to see whether their aCL responses were different. Twenty-one patients with acute Kawasaki disease and 16 patients with an acute febrile illness were recruited. The aCL levels were measured in the sera of febrile patients and in Kawasaki disease patients prior to immunoglobulin therapy. There was no significant difference between the IgG aCL levels (p = 0.87) between the Kawasaki disease and febrile patients. However, the IgM (p = 0.01) and IgA (p = 0.03) aCL were significantly higher in patients with acute Kawasaki disease than in febrile children. Elevation of IgA aCL has been reported in association with other vasculitides and IgA-secreting plasma cells have been demonstrated in the vascular tissue in Kawasaki disease. Copyright 2002 S. Karger AG, Basel

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          Immunoregulatory abnormalities in mucocutaneous lymph node syndrome.

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            Antiphospholipid antibody syndrome: Immunologic and clinical aspects

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              Anticardiolipin antibodies in acquired immunodeficiency syndrome.

              We undertook a prospective study of IgG and IgM anticardiolipin antibodies (ACAs) to determine their clinical significance in patients with acquired immunodeficiency syndrome (AIDS). IgG ACAs were found in 24 (92.3%) of 26 patients with AIDS who were hospitalized for pulmonary complaints (group 1) and in 13 (93%) of 14 patients with AIDS-related complex (group 2). In addition, 17 (94%) of 18 patients with AIDS (group 3) who had coagulation tests and were studied retrospectively had IgG ACAs. The prevalence of IgG ACAs in these three groups was significantly higher than in healthy controls, but was comparable to that in 31 consecutive patients with systemic lupus erythematosus (67.7%). The mean titer of IgG ACAs in group 1 was higher than in groups 2 and 3 but was not different from that in the patients with systemic lupus erythematosus. The frequency and titer of IgM ACAs in group 1 (7.6%) or group 2 (14.3%) were not significantly different from those in normal controls (4.7%). In contrast, half of the patients in group 3 had low-titer IgM ACAs. The serum titer of IgG ACAs in patients with AIDS with thrombocytopenia was significantly higher than it was in those with normal platelet counts. There was no association between ACAs and Pneumocystis carinii pneumonia or other infections, cancer, thrombosis, positive VDRL test, or presence of the lupus anticoagulant. The prevalence and titer of IgG or IgM ACAs were not associated with abnormal results of any coagulation test. Although we found IgG ACAs to be associated with thrombocytopenia in AIDS, their presence does not carry exactly the same clinical significance as it does in systemic lupus erythematosus. The high prevalence of ACAs in AIDS, in AIDS-related complex, and in otherwise healthy contacts with antibodies to human immunodeficiency virus suggests that their occurrence may be related to the underlying human immunodeficiency virus infection.
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