Volume 30, Issue 4 pp. 382-388
Article
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Anticardiolipin antibodies in patients with systemic lupus erythematosus

Gunnar Sturfelt MD, PhD

Corresponding Author

Gunnar Sturfelt MD, PhD

Associate Professor, Department of Rheumatology

Department of Rheumatology, University Hospital, Lund, Sweden, and the Department of Immunology, the National Bacteriological Laboratory, Stockholm, Sweden

Department of Rheumatology, University Hospital, S-221 85 Lund, SwedenSearch for more papers by this author
Ola Nived MD, PhD

Ola Nived MD, PhD

Professor, Department of Immunology

Department of Rheumatology, University Hospital, Lund, Sweden, and the Department of Immunology, the National Bacteriological Laboratory, Stockholm, Sweden

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Renée Norberg MD, PhD

Renée Norberg MD, PhD

Professor, Department of Immunology

Department of Rheumatology, University Hospital, Lund, Sweden, and the Department of Immunology, the National Bacteriological Laboratory, Stockholm, Sweden

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Rigmor Thorstensson PhD

Rigmor Thorstensson PhD

Department of Immunology

Department of Rheumatology, University Hospital, Lund, Sweden, and the Department of Immunology, the National Bacteriological Laboratory, Stockholm, Sweden

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Katarina Krook

Katarina Krook

Laboratory Assistant, Department of Immunology

Department of Rheumatology, University Hospital, Lund, Sweden, and the Department of Immunology, the National Bacteriological Laboratory, Stockholm, Sweden

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First published: April 1987
Citations: 104

Abstract

We studied a group of 59 unselected patients with systemic lupus erythematosus (SLE); these patients were from a defined population who lived in southern Sweden. We found that serum concentrations of anticardiolipin antibodies were increased in 32 SLE patients (54.2%). No significant correlation between increased amounts of anticardiolipin antibodies and clinical symptoms, such as thrombocytopenia or thrombosis, was found. Serial serum samples from 28 patients (12 patients were from the epidemiologic cohort) were analyzed. Sixteen of these 28 patients (57.1%) had increased levels of anticardiolipin antibodies; in most cases, there was no variation in these values with regard to clinical disease flares or treatment. Increased concentrations of anticardiolipin were observed in 4 patients with cerebral infarction. However, very high concentrations of anticardiolipin antibodies were observed in several patients with inactive SLE who had no history of thrombosis or thrombocytopenia. Our results underscore the importance of studying unselected patient groups when correlating laboratory data with clinical manifestations of disease.

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