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Poster Session
SLE Organ manifestations: clinical and pathogenesis
237 Ischaemic stroke in systemic lupus erythematosus, -distribution of subtypes and a risk genotype in the stat4 gene
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  1. E Svenungsson1,
  2. L Hopia2,
  3. A Laveskog3,
  4. A Jönsen4,
  5. D Leonard5,
  6. JT Gustafsson1,
  7. I Gunnarsson1,
  8. A Zickert6,
  9. G Nordmark5,
  10. AA Bengtsson4,
  11. K Elvin7,
  12. JK Sandling8,
  13. AC Syvänen8,
  14. L Rönnblom5 and
  15. M Andersson2
  1. 1Karolinska Institutet, Unit of Rheumatology- Department of Medicine- Solna, Stockholm, Sweden
  2. 2Karolinska Institutet, Department of Clinical Neuroscience, Stockholm, Sweden
  3. 3Karolinska Institutet, Department of Neuroradiology, Stockholm, Sweden
  4. 4Lund University, Department of Clinical Sciences- Section of Rheumatology, Lund, Sweden
  5. 5Uppsala University, Department of Medical Sciences- Section of Rheumatology, Uppsala, Sweden
  6. 6Karolinska Institutet, Unit of Rheumatology- Department of Medicine- Huddinge, Stockholm, Sweden
  7. 7Karolinska Institutet, Unit of Clinical Immunology- Department of Clinical Immunology and Transfusion Medicine-, Stockholm, Sweden
  8. 8Uppsala University, Department of Medical Sciences- Molecular Medicine, Uppsala, Sweden

Abstract

Background and aims We investigated the distribution of ischaemic stroke subtypes, classified according the Trial of Org 10 172 in Acute Stroke Treatment (TOAST) system, among patients with systemic lupus erythematosus (SLE). Genetic susceptibility in the signal transducer and activator of transcription factor 4 (STAT4) gene, defined by the single nucleotide polymorphism (SNP) rs10181656(G) were explored.

Methods We identified 69/665 SLE patients with stroke. Medical charts were retrieved and brain, cardiac and vascular imaging at the time of stroke were examined. Classification was performed according to TOAST: large-artery atherosclerosis (LAA), cardioembolism (CE), small-artery occlusion (SAO), stroke of other determined aetiology (OC) and stroke of undetermined aetiology (UE). Occurrence of the anti-phospholipid syndrome (APS) was documented. Evaluators were blinded to genotypes. General population controls (n=658) and SLE patients free from previous cerebrovascular disease (n=517) were used as comparators.

Results 56/69 patients with ischaemic stroke had charts with sufficient information for TOAST classification. Median age was 52 (17-84) years, 91% were female. All strokes classified as OC were attributed to APS. TOAST classification is presented in Table 1. Stroke of OE/APS and CE origin were associated with the STAT4 risk genotype as presented in Table 2.

Abstract 237 Table 1
Abstract 237 Table 1

Distribution of ischemic stroke subtypes in patients with SLE according to TOAST classification

Abstract 237 Table 2
Abstract 237 Table 2

Association of the risk allele, STAT4 single nucleotide polymorphism (SNP) rs10181656 (G), in SLE patients with ischemic stroke overall and stroke subtypes, specified according to the TOAST classification

Conclusions The majority of ischaemic strokes among SLE patients were of APS or CE origin. These two subtypes were associated with genetic susceptibility in the STAT4 gene. Patients with APS associated strokes were remarkably young. STAT4 genotype could, in addition to antiphospholipid antibodies and echocardiography, add information about stroke risk and help identify patients who will benefit from prophylactic anticoagulation treatment.

https://doi.org/10.1136/lupus-2017-000215.237

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