Full Papers
A one-point increase in the Damage Index for Antiphospholipid Syndrome (DIAPS) predicts mortality in thrombotic antiphospholipid syndrome
P. Gaspar1, F. Farinha2, Z. Sayar3, M. Efthymiou4, H. Cohen5, D.A. Isenberg6
- Department of Internal Medicine 2, North Lisbon University Hospital Centre, Lisbon, and Instituto de Medicina Molecular João Lobo Antunes, Faculty of Medicine, University of Lisbon, Portugal. pedrosilvagaspar@gmail.com
- Centre for Rheumatology, Division of Medicine, University College London, UK.
- Department of Haematology, University College London Hospitals NHS Foundation Trust, London, UK.
- Haemostasis Research Unit, Department of Haematology, University College London, UK.
- Department of Haematology, University College London Hospitals NHS Foundation Trust, London, and Haemostasis Research Unit, Department of Haematology, University College London, UK.
- Centre for Rheumatology, Division of Medicine, University College London, and Department of Rheumatology, University College London Hospitals NHS Foundation Trust, London, UK.
CER15635
2023 Vol.41, N°3
PI 0605, PF 0612
Full Papers
PMID: 35819804 [PubMed]
Received: 28/02/2022
Accepted : 09/05/2022
In Press: 11/07/2022
Published: 23/03/2023
Abstract
OBJECTIVES:
To determine whether early damage and its kinetics measured by the Damage Index for Antiphospholipid Syndrome (DIAPS) predicts mortality.
METHODS:
We carried out a single-centre retrospective analysis of thrombotic APS patients (2006 Sydney criteria), using the DIAPS for damage assessment. Early damage was considered to be at six months after disease onset; early damage increase (delta-DIAPS) was deemed to be at least a one-point rise in DIAPS within the first five years of illness. Groups were compared using appropriate statistical tests. Survival was analysed by the Kaplan-Meier method. Cox regression analysis was performed to investigate predictors of mortality.
RESULTS:
A total of 197 patients (71.1% female; 65.9% primary APS; 72.4% Caucasian) were followed for up to 43 years (median 10). Damage developed in 143 (73.6%) patients. Twenty-three patients (12%) died. Secondary APS (HR 3.07, 95%CI 1.32–7.12, p=0.009), male sex (HR 3.14, 95%CI 1.35–7.33, p=0.008) and age at APS onset ≥40 years (HR 5.34, 95%CI 1.96–14.53, p=0.001) were risk factors for death. Early damage (n=69, 35.0%) was not associated with death (p=0.231). Having a first arterial event was associated with early damage (p<0.001), but not with delta-DIAPS (p=0.539) nor with the risk of death (p=0.151). Delta-DIAPS (n=53/181, 29.3%) predicted mortality (HR 5.40, 95%CI 2.33–12.52, p<0.001), even after adjusting individually for APS category (secondary), sex (male), early damage and age at APS onset (≥40 years) (all p<0.005).
CONCLUSIONS:
Evolving damage in the first five years of illness, but not early damage, predicted mortality regardless of the nature of the first thrombotic event, sex, APS category and age.
