Dataset Information

Sex Differences in Clinical Characteristics and Prognosis in Primary Thrombotic Antiphospholipid Syndrome.

ABSTRACT:

Objectives

This study aimed to investigate whether there are sex differences in clinical characteristics and prognosis in patients with primary thrombotic antiphospholipid syndrome (ptAPS).

Methods

From January 2013 to July 2021, 154 consecutive patients diagnosed with ptAPS were prospectively recruited. Multivariable Cox regression was used to evaluate the association between gender and the composite endpoint including thromboembolic recurrence or all-cause death during follow-up.

Results

Totally, 80 (52%) male and 74 (48%) female patients with ptAPS were included, and men had a higher percentage of smokers/ex-smokers [50 (62%) vs. 6 (8%), p < 0.001] and hyperhomocysteinemia [26 (32%) vs. 9 (12%), p = 0.003]. The baseline thromboembolic events were similar in two genders, except for limb ischemia [15 (19%) in men vs. 1 (1%) in women, p < 0.001]. During a median follow-up of 42 months, the composite endpoint occurred in 30 (38%) male and 15 (20%) female patients (p = 0.019). Male gender [HR 2.499, 95% CI (1.316, 4.743), p = 0.005] and warfarin administration [HR 0.482, 95% CI (0.257, 0.905), p = 0.023] remained independent risk factors for the composite endpoint. Male gender [HR 3.699, 95% CI (1.699, 8.246), p = 0.001] and isolated lupus anticoagulant positivity [HR 2.236, 95% CI (1.039, 4.811), p = 0.040] were independent risk factors for thromboembolic recurrence.

Conclusion

There are sex disparities in the clinical characteristics in patients with ptAPS and the male gender is an independent risk factor for the poor prognosis. Male patients with isolated lupus anticoagulant (LA) positivity have the highest risk of thromboembolic recurrence.

SUBMITTER: Huang Y

PROVIDER: S-EPMC9289156 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by pregnancy morbidity or thrombosis and persistent antiphospholipid antibodies (aPL) that bind to the endothelium and induce endothelial activation, which is evidenced by the expression of adhesion molecules and the production of reactive oxygen species (ROS) and subsequent endothelial dysfunction marked by a decrease in the synthesis and release of nitric oxide (NO). These endothelial alterations are the key components for the development of severe pathological processes in APS. Patients with APS can be grouped according to the presence of other autoimmune diseases (secondary APS), thrombosis alone (thrombotic APS), pregnancy morbidity (obstetric APS), and refractoriness to conventional treatment regimens (refractory APS). Typically, patients with severe and refractory obstetric APS exhibit thrombosis and are classified as those having primary or secondary APS. The elucidation of the mechanisms underlying these alterations according to the different groups of patients with APS could help establish new therapies, particularly necessary for severe and refractory cases. Therefore, this study aimed to evaluate the differences in endothelial activation and dysfunction induced by aPL between patients with refractory obstetric APS and other APS clinical manifestations. Human umbilical vein endothelial cells (HUVECs) were stimulated with polyclonal immunoglobulin-G (IgG) from different groups of patients n = 21), including those with primary (VTI) and secondary thrombotic APS (VTII) and refractory primary (RI+), refractory secondary (RII+), and non-refractory primary (NR+) obstetric APS. All of them with thrombosis. The expression of adhesion molecules; the production of ROS, NO, vascular endothelial growth factor (VEGF), and endothelin-1; and the generation of microparticles were used to evaluate endothelial activation and dysfunction. VTI IgG induced the expression of adhesion molecules and the generation of microparticles and VEGF. RI+ IgG induced the expression of adhesion molecules and decreased NO production. RII+ IgG increased the production of microparticles, ROS, and endothelin-1 and reduced NO release. NR+ IgG increased the production of microparticles and endothelin-1 and decreased the production of VEGF and NO. These findings reveal differences in endothelial activation and dysfunction among groups of patients with APS, which should be considered in future studies to evaluate new therapies, especially in refractory cases.