TOPLINE:

In patients with persistently positive antiphospholipid (aPL) antibodies, both a history of thrombosis and hematologic disease (autoimmune hemolytic anemia and/or thrombocytopenia) independently conferred an approximately twofold increased risk for incident thrombosis. 

METHODOLOGY:

• Researchers aimed to identify independent demographic, clinical, and laboratory risk factors for incident thrombosis among 1067 patients with persistently positive aPL antibodies (mean age > 43 years; ≥ 70% women) who were followed up for at least 1 year.
• Participants were required to meet the Revised Sapporo Classification Criteria for aPL antibody positivity; data were collected at enrollment and every 12 ± 3 months via a web-based application and included demographics, aPL antibody-related clinical characteristics, and laboratory values.
• Thrombosis was prospectively ascertained from patient reports; events included macrovascular arterial events such as myocardial infarction and cerebrovascular accident, macrovascular venous events such as venous thromboembolism and hepatic vein thrombosis, and catastrophic aPL syndrome.
• The mean follow‑up duration in this cohort was 4.43 years.

TAKEAWAY:

• A history of thrombosis emerged as an independent predictor of new thrombotic events (hazard ratio [HR], 2.34; P = .02).
• A history of hematologic disease (defined as persistent autoimmune hemolytic anemia or otherwise unexplained thrombocytopenia with platelet nadir < 100,000/μL) was also an independent predictor of incident thrombosis (HR, 1.95; P = .01).
• Among patients with hematologic disease, thrombocytopenia was significantly associated with thrombosis (P = .005), whereas autoimmune hemolytic anemia was not (P = .85).

IN PRACTICE:

“History of thrombosis is already widely regarded to be a significant risk factor for future thrombosis, not only among aPL-positive individuals but also in the general population,” the authors wrote.

“The finding that aPL-associated haematologic disease confers increased risk for thrombosis among aPL-positive patients is novel,” they added.

SOURCE:

The study was led by Jonathan Thaler, MD, Hospital for Special Surgery in New York City. It was published online on November 19, 2025, in Annals of the Rheumatic Diseases.

LIMITATIONS:

The number of patients with at least one thrombotic event was small. The retrospective nature of baseline data collection may have introduced potential bias. Additionally, reliance on investigator-reported causes of death may have affected the accuracy of outcome classification.

DISCLOSURES:

This study did not receive any specific grant. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.