Background/Purpose:   Infection has been increasingly reported in the literature as an environmental trigger inducing the development of anti-phospholipid antibodies or antiphospholipid syndrome in genetically predisposed individuals. We conducted a systematic review and meta-analysis of observational studies to evaluate the risk of developing positive antiphospholipid (aPL) antibodies following infection compared to controls and determine whether these antibodies are associated with any clinical consequences.

Methods: We conducted a literature search using Medline, EMBASE, Web of Science, and the Cochrane CENTRAL databases with no language restriction to identify observational studies reporting on patients who develop positive aPL antibodies after infection from inception up to October 2013. Two independent reviewers assessed the studies for inclusion and for quality, and extracted relevant data. We extracted data on the related infection, profile and prevalence of aPL antibody, and patient clinical outcomes. We performed a meta-analysis and estimated relative risks (RR) with 95% confidence intervals (CI) of developing antibodies after an infection compared to controls

Results:  From 2,257 unique citations, 320 publications met our inclusion criteria; from these, we selected 216 studies with controls to estimate risk. The most commonly reported infections were viral and bacterial. Compared to controls, patients with an infection were 10.9 times more likely to develop positive IgG anticardiolipin (aCL) antibodies after the infection (95% confidence Intervals (CI) 5.6-21.2). The highest risk ratio (RR) was observed after infection with tuberculosis (47.5; 95% CI 3.0-753.8), Q fever (44.0; 95% CI 2.8-702.5), and Hepatitis C virus infection (21.4; 95% CI 3.6-127.1). After an infection with Epstein Bar virus individuals were 33 times more likely to develop positive IgM aCL (95%CI 1.9-586.2) compared to controls. The RRs for developing lupus anticoagulant or and anti-β2 glycoprotein-I (GPI) antibodies were 2.4 (95% CI 1.3-4.5), and 2.3 (95%CI 1.2-4.4), respectively. For studies without controls (104), the pooled incidence of positive IgG aCL after infection was 36% (95% CI 27%-45%). The highest incidence was found in individuals with human immunodeficiency virus (HIV) (51%; 95% CI 38%-63%). Development of clinical manifestations of aPL syndrome was reported in 52.3% of the included studies. The most common manifestations were thromboembolic events or pregnancy related complications, occurring in 23.1% of individuals.

Conclusion:  Various viral and bacterial infections can frequently induce the development of aPL antibodies, and can cause thromboembolic manifestations fulfilling the diagnosis of APS.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/risk-of-developing-antiphospholipid-syndrome-following-infection-a-systematic-review-and-meta-analysis-of-observational-studies/