The objective of this study was to conduct a systematic review of case reports documenting the development of antiphospholipid syndrome or antiphospholipid syndrome-related features after an infection.

We searched Medline, EMBASE, Web of Science, PubMed ePubs, and The Cochrane Library - CENTRAL through March 2015 without restrictions. Studies reporting cases of antiphospholipid syndrome or antiphospholipid syndrome-related features following an infection were included.

Two hundred and fifty-nine publications met inclusion criteria, reporting on 293 cases. Three different groups of patients were identified; group 1 included patients who fulfilled the criteria for definitive antiphospholipid syndrome (24.6%), group 2 included patients who developed transient antiphospholipid antibodies with thromboembolic phenomena (43.7%), and group 3 included patients who developed transient antiphospholipid antibodies without thromboembolic events (31.7%). The most common preceding infection was viral (55.6%). In cases that developed thromboembolic events Human immunodeficiency and Hepatitis C viruses were the most frequently reported. Parvovirus B19 was the most common in cases that developed antibodies without thromboembolic events. Hematological manifestations and peripheral thrombosis were the most common clinical manifestations. Positive anticardiolipin antibodies were the most frequent antibodies reported, primarily coexisting IgG and IgM isotypes. Few patients in groups 1 and 2 had persistent antiphospholipid antibodies for more than 6 months. Outcome was variable with some cases reporting persistent antiphospholipid syndrome features and others achieving complete resolution of clinical events.

Development of antiphospholipid antibodies with all traditional manifestations of antiphospholipid syndrome were observed after variety of infections, most frequently after chronic viral infections with Human immunodeficiency and Hepatitis C. The causal relationship between infection and antiphospholipid syndrome cannot be established, but the possible contribution of various infections in the pathogenesis of antiphospholipid syndrome need further longitudinal and controlled studies to establish the incidence, and better quantify the risk and the outcomes of antiphospholipid-related events after infection.

The association between the hepatitis C virus (HCV) infection and the risk of myocardial infarction (MI) and stroke has been previously investigated. However, the association between the HCV infection and the risk of venous thromboembolism (VTE) has not been extensively discussed. Using the Longitudinal Health Insurance Database 2000 (LHID2000), we selected 3686 patients with newly diagnosed HCV infection. We randomly selected 14,744 people with no HCV or hepatitis B virus (HBV) infection as comparison group and frequency matched them with patients with HCV infection according to their age, sex, and index year. The incidence density rates and hazard ratios (HRs) of deep vein thrombosis (DVT) and pulmonary embolism (PE) were calculated until the end of 2011. The mean follow-up duration of 5.14 years for the HCV cohort and 5.61 years for the non-HCV cohort, the overall incidence density rates of DVT were 7.92 and 3.51 per 10,000 person-years in the non-HCV group, and the HCV groups, respectively (crude HR = 2.25; 95% confidence interval [CI] = 1.21-4.21). After adjusted for age, sex, and comorbidities, the risk of DVT remained significantly higher in the HCV group than in the non-HCV group (adjusted HR = 1.96; 95% CI = 1.03-3.73). The overall incidence density rates of PE in the HCV and non-HCV groups were not significantly different (crude HR = 2.20; 95% CI = 0.94-5.14). HCV infection is associated with the risk of DVT in a long-term follow-up period.

Many infections are associated with antiphospholipid antibodies (aPLs). The purpose of this study was to investigate the prevalence, persistence, clinical significance, and characteristics of aPLs in hepatitis B virus (HBV)-infected patients.

This study included 143 patients with HBV infection and 32 healthy individuals as controls. The presence of anticardiolipin antibodies (aCL Ab), anti-β(2)-glycoprotein I antibodies (β(2)GPI Ab), and lupus anticoagulant (LA) was assessed.

The total prevalence of aPLs in HBV-infected patients was 12.6% (18 of 143). Of these 18 patients, 15 had low to medium titers of aCL Ab (10 with IgM, 4 with IgG, and 1 with both isotypes). β(2)GPI Ab and LA were detected in 3 (2.1%) and 2 (1.4%) patients with HBV infection, respectively. In follow-up specimens from 14 patients with elevated levels of aCL Ab or β(2)GPI Ab, 10 (71.4%) showed the persistent presence of aPLs. No clinical manifestations related to aPLs were identified.

In HBV-infected patients, the most frequently detected antiphospholipid antibodies were IgM aCL Ab, which have a weak association with the clinical manifestations of APS. Unlike the transient presence reported for other infection-associated aPLs, most aPLs were persistently detected over a 12-week period in patients with HBV infection.