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Published on: September 9, 2012
Antiphospholipid antibodies in pediatric patients with prolonged activated partial thromboplastin time during
Katrin Frauenknecht1, Karl Lackner, Philipp von Landenberg
1Institute for Clinical Chemistry and Laboratory Medicine, Johannes Gutenberg University of Mainz, 55131 Mainz, Germany.
Insights
Infections can commonly cause elevated antiphospholipid antibodies (aPL), which may explain prolonged activated partial thromboplastin time (aPTT) in children. This suggests aPL presence during infection may precede autoimmune activity.
Area of Science:
- Immunology
- Hematology
- Pediatrics
Background:
- Antiphospholipid antibodies (aPL) are associated with thrombotic events.
- The role of infection-induced aPL and their association with prolonged activated partial thromboplastin time (aPTT) in children requires further investigation.
Purpose of the Study:
- To investigate the association between infection-related antiphospholipid antibodies (aPL) and prolonged activated partial thromboplastin time (aPTT) in children.
- To determine the prevalence of specific aPL (anti-cardiolipin, anti-phosphatidylserine, anti-beta2-glycoprotein I) in children with and without infections and prolonged aPTT.
Main Methods:
- Sera from 122 children were analyzed using ELISA for aPL (cardiolipin, phosphatidylserine, beta2-glycoprotein I).
- Groups included children with infections and prolonged aPTT, children with prolonged aPTT without infection, children with infections, and healthy controls.
- Lupus anticoagulant and Factor XII were also assessed.
Main Results:
- Elevated aPL were detected in 89.2% of infected children with prolonged aPTT.
- IgM anti-beta2-glycoprotein I antibodies were significantly higher in infected children with prolonged aPTT compared to controls.
- Increased IgG and IgM anti-phosphatidylserine antibodies and IgG anti-cardiolipin antibodies were observed in infected children and those with prolonged aPTT.
Conclusions:
- Infections commonly lead to elevated aPL in children, potentially explaining mild aPTT prolongation.
- The presence of aPL during infection may be an early indicator, possibly preceding autoimmune disease development.
- No significant difference in specificity was found compared to pathogenic aPL; duration of presence may trigger autoimmunity.
Objective:
To investigate the close association between different antiphospholipid antibodies (aPL) caused by infection and their appearance together with a prolonged activated partial thromboplastin time (aPTT).
Methods:
Sera from 122 children were evaluated in this study. Thirty-seven children with mild to medium prolonged aPTT (>37.2s) and elevated C-reactive protein (CRP) levels during various forms of infections (group 2), 18 children without infections (group 3) but with mild to medium prolonged aPTT and 13 children with infections (group 4) and with elevated CRP-level as well as a control group (group 1) of 54 patients without any infection and normal aPTT and negative CRP levels were investigated with commercially available ELISA tests (AESKU.Diagnostics, Wendelsheim, Germany) for the presence of antibodies directed against cardiolipin (CL), phosphatidylserine (PS) and beta2-glycoprotein I (beta 2GPI). The cutoff for positive results was defined with the healthy, aged matched control group (group 1) using the mean OD values plus 2 standard deviations. The lupus anticoagulant (dilute Russell's Viper Venom time, dRVVT) and coagulation Factor XII were determined with routine tests (Dade Behring).
Results:
Detection of at least one antibody to phospholipids was possible in 89.2% of group 2. It could be shown that IgM anti-beta 2GPI antibodies were found in 27 (59.5%) of group 2, but only in 1 (5.6%) of group 3 (p=0.024) and only in 4 (7.4%) of the controls (p=0.014). The presence of IgG-anti-beta 2GPI antibodies showed no significant difference in the different groups. Furthermore, children of groups 2, 3 and 4 had statistically significant higher levels of antibodies against PS IgG and PS IgM than controls. Also, antibodies to CL of the IgG-type were more frequently detected in children of group 2 than in controls (p=0.038). Detection of CL-IgM antibodies did not reach a significant level in the comparison of the different groups.
Conclusion:
During commonly acquired infections elevation of aPL of nearly all types seems to be a common process. Mild prolongation of aPTT might reflect this presence of aPL in the course of the infectious disease. Our data suggest that there exists no differences in specificity in comparison to the "pathogenic" aPL but the presence over time might be the trigger for the autoimmune activity to begin.
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