Pentasystem embolism associated with transient antiphospholipid antibodies in severe M. pneumoniae pneumonia: a “Dual-Hit” case report and systematic review
- 1Department of Pediatric Critical Care Medicine, Sichuan Provincial Maternity and Child Health Care Hospital , , ,
- 2Department of Radiology, Sichuan Provincial Maternity and Child Health Care Hospital , , ,
Abstract
Background: Thromboembolism is a critical complication of severe Mycoplasma pneumoniae pneumonia (SMPP) in children, yet its clinical spectrum and immunothrombotic mechanisms remain poorly defined. The “dual-hit” hypothesis—synergy between infection-induced inflammation and transient antiphospholipid antibodies (aPLs)—lacks integrated clinical validation.
Methods: We report a case of extensive multi-system thrombosis in a 6-year-old boy with SMPP. A systematic review of literature (January 2020–December 2025) identified 19 studies comprising 199 pediatric cases.
Results: In the index case, thrombosis coincided with hyperinflammation and transient aPLs, which seroconverted to negative upon recovery. Pooled analysis showed multi-system involvement in 27.1% of cases (54/199). Among tested patients (n = 65; 32.7% of the cohort), aPL positivity was 69.2% (45/65). Most patients achieved favorable outcomes with anticoagulation and immunomodulation.
Conclusion: This study is consistent with the “dual-hit” model in SMPP, where systemic inflammation may prime the endothelium and transient aPL positivity coincides with an extensive thrombotic burden. The high prevalence of multi-system involvement supports low-threshold vascular imaging and aPLs screening, along with biomarker-guided management. Transient aPLs should be interpreted as a potential risk-amplifying biomarker rather than a proven causal driver of thrombosis.
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BibTeX
@article{hu2026pentasystem,
title = {{Pentasystem embolism associated with transient antiphospholipid antibodies in severe M. pneumoniae pneumonia: a “Dual-Hit” case report and systematic review}},
author = {Yuhang Hu and Jian Chen and Lijuan Wu and Jing Xu and Xuemei Xu and Juan Du and Min Kang and Xianmin Wang},
journal = {Frontiers in immunology},
year = {2026},
month = sep,
doi = {10.3389/fimmu.2026.1845246},
url = {https://europepmc.org/article/PMC/PMC13661489},
note = {CC BY},
}
RIS
TY - JOUR
TI - Pentasystem embolism associated with transient antiphospholipid antibodies in severe M. pneumoniae pneumonia: a “Dual-Hit” case report and systematic review
AU - Yuhang Hu
AU - Jian Chen
AU - Lijuan Wu
AU - Jing Xu
AU - Xuemei Xu
AU - Juan Du
AU - Min Kang
AU - Xianmin Wang
PY - 2026
DA - 2026/09/30
JO - Frontiers in immunology
DO - 10.3389/fimmu.2026.1845246
UR - https://europepmc.org/article/PMC/PMC13661489
AB - Background: Thromboembolism is a critical complication of severe Mycoplasma pneumoniae pneumonia (SMPP) in children, yet its clinical spectrum and immunothrombotic mechanisms remain poorly defined. The “dual-hit” hypothesis—synergy between infection-induced inflammation and transient antiphospholipid antibodies (aPLs)—lacks integrated clinical validation. Methods: We report a case of extensive multi-system thrombosis in a 6-year-old boy with SMPP. A systematic review of literature (January 2020–December 2025) identified 19 studies comprising 199 pediatric cases. Results: In the index case, thrombosis coincided with hyperinflammation and transient aPLs, which seroconverted to negative upon recovery. Pooled analysis showed multi-system involvement in 27.1% of cases (54/199). Among tested patients (n = 65; 32.7% of the cohort), aPL positivity was 69.2% (45/65). Most patients achieved favorable outcomes with anticoagulation and immunomodulation. Conclusion: This study is consistent with the “dual-hit” model in SMPP, where systemic inflammation may prime the endothelium and transient aPL positivity coincides with an extensive thrombotic burden. The high prevalence of multi-system involvement supports low-threshold vascular imaging and aPLs screening, along with biomarker-guided management. Transient aPLs should be interpreted as a potential risk-amplifying biomarker rather than a proven causal driver of thrombosis.
SN - 1664-3224
ER -