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Combined Near-infrared Fluorescent Imaging and Micro-computed Tomography for Directly Visualizing Cerebral Thromboemboli
Published on: September 25, 2016
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Influenza-associated thrombotic microangiopathies
1Division of Nephrology, The Montreal Children's Hospital, McGill University Health Centre, 1001, boul. Décarie-Room B RC.6651, Montréal, QC, H4A 3J1, Canada. martin.bitzan@mcgill.ca.
Pediatric Nephrology (Berlin, Germany)
|September 9, 2017
Summary
Influenza virus can trigger thrombotic microangiopathy (TMA), including hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Many patients had complement gene mutations, suggesting infection uncovers underlying genetic predispositions.
Area of Science:
- Hematology
- Virology
- Genetics
Background:
- Thrombotic microangiopathy (TMA) encompasses disorders like hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).
- The role of influenza virus as a trigger for HUS or TTP is not fully understood.
Purpose of the Study:
- To review and analyze cases of influenza-associated TMA.
- To investigate the clinical and epidemiological characteristics of influenza-triggered HUS/TTP.
Main Methods:
- Literature survey in PubMed and Google Scholar using keywords: HUS, TTP, TMA, influenza.
- Extraction and analysis of reported epidemiological and clinical data from identified cases.
Main Results:
- 25 cases of influenza-associated TMA identified; 5 linked to influenza vaccination.
- Influenza A was prevalent (83%), particularly during the 2009 A(H1N1) pandemic.
- Complement gene mutations were found in 7/8 tested patients, suggesting genetic predisposition.
Conclusions:
- Influenza-mediated HUS/TTP is rare but can be severe, with significant mortality (12%).
- Infection may unmask underlying complement pathway dysregulation.
- Further research is needed on viral factors, complement activation, ADAMTS13 antibodies, and treatment strategies.
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