Status:
Ready to upload
Record number:
1425
Adverse Occurrence type:
MPHO Type:
Time to detection:
3 - 8 months
Alerting signals, symptoms, evidence of occurrence:
A kidney transplant recipient underwent plasma exchange between March and June 2012 and received 59 units of blood products. Signs of liver cytolysis were noted from June 2012, with detection of HEV RNA and weakly reactive IgM a few months later. A second patient, a liver transplant recipient, received 93 units of blood products and was found to be HEV RNA positive 8 months post-transplant. Both patients and their respective organ donors tested negative for HEV RNA at time of transplant; they received FFP from a common donor who was shown to be viraemic at the time of apheresis donation.
Demonstration of imputability or root cause:
Two cases of HEV transmission by 2 units of Intercept-treated plasma; the incriminated FFPs resulted from the same apheresis donation that was amotosalen/UVA light treated before segmentation in 3 units. Two of the 3 units were transfused to the 2 patients described above; the third was transfused to a patient who died 2 days following transfusion. The 2 FFP recipients and the donor were infected by a genotype 3f strain presenting a strict homology on partial sequences of the open reading frame 1 (ORF1) and ORF2 regions. All other blood donations for these patients tested negative for HEV RNA.
Imputability grade:
3 Definite/Certain/Proven
Groups audience:
Keywords:
Suggest new keywords:
FFP
plasmapheresis
amotosalen
UVA
Intercept
pathogen reduction
pathogen inactivation
HEV
Reference attachment:
Suggest references:
Hauser, L., Roque-Alfonso, A.M., Beyloune, A., Simonet, M., Deau Fischer, B., Burin des Toziers, N.,Mallet,V., Tiberghien, P. and Bierling, P. (2014). Hepatitis E transmission by transfusion of Intercept blood system-treated plasma.Blood 123(5):796-797.
Expert comments for publication:
Non-enveloped viruses such as HEV are known to be resistant to pathogen reduction strategies such as solvent/detergent treatment. In the case of amotosalen/UVA treatment, the difficulty in amotosalen penetration through tight non-enveloped viral capsids may explain the lack or low level of activity.