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Long-lasting chronic high load carriage of Epstein-Barr virus is more common in young pediatric renal transplant recipients.

Artikel i vetenskaplig tidskrift
Författare Susanne Westphal Ladfors
Jenny K Lindahl
Sverker Hansson
Per Brandström
Rune Andersson
Marianne Jertborn
Magnus Lindh
Susanne Woxenius
Vanda Friman
Publicerad i Pediatric nephrology (Berlin, Germany)
Volym 35
Nummer/häfte 3
Sidor 427-439
ISSN 1432-198X
Publiceringsår 2019
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 427-439
Språk en
Länkar dx.doi.org/10.1007/s00467-019-04401...
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Chronic high load carrier ,Barr virus. EBV DNA, Infection. Pediatric, Renal transplantation.
Ämneskategorier Urologi och njurmedicin

Sammanfattning

Epstein-Barr virus (EBV) infections can induce post-transplant lymphoproliferative disorder (PTLD). A chronic high load (CHL), as indicated by long-term high EBV DNA levels after transplantation, has been associated with an enhanced risk of PTLD. We aimed to evaluate incidence, time of occurrence, risk factors, and outcome of EBV CHL carrier state after pediatric renal transplantation.A retrospective study of 58 children aged 1-17 years (median 10), who underwent renal transplantation between January 2004 and June 2017 at a single medical center. EBV IgG antibodies in serum were analyzed before and yearly after transplantation. EBV DNA in whole blood were analyzed weekly for the first 3 months post-transplant, monthly up to 1 year and then at least once yearly. CHL was defined as EBV DNA ≥ 4.2 log10 Geq/ml in > 50% of the samples during ≥ 6 months.At transplantation, 31 (53%) patients lacked EBV IgG and 25 (81%) of them developed primary EBV infection post-transplant. Of the 27 seropositive patients, 20 (74%) experienced reactivation of EBV. Altogether, 14 (24%) children developed CHL, starting at a median of 69 days post-transplant and lasting for a median time of 2.3 years (range 0.5-6.5), despite reduction of immunosuppression. Patients with CHL were younger and 11/14 were EBV seronegative at transplantation. No child developed PTLD during median clinical follow-up of 7.8 years (range 0.7-13).CHL was frequent, long lasting, and occurred mainly in young transplant recipients. The absence of PTLD suggests that monitoring of EBV DNA to guide immunosuppression was effective.

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