Title: Procalcitonin in early allograft dysfunction after orthotopic liver transplantation: A
retrospective single centre study
Version: 1 Date: 22 Jul 2022
Reviewer's report:
Frick et al report on the impact of early allograft dysfunction and Ischemia reperfusion injury
on early post transplant procalcitonin levels. This is a single center retrospective study of 110
patients who underwent LTx between 2016 and 2020. The authors report higher levels of peak
procalcitonin levels in patients developing EAD and IRI, but better graft survival in patients with
IRI who have elevated procalcitonin levels. The authors suggest that procalcitonin can serve as
an early marker of adverse outcomes in patients manifesting IRI.
The hypothesis is interesting and needs further study in larger studies.
1. The present study itself has drawbacks due to its retrospective nature, significant missing data
and significant skewing of patient enrolment towards sicker recipients.
2. The key point appears to be the inability of the graft liver to produce procalcitonin despite
significant IRI is a predictor of graft loss. Were there any differences in donor or graft parameters
between IRI+PCT<15 and IRI+PCT>15 groups which could have predicted worse outcomes.
3. In Table 4, nearly half of recipients needed RRT in the post-operative period. This is a very
high incidence of RRT? Does this affect Procalcitonin levels?
4. How the authors explain the high incidence of reoperation and arterial complications, which
are essentially surgical complications in the EAD group. Does a proinflammatory milieu
increase risk of these complications?
Title: Procalcitonin in early allograft dysfunction after orthotopic liver transplantation: A
retrospective single centre study
Version: 1 Date: 22 Jul 2022
Reviewer's report:
Frick et al report on the impact of early allograft dysfunction and Ischemia reperfusion injury
on early post transplant procalcitonin levels. This is a single center retrospective study of 110
patients who underwent LTx between 2016 and 2020. The authors report higher levels of peak
procalcitonin levels in patients developing EAD and IRI, but better graft survival in patients with
IRI who have elevated procalcitonin levels. The authors suggest that procalcitonin can serve as
an early marker of adverse outcomes in patients manifesting IRI.
The hypothesis is interesting and needs further study in larger studies.
1. The present study itself has drawbacks due to its retrospective nature, significant missing data
and significant skewing of patient enrolment towards sicker recipients.
2. The key point appears to be the inability of the graft liver to produce procalcitonin despite
significant IRI is a predictor of graft loss. Were there any differences in donor or graft parameters
between IRI+PCT<15 and IRI+PCT>15 groups which could have predicted worse outcomes.
3. In Table 4, nearly half of recipients needed RRT in the post-operative period. This is a very
high incidence of RRT? Does this affect Procalcitonin levels?
4. How the authors explain the high incidence of reoperation and arterial complications, which
are essentially surgical complications in the EAD group. Does a proinflammatory milieu
increase risk of these complications?
Please review this paper.
user
Title: Procalcitonin in early allograft dysfunction after orthotopic liver transplantation: A
retrospective single centre study
Version: 1 Date: 22 Jul 2022
Reviewer's report:
Frick et al report on the impact of early allograft dysfunction and Ischemia reperfusion injury
on early post transplant procalcitonin levels. This is a single center retrospective study of 110
patients who underwent LTx between 2016 and 2020. The authors report higher levels of peak
procalcitonin levels in patients developing EAD and IRI, but better graft survival in patients with
IRI who have elevated procalcitonin levels. The authors suggest that procalcitonin can serve as
an early marker of adverse outcomes in patients manifesting IRI.
The hypothesis is interesting and needs further study in larger studies.
1. The present study itself has drawbacks due to its retrospective nature, significant missing data
and significant skewing of patient enrolment towards sicker recipients.
2. The key point appears to be the inability of the graft liver to produce procalcitonin despite
significant IRI is a predictor of graft loss. Were there any differences in donor or graft parameters
between IRI+PCT<15 and IRI+PCT>15 groups which could have predicted worse outcomes.
3. In Table 4, nearly half of recipients needed RRT in the post-operative period. This is a very
high incidence of RRT? Does this affect Procalcitonin levels?
4. How the authors explain the high incidence of reoperation and arterial complications, which
are essentially surgical complications in the EAD group. Does a proinflammatory milieu
increase risk of these complications?
assistant