Procalcitonin in Pediatric Allogeneic Hematopoietic Stem Cell Transplant (aHSCT) Recipients
Year: 2011
Type: article
Study design: Observational Study
Abstract: The mortality of aHSCT remains unacceptably high and is often related to inflammation from infection and/or graft-versus-host disease (GVHD). Identifying markers of inflammation may allow tailoring of therapy in high-risk patients (pts). Studies show PCT as a useful marker in assessing the severity of bacterial infections. We conducted a prospective pilot study measuring serial procalcitonin (PCT) and other inflammatory markers in pediatric aHSCT pts. The goal of this ongoing study is to identify biomarkers that would be predictive of infection and other post-transplant complications. Pts were enrolled prior to preparative regimen, and serum was collected pre-transplant, day of stem cell infusion (D0), biweekly until engraftment, and on day 30, 60, and 100. Samples were run using Time Resolved Amplified Cryptate Emission technology. Thirteen pts have been enrolled, with a median age of 10 (1-21) years and the following diagnoses: AML (4), ALL (2), bone marrow failure (4), thalassemia (2), and sickle cell disease (1). Stem cell sources include HLA matched related donor (4), matched unrelated donor (8), and sibling cord (1). The conditioning regimen was ablative in 7 and reduced intensity in 6. To date, we have pre-transplant and D0 data on all pts. Median PCT values showed significant differences at the 2 time points (pre-transplant 0.105 ng/dl [0.000-0.350] vs D0 0.315 ng/dl [0.035-7.230], p 0.02] with no effect from conditioning regimen. Of pts with blood culture positive sepsis (2), neither had PCT > 2.0 ng/dl. Pts with GVHD (6) did not have an elevation in PCT. One pt requiring intensive care for acute renal failure and development of respiratory failure due to parainfluenza had significantly elevated PCT (peak 20 ng/dl). This data suggest that an elevation in PCT on D0 is associated with inflammation caused by preparative regimens. Although the exact mechanism of PCT is unknown, it is hypothesized that PCT synthesis is induced by TNF-α or IL-6, which are known to play a role in preparative regimen-induced inflammation. We are currently measuring GM-CSF, IFN-γ, IL-1β, IL-2, IL-6, IL-8, IL-10, IL-12p70, and TNF-α by multiplex assay to correlate with PCT levels and clinical outcomes. We hypothesize that PCT will be lower on DO after reduced intensity regimens given less inflammation and toxicity. More subjects need to be enrolled to determine whether D0 levels are predictive of toxicity and whether post-transplant PCT can predict GVHD and/or infection.
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $3,650
OpenAlex ID: W2004668936