Heparin-binding protein as a biomarker of gastrointestinal dysfunction in critically ill patients: a retrospective cross-sectional study in China

Abstract

<jats:sec><jats:title>Objective</jats:title><jats:p>To investigate the association of plasma heparin-binding protein (HBP) with the development of acute gastrointestinal injury (AGI) in critically ill patients.</jats:p></jats:sec><jats:sec><jats:title>Design</jats:title><jats:p>Clinical retrospective cross-sectional study.</jats:p></jats:sec><jats:sec><jats:title>Setting</jats:title><jats:p>A general teaching hospital in China.</jats:p></jats:sec><jats:sec><jats:title>Participants</jats:title><jats:p>Adult patients (age ≥18 years) admitted to our department with an intensive care unit (ICU) stay ≥5 days.</jats:p></jats:sec><jats:sec><jats:title>Main outcome measures</jats:title><jats:p>HBP levels were recorded twice or more within 5 days after admission. The initial AGI grades and the worst AGI grades within 5 days after admission, the number of patients receiving total enteral nutrition (TEN) and the number of patients with feeding intolerance (FI) and with sepsis were also recorded, along with some clinical severity and outcome variables.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>From June 2018 to May 2019, 221 patients were enrolled in this study. We divided patients into four groups based on the HBP values: HBP ≤20 ng/mL, 20&lt;HBP ≤50 ng/mL, 50&lt;HBP ≤100 ng/mL and HBP &gt;100 ng/mL. Significant differences were found in the ratios of AGI deterioration and TEN and the incidence rates of FI and sepsis among the four groups. Differences were also found among the groups regarding the worst AGI grades. The area under receiver operating characteristic curves for AGI deterioration, severe AGI (grades II or above), TEN and FI were 0.738 (p=0.001), 0.774 (p&lt;0.001), 0.810 (p&lt;0.001) and 0.729 (p=0.001), respectively. The optimal HBP cut-off values for AGI deterioration and severe AGI were 53.27 ng/mL and 41.26 ng/mL, respectively. However, no differences in ICU duration or 28-day mortality were found.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>HBP levels were associated with gastrointestinal dysfunction in critically ill patients. Increased HBP was positively correlated with sepsis but it was not correlated with 28-day mortality.</jats:p></jats:sec>

The need for biomarkers to determine response to enteral nutrition during and after critical illness: an update

“…Studied biomarkers are summarized in Table 1, which needs to be interpreted with caution as none of the presented studies is able to provide definitive answers regarding the dynamics and usefulness of putative markers [4 ▪▪ ,20,21,33,34,36 ▪ ,37,39–42,53,54]. Very recently, Jenkins and colleagues have reached similar conclusions regarding both the current absence and the future necessity of biomarkers of GI dysfunction [55 ▪ ].…”

“…Trefoil factor 3 (TFF3), another marker potentially reflecting intestinal epithelial damage, has been shown to discriminate between abdominal sepsis and other GI surgery as well as between survivors and nonsurvivors [40]. Heparin-binding protein (HBP) has been shown to associate independently with EFI and with the severity of the acute gastrointestinal injury (AGI) [41].…”

A scoping review considering potential biomarkers or functional measures of gastrointestinal dysfunction and enteral feeding intolerance in critically ill adults

“…The majority of studies (n=17; 77%) were in a mixed ICU population (1,(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34). Three studies (14%) were conducted in surgical/trauma patients (35)(36)(37) and the remaining two studies (9%) in medical ICU patients (38,39).…”

Azurocidin 1 inhibits the aberrant proliferation of triple‑negative breast cancer through the regulation of pyroptosis

“…As an inflammatory mediator, AZU1 can increase the permeability of vascular endothelial cells, thus leading to vascular leakage and neutrophil extravasation ( 16 ). In addition, it could also activate inflammatory cells to release pro-inflammatory factors and cause systemic inflammatory response syndrome in severe cases, such as sepsis, in which the expression level of AZU1 is positively associated with the severity of disease ( 17 , 18 ). However, its role in TNBC remains unclear.…”