Hepcidin discriminates sepsis from other critical illness at admission to intensive care

Abstract

Initial differential diagnosis and prognosis for patients admitted to intensive care with suspected sepsis remain arduous. Hepcidin has emerged as a potential biomarker for sepsis. Here we report data on the relevance of levels of hepcidin versus other biomarkers as a diagnostic and prognostic tool for sepsis. 164 adult patients admitted to the intensive care unit (ICU) within 24 h upon arrival to the hospital were included. Blood samples collected daily for seven consecutive days and hepcidin levels, heparin binding protein (HBP) levels and standard biomarkers were determined. Blood cultures were initiated at inclusion. Clinical scores were evaluated daily and mortality after 28- and 180-days was recorded. One hundred of the patients were found to fulfil the criteria for sepsis whereas 64 did not. Hepcidin levels at admission were significantly higher in the septic than in the non-septic patients. In septic patients hepcidin levels declined significantly already at 24 h followed by a steady decline. A significant negative correlation was observed between hepcidin levels and SAPS 3 in patients with sepsis. Hepcidin levels at inclusion were significantly higher among septic patients that survived 180-days and predicted mortality. Our data show that hepcidin levels are indicative of sepsis in patients admitted to the ICU and has a prognostic value for mortality.

Hepcidin, in contrast to heparin binding protein, does not portend acute kidney injury in patients with community acquired septic shock

“…In agreement with our earlier reported data, significantly increased levels of both hepcidin and HBP were recorded in the sepsis group compared to the non-sepsis group [ 37 ]. Median levels of hepcidin in the sepsis group at inclusion was 41.0 nmol/L, (IQR 21.5–66.5), compared to 14.0 nmol/L (IQR 4.2–37.0) in the non-sepsis group (p<0.001) ( Fig 2 ).…”

“…The patient cohort investigated herein does not include patients with CKD but were extracted from the same cohort as described by Olinder et al . where analysis of kidney failure was not reported [ 37 ]. The omission of patients with CKD, did not change the overall differences in hepcidin or HBP levels between sepsis and non-sepsis patients.…”

“…The patient cohort investigated in the present study has been described previously [ 37 ]. The sepsis patients were enrolled in line with the sepsis-3 definition–anamnesis/history of infection and SOFA score ≥ 2, and the patients in the non-sepsis group were admitted with totally different diagnosis, e .…”

Propofol and Dexmedetomidine Ameliorate Endotoxemia-Associated Encephalopathy via Inhibiting Ferroptosis

“…50 Some researchers contend that the anti-inflammatory effects of hepcidin, along with its increase during inflammation, make it a promising novel biomarker of sepsis. 53,54 During the inflammatory phase, microglia encounter LPS signals with toll-like receptor (TLR) 4. Through the secretion of IL-6, microglia stimulate astrocytes to increase hepcidin production.…”

Identifying biomarkers deciphering sepsis from trauma-induced sterile inflammation and trauma-induced sepsis

“…The sepsis group contained 23 patients with community acquired sepsis, included after admission to the ICU within 24 hours of arrival to the hospital in Helsingborg, Sweden. These sepsis patients were a subgroup of patients included in an earlier reported cohort (48). Inclusion criteria were; non-pregnant adults >18 years old with no surgery or blood transfusion during the 7 preceding days, and an expected ICU stay > 2 days (49).…”