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  • 1. Bergquist, Maria
    et al.
    Samuelsson, Line
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Larsson, Anders
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Johansson, Joakim
    Lipcsey, Miklos
    TNFR1, TNFR2, neutrophil gelatinase-associated lipocalin and heparin binding protein in identifying sepsis and predicting outcome in an intensive care cohort2020In: Scientific Reports, E-ISSN 2045-2322, Vol. 10, no 1, article id 15350Article in journal (Refereed)
    Abstract [en]

    To date no biomarkers can aid diagnosing sepsis with adequate accuracy. We set out to assess the ability of Tumor necrosis factor receptor (TNFR) 1 and 2, Neutrophil gelatinase-associated lipocalin (NGAL) and Heparin binding protein (HBP) to discriminate sepsis from non-infected critically ill patients in a large ICU cohort, and to evaluate their value to predict mortality at 30 days. Adult patients admitted to the ICU with an arterial catheter were included. Clinical data and blood samples were prospectively recorded daily. Diagnoses were set retrospectively. Descriptive statistics and logistic regression models were used. NGAL, TNFR1 and TNFR2 were higher in sepsis patients compared to other diagnoses, as well as in non-survivors compared to survivors. In addition, these biomarkers increased with increasing stages of acute kidney injury. TNFR1 and TNFR2 performed similarly to NGAL and CRP in identifying sepsis patients, but they performed better than CRP in predicting 30-day mortality in this ICU cohort. Thus, TNFR1 and TNFR2 may be particularly useful in identifying high risk sepsis patients and facilitate relevant health care actions in this group of sepsis patients.

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  • 2.
    Larsson, Anders
    et al.
    Dept of Medical Scienses, Clinical Chemistry, Uppsala University.
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Lipcsey, Miklos
    Dept of Surgical Scienses, Anaesthesiology and Intensive Care, Uppsala University.
    Bergquist, Maria
    Dept of Surgical Scienses, Anaesthesiology and Intensive Care, Uppsala University.
    Kultima, Kim
    Dept of Medical Scienses, Clinical Chemistry, Uppsala University.
    Mandic-Havelka, Aleksandra
    Dept of Molecular Medicine and Surgery, Karolinska University Hospital.
    Calprotectin is superior to procalcitonin as a sepsis marker and predictor of 30-day mortality in intensive care patients2020In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 80, no 2, p. 156-161Article in journal (Refereed)
    Abstract [en]

    Sepsis is the most frequent cause of death in the intensive care unit (ICU). A rapid and correct diagnosis and initiation of therapy is crucial for improving patient outcomes. The aim of this study was to compare the performance of calprotectin with the more widely used sepsis biomarker procalcitonin (PCT) in ICU patients. The performance of calprotectin and PCT as sepsis and prognostic markers for 30-d mortality was compared in a prospective, observational study in an eight-bed ICU. We investigated concentrations of the biomarkers in plasma collected at admission from all ICU patients admitted during a year (2012-2013, n = 271) together with simplified acute physiology 3 scores (SAPS3) and sequential organ failure assessment (SOFA) scores. The receiver operating characteristic (ROC) analysis showed a higher area under the curve (AUC) value for calprotectin (0.79) than for PCT (0.49) when used as a sepsis marker. The calprotectin concentrations at admission were higher in non-survivors than in survivors at day 30. In our study, calprotectin was superior to PCT for distinguishing between ICU patients with sepsis and non-sepsis patients. Calprotectin also had higher predictive ability regarding 30-d mortality.

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  • 3.
    Larsson, Niklas
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Gouveia-Figueira, Sandra
    Umeå University.
    Claesson, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Lehtipalo, Stefan
    Umeå University.
    Behndig, Anders
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Ophthalmology.
    Tyden, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Pinto, Rui
    Umeå University.
    Nording, M. L.
    Umeå University.
    Oxylipin Profiling In The Acute Respiratory Distress Syndrome2016In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 193, article id A4419Article in journal (Refereed)
  • 4.
    Larsson, Niklas
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Nording, Malin L.
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Lindberg, Richard
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Haney, Michael
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Oxylipin profiles during the first day of mechanical ventilation in an intensive care unit cohort: research letter2023In: Anesthesiology, ISSN 0003-3022, E-ISSN 1528-1175, Vol. 138, no 5, p. 561-563Article in journal (Other academic)
  • 5. Nelson, Axel
    et al.
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology. Unit of Research, Education and Development, Östersund.
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology. Unit of Research, Education and Development, Östersund.
    Bodelsson, Mikael
    Circulating syndecans during critical illness2017In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 125, no 5, p. 468-475Article in journal (Refereed)
    Abstract [en]

    Circulating syndecans are proposed to be markers of glycocalyx degradation and previous investigations have found higher plasma levels of syndecan-1 among patients with different pathological conditions. We wanted to investigate if levels of other syndecans (-2,-3 and -4) are altered during critical illness and compare the levels to syndecan-1. In 137 consecutive intensive care unit (ICU) patients with sepsis, cardiac arrest, gastrointestinal bleeding, intoxication or trauma, plasma levels of syndecan-1, -2, -3 and -4 were measured using ELISA. Syndecan-1 and syndecan-3 levels were similar among the different ICU patient groups but higher than controls. No differences in plasma levels of syndecan-2 or syndecan-4 were found neither among the different ICU patient groups nor compared to controls. All syndecans showed an association with mortality and the levels of syndecan-1 and -3 and correlated with each other. The results indicate that syndecan release is triggered by the physiological stress of critical illness in general and involves several subtypes such as syndecan-1 and syndecan-3.

  • 6.
    Ruge, Toralph
    et al.
    Department of Emergency and Internal Medicine, Skåne University Hospital, Malmö, Sweden; Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
    Larsson, Anders
    Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.
    Lipcsey, Miklós
    Department of Surgical Sciences, Anaesthesiology and Intensive Care Medicine, Uppsala University, Uppsala, Sweden.
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Eriksson, Mats
    Department of Surgical Sciences, Anaesthesiology and Intensive Care Medicine, Uppsala University, Uppsala, Sweden.
    A comparison between endostatin and conventional biomarkers on 30-day mortality and renal replacement therapy in unselected intensive care patients2021In: Biomedicines, E-ISSN 2227-9059, Vol. 9, no 11, article id 1603Article in journal (Refereed)
    Abstract [en]

    Endostatin may predict mortality and kidney impairment in general populations as well as in critically ill patients. We decided to explore the possible role of endostatin as a predictor of 30-day mortality, acute kidney injury (AKI), and renal replacement therapy (RRT) in a cohort of unselected intensive care unit (ICU) patients. Endostatin and creatinine in plasma were analyzed and SAPS3 was determined in 278 patients on ICU arrival at admission to a Swedish medium-sized hospital. SAPS3 had the highest predictive value, 0.85 (95% C.I.: 0.8–0.90), for 30-day mortality. Endostatin, in combination with age, predicted 30-day mortality by 0.76 (95% C.I.: 0.70–0.82). Endostatin, together with age and creatinine, predicted AKI with 0.87 (95% C.I.: 0.83–0.91). Endostatin predicted AKI with [0.68 (0.62–0.74)]. Endostatin predicted RRT, either alone [0.82 (95% C.I.: 0.72–0.91)] or together with age [0.81 (95% C.I.: 0.71–0.91)]. The predicted risk for 30-day mortality, AKI, or RRT during the ICU stay, predicted by plasma endostatin, was not influenced by age. Compared to the complex severity score SAPS3, circulating endostatin, combined with age, offers an easily managed option to predict 30-day mortality. Additionally, circulating endostatin combined with creatinine was closely associated with AKI development.

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  • 7.
    Samuelsson, Line
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Tyden, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Herwald, Heiko
    Hultin, Magnus
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Walldén, Jakob
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Steinvall, Ingrid
    Sjöberg, Folke
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Renal clearance of heparin-binding protein and elimination during renal replacement therapy: Studies in ICU patients and healthy volunteers2019In: PLOS ONE, E-ISSN 1932-6203, Vol. 14, no 8, article id e0221813Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Heparin-binding protein (HBP) is released by neutrophils upon activation, and elevated plasma levels are seen in inflammatory states like sepsis, shock, cardiac arrest, and burns. However, little is known about the elimination of HBP. We wanted to study renal clearance of HBP in healthy individuals and in burn patients in intensive care units (ICUs). We also wished to examine the levels of HBP in the effluent of renal replacement circuits in ICU patients undergoing continuous renal replacement therapy (CRRT).

    METHODS: We measured plasma and urine levels of HBP and urine flow rate in 8 healthy individuals and 20 patients in a burn ICU. In 32 patients on CRRT, we measured levels of HBP in plasma and in the effluent of the CRRT circuit.

    RESULTS: Renal clearance of HBP (median (IQR) ml/min) was 0.19 (0.08-0.33) in healthy individuals and 0.30 (0.01-1.04) in burn ICU patients. In ICU patients with cystatin C levels exceeding 1.44 mg/l, clearance was 0.45 (0.15-2.81), and in patients with cystatin C below 1.44 mg/l clearance was lower 0.28 (0.14-0.55) (p = 0.04). Starting CRRT did not significantly alter plasma levels of HBP (p = 0.14), and the median HBP level in the effluent on CRRT was 9.1 ng/ml (IQR 7.8-14.4 ng/ml).

    CONCLUSION: In healthy individuals and critically ill burn patients, renal clearance of HBP is low. It is increased when renal function is impaired. Starting CRRT in critically ill patients does not alter plasma levels of HBP significantly, but HBP can be found in the effluent. It seems unlikely that impaired kidney function needs to be considered when interpreting concentrations of HBP in previous studies. Starting CRRT does not appear to be an effective way of reducing HBP concentrations.

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  • 8.
    Strålin, Kristoffer
    et al.
    Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden; National Program Group for Infectious Diseases, National System for Knowledge-Driven Management within Swedish Healthcare, Sweden’s Regions in Collaboration, Sweden.
    Linder, Adam
    Department of Infectious Diseases, Skåne University Hospital, Lund, Sweden; Department of Clinical Sciences, Division of Infection Medicine, Lund University, Lund, Sweden.
    Brink, Magnus
    National Program Group for Infectious Diseases, National System for Knowledge-Driven Management within Swedish Healthcare, Sweden’s Regions in Collaboration, Sweden; Department of Infectious Diseases, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Benjaminsson-Nyberg, Patrik
    Department of Emergency Medicine, Linköping University Hospital, Linköping, Sweden; Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Svefors, Jesper
    Department of Infectious Diseases, Ryhov Hospital, Jönköping, Sweden.
    Bengtsson-Toni, Maria
    Department of Internal Medicine, Skåne University Hospital, Malmö, Sweden.
    Abelson, Christina
    Funäsdalen Primary Healthcare Centre, Funäsdalen, Sweden.
    Offenbartl, Karsten
    Expert and Consultant in Surgery, Jönköping County, Jönköping, Sweden.
    Björkqvist, Kristina
    Sepsisföreningen (Patient Organization), Sweden.
    Rosenqvist, Mari
    Department of Infectious Diseases, Skåne University Hospital, Malmö, Sweden.
    Rönnkvist, Annica
    Division of Inflammation and ageing, Karolinska University Hospital, Stockholm, Sweden.
    Svärd-Backlund, Jenny
    Health and Medical Care Administration, Stockholm, Sweden.
    Wallgren, Karin
    Department of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden.
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology. Department of Anesthesiology and Intensive Care, Östersund Hospital, Östersund, Sweden.
    Wallgren, Ulrika
    Fisksätra Primary Healthcare Centre, Stockholm, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Vicente, Veronica
    Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Ambulance Medical Service in Stockholm, Stockholm, Sweden.
    Cajander, Sara
    Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden; Department of Infectious Diseases, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Lipcsey, Miklós
    Department of Anesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, Sweden; Department of Surgical Sciences, Anesthesiology and Intensive Care Medicine, Uppsala University, Uppsala, Sweden.
    Nauclér, Pontus
    Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Kurland, Lisa
    Department of Emergency Medicine, Örebro University Hospital, Örebro, Sweden; Department of Medical Sciences, Örebro University, Örebro, Sweden; National Program Group for Emergency Care, National System for Knowledge-Driven Management within Swedish Healthcare, Sweden’s Regions in Collaboration, Sweden.
    Design of a national patient-centred clinical pathway for sepsis in Sweden2023In: Infectious Diseases, ISSN 2374-4235, E-ISSN 2374-4243, Vol. 55, no 10, p. 716-724Article in journal (Refereed)
    Abstract [en]

    Background: The World Health Organization has adopted a resolution on sepsis and urged member states to develop national processes to improve sepsis care. In Sweden, sepsis was selected as one of the ten first diagnoses to be addressed, when the Swedish government in 2019 allocated funds for patient-centred clinical pathways in healthcare. A national multidisciplinary working group, including a patient representative, was appointed to develop the patient-centred clinical pathway for sepsis.

    Methods: The working group mapped challenges and needs surrounding sepsis care and included a survey sent to all emergency departments (ED) in Sweden, and then designed a patient-centred clinical pathway for sepsis.

    Results: The working group decided to focus on the following four areas: (1) sepsis alert for early detection and management optimisation for the most severely ill sepsis patients in the ED; (2) accurate sepsis diagnosis coding; (3) structured information to patients at discharge after sepsis care and (4) structured telephone follow-up after sepsis care. A health-economic analysis indicated that the implementation of the clinical pathway for sepsis will most likely not drive costs. An important aspect of the clinical pathway is implementing continuous monitoring of performance and process indicators. A national working group is currently building up such a system for monitoring, focusing on extraction of this information from the electronic health records systems.

    Conclusion: A national patient-centred clinical pathway for sepsis has been developed and is currently being implemented in Swedish healthcare. We believe that the clinical pathway and the accompanying monitoring will provide a more efficient and equal sepsis care and improved possibilities to monitor and further develop sepsis care in Sweden.

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  • 9.
    Svensk, Erik
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Wallden, Jakob
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Limitations of care and comorbidities are associated with increased mortality in patients treated with non-invasive ventilation: a retrospective observational study in a single-center ICU2021In: F1000 Research, E-ISSN 2046-1402, Vol. 10, article id 865Article in journal (Refereed)
    Abstract [en]

    Background: Non-invasive ventilation (NIV) is a common treatment for acute respiratory failure in intensive care units (ICU). While there is increasing data on outcomes after NIV treatment, there are large variations in staffing and monitoring where NIV is provided, making results hard to generalize. The aim of this study was to characterize patients treated with NIV, describe outcomes, and identify factors associated with outcome in an ICU at a Swedish county hospital.

    Methods: A single-centre retrospective observational study during 2018 of patients treated with NIV in a six-bed ICU at a Swedish county hospital. Patient characteristics, including comorbidities, details of ICU stay, simplified acute physiology score (SAPS-3), details of NIV treatment and 30-day mortality were collected, and the Charlson co-morbidity index (CCI) was calculated. Primary outcomes were 30-day mortality and associated factors.

    Results: 92 patients with mean age (71,3, SD 12,1) were treated with NIV during the study period. 42 (46%) were women. Median CCI was 3 (25th-75th percentiles 1.4)) and median SAPS-3 score was 66 (25th-75th percentiles 58). The 30-day mortality was 37% and in the univariate analysis, SAPS-3 score >66, Charlson comorbidity index, CCI>=3, pCO2 <5.5 and limitation of care were factors associated with increased 30-day mortality. pH <7.35 and pO2<8 at admission showed no associations with 30-day mortality.

    Conclusions: We found that patients treated with NIV in ICU were a diverse population where comorbidities and presence of limitations of care might be considered as better predictors of 30-day mortality, rather than physiological parameters.

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  • 10.
    Tydén, Jonas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Heparin-binding protein and organ failure in critical illness2019Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Background: For patients severely ill enough to require care in an intensive care unit (ICU), both the disease itself (e.g. bacteria in the blood in sepsis or fractures after trauma) and effects of the immune system can cause circulatory, pulmonary, or renal dysfunction. Leukocytes play a dominant role in the immune system.  When activated they release a range of small proteins with different properties Heparin-binding protein (HBP) being one of these proteins, has many functions, including to increase vascular permeability. Heparin-binding protein causes plasma leakage from blood vessels into surrounding tissue (oedema), which can lead to  organ dysfunction depending on the site and degree of oedema formation. Increased concentration of HBP in plasma is associated with failing circulation and lung function in subgroups of critically ill patients.

    Aims: We investigated the possibility of using concentration of HBP in plasma for predicting circulatory, respiratory or renal failure in an ICU population with mixed diagnosis. We assessed concentration of HBP in alveoli in ventilator induced lung injury (VILI), and finally assessed elimination of HBP in urine and effluent fluid from continuous dialysis.

    Methods: In Papers I and II, HBP concentration in plasma was measured in 278 patients on admission to ICU. Sequential organ failure assessment (SOFA) scores and acute kidney injury (AKI) stage were recorded daily. In Paper III HBP concentration in bronco-alveolar fluid was measured in a pig model of ventilatory induced lung injury, in 16 healthy volunteers and in 10 intubated ICU patients. In Paper IV plasma and urine concentration of HBP was measured in 8 healthy volunteers and 20 burn ICU patients. In addition, HBP was sampled in plasma and effluent fluid in 32 ICU patients on continuous renal replacement therapy (CRRT).

    Results: In Paper I, patients developing circulatory failure (circulatory sub-score of SOFA = 4) had higher plasma concentration of HBP compared to those who did not (median(IQR)ng/ml) (63.5(32–105) vs 36.4(24–59)) p<0.01), and patients developing respiratory failure (P:F ratio < 27) had higher HBP concentration than those who did not (44.4(30-109) vs 35.2(23-57) p<0.01). Discriminatory capacity was (ROC AUC (95%CI)) (0.65 (0.54–0.76)) for circulatory failure and (0.61(0.54–0.69)) for respiratory failure. In Paper II, patients developing renal failure (AKI stage 2-3) had higher plasma concentration of HBP compared to those who did not (72.1 (13.0–131.2) vs 34.5 (19.7–49.3) p<0.01). Discriminatory capacity for AKI stage 3 was 0.68(0.54-0.83) (ROC AUC (95%CI)). In the subgroup with severe sepsis, it was  0.93 (0.85–1.00). In Paper III, HBP concentration in bronchoalveolar lavage was higher in pigs subjected to injurious ventilation over 6 hours ventilation compared to controls (1144(359–1636) vs 89(33–191) p=0.02) (median(IQR)ng/ml). The median HBP concentration in bronchoalveolar lavage from healthy volunteers was 0.90(0.79– 1.01) compared to 1959(612–3306) from intubated ICU patients (p < 0.01).In Paper IV, renal clearance of HBP was 0.19 (0.08-0.33) in healthy individuals and 0.30 (0.01-1.04)  (median, IQR, ml/min)  in burn ICU patients. Clearance of HBP was higher in burn patients with increased cystatin C (0.45(0.15-2.81) vs. 0.28(0.14-0.55) p=0.04). Starting CRRT did not alter plasma concentration of HBP (p=0.14). Median HBP concentration in effluent fluid on CRRT was 9.1 ng/ml (7.8-14.4).

    Conclusions: Papers I and II:There is an association between high concentration of HBP in plasma on ICU admission and circulatory, respiratory and renal failure. For the individual patient, the predictive value of a high HBP concentration is low, with the possible exception of renal failure in septic patients. Paper III:HBP concentration in alveoli increases in pigs subjected to injurious ventilation. HBP concentration in alveoli of intubated ICU patients ventilated protectively is elevated to similar levels, a factor of approximately 1000 times higher than the concentration seen in healthy controls. Paper IV:In healthy study participants, renal clearance of HBP is low. In critically ill burn patients with impaired renal function, clearance of HBP is increased. Starting CRRT in critically ill patients does not alter plasma concentration of HBP. Still, HBP is found in the CRRT effluent fluid, and concentration does not appear to be dependent on plasma concentration.

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  • 11.
    Tydén, Jonas
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Herwald, H.
    Hultin, Magnus
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Walldén, Jakob
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Heparin-binding protein as a biomarker of acute kidney injury in critical illness2017In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 61, no 7, p. 797-803Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: There is no biomarker with high sensitivity and specificity for the development of acute kidney injury (AKI) in a mixed intensive care unit (ICU) population. Heparin-binding protein (HBP) is released from granulocytes and causes increased vascular permeability which plays a role in the development of AKI in sepsis and ischemia. The aim of this study was to investigate whether plasma levels of HBP on admission can predict the development of AKI in a mixed ICU population and in the subgroup with sepsis. METHODS: Longitudinal observational study with plasma HBP levels from 245 patients taken on admission to ICU. Presence and severity of AKI was scored daily for 1 week. RESULTS: Mean (95% CI) plasma concentrations of log HBP (ng/ml) in the groups developing different stages of AKI were: stage 0 (n = 175), 3.5 (3.4-3.7); stage 1 (n = 33), 3.7 (3.5-4.0), stage 2 (n = 20), 4.4 (3.5-4.8); and stage 3 (n = 17), 4.6 (3.8-5.2). HBP levels were significantly higher in patients developing AKI stage 3 (P < 0.01) compared to AKI stage 0 and 1. The area under the curve (AUC) for HBP to discriminate the group developing AKI stage 2-3 was 0.70 (CI: 0.58-0.82) and in the subgroup with severe sepsis 0.88 (CI: 0.77-0.99). CONCLUSION: Heparin-binding protein levels on admission to ICU are associated with the development of severe kidney injury. The relationship between HBP and AKI needs to be further validated in larger studies.

  • 12.
    Tydén, Jonas
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology. Department of Anaesthesiology and Intensive Care, Östersund Hospital, Östersund, Sweden.
    Herwald, Heiko
    Sjoberg, Folke
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology. Department of Surgical and Perioperative Sciences, Anaesthesiology and Intensive Care, Umeå University, Umeå, Sweden.
    Increased Plasma Levels of Heparin-Binding Protein on Admission to Intensive Care Are Associated with Respiratory and Circulatory Failure2016In: PLOS ONE, E-ISSN 1932-6203, Vol. 11, no 3, article id e0152035Article in journal (Refereed)
    Abstract [en]

    Purpose: Heparin-binding protein (HBP) is released by granulocytes and has been shown to increase vascular permeability in experimental investigations. Increased vascular permeability in the lungs can lead to fluid accumulation in alveoli and respiratory failure. A generalized increase in vascular permeability leads to loss of circulating blood volume and circulatory failure. We hypothesized that plasma concentrations of HBP on admission to the intensive care unit (ICU) would be associated with decreased oxygenation or circulatory failure.

    Methods: This is a prospective, observational study in a mixed 8-bed ICU. We investigated concentrations of HBP in plasma at admission to the ICU from 278 patients. Simplified acute physiology score (SAPS) 3 was recorded on admission. Sequential organ failure assessment (SOFA) scores were recorded daily for three days.

    Results: Median SAPS 3 was 58.8 (48-70) and 30-day mortality 64/278 (23%). There was an association between high plasma concentrations of HBP on admission with decreased oxygenation (p<0.001) as well as with circulatory failure (p<0.001), after 48-72 hours in the ICU. There was an association between concentrations of HBP on admission and 30-day mortality (p = 0.002). ROC curves showed areas under the curve of 0,62 for decreased oxygenation, 0,65 for circulatory failure and 0,64 for mortality.

    Conclusions: A high concentration of HBP in plasma on admission to the ICU is associated with respiratory and circulatory failure later during the ICU care period. It is also associated with increased 30-day mortality. Despite being an interesting biomarker for the composite ICU population it's predictive value at the individual patient level is low.

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  • 13.
    Tydén, Jonas
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology. Anestesiläkaravdelningen, Östersund Hospital, Östersund, Sweden.
    Larsson, Niklas
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Lehtipalo, Stefan
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Herwald, H
    Hultin, Magnus
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Walldén, Jakob
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Behndig, Annelie F.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Johansson, Joakim
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Anaesthesiology.
    Heparin-binding protein in ventilator-induced lung injury.2018In: Intensive Care Medicine Experimental, E-ISSN 2197-425X, Vol. 6, no 1, article id 33Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Although mechanical ventilation is often lifesaving, it can also cause injury to the lungs. The lung injury is caused by not only high pressure and mechanical forces but also by inflammatory processes that are not fully understood. Heparin-binding protein (HBP), released by activated granulocytes, has been indicated as a possible mediator of increased vascular permeability in the lung injury associated with trauma and sepsis. We investigated if HBP levels were increased in the bronchoalveolar lavage fluid (BALF) or plasma in a pig model of ventilator-induced lung injury (VILI). We also investigated if HBP was present in BALF from healthy volunteers and in intubated patients in the intensive care unit (ICU).

    METHODS: Anaesthetized pigs were randomized to receive ventilation with either tidal volumes of 8 ml/kg (controls, n = 6) or 20 ml/kg (VILI group, n = 6). Plasma and BALF samples were taken at 0, 1, 2, 4, and 6 h. In humans, HBP levels in BALF were sampled from 16 healthy volunteers and from 10 intubated patients being cared for in the ICU.

    RESULTS: Plasma levels of HBP did not differ between pigs in the control and VILI groups. The median HBP levels in BALF were higher in the VILI group after 6 h of ventilation compared to those in the controls (1144 ng/ml (IQR 359-1636 ng/ml) versus 89 ng/ml (IQR 33-191 ng/ml) ng/ml, respectively, p = 0.02). The median HBP level in BALF from healthy volunteers was 0.90 ng/ml (IQR 0.79-1.01 ng/ml) as compared to 1959 ng/ml (IQR 612-3306 ng/ml) from intubated ICU patients (p < 0.001).

    CONCLUSIONS: In a model of VILI in pigs, levels of HBP in BALF increased over time compared to controls, while plasma levels did not differ between the two groups. HBP in BALF was high in intubated ICU patients in spite of the seemingly non-harmful ventilation, suggesting that inflammation from other causes might increase HBP levels.

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