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Urinary excretion of histamine and methylhistamine after burns
Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medical and Health Sciences, Rehabilitation Medicine. Linköping University, Faculty of Health Sciences.ORCID iD: 0000-0003-4420-418X
Linköping University, Department of Medical and Health Sciences, Clinical Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Clinical Physiology UHL.
Linköping University, Department of Clinical and Experimental Medicine, Burn Center. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Sinnescentrum, Department of Plastic Surgery, Hand surgery UHL. Östergötlands Läns Landsting, Sinnescentrum, Department of Anaesthesiology and Surgery UHL.
2012 (English)In: Burns, ISSN 0305-4179, E-ISSN 1879-1409, Vol. 38, no 7, 1005-1009 p.Article in journal (Refereed) Published
Abstract [en]

Background: The increased vascular permeability seen after burn contribute to morbidity and mortality as it interferes with organ function and the healing process. Large efforts have been made to explore underlying pathophysiological mechanisms that generate increased vascular permeability after burns. Many different substances have been proposed as mediators of which histamine, serotonin and oxygen radicals are claimed most important. However, no specific blocker has convincingly been shown to be clinically effective. Early work has claimed increased histamine plasma-concentrations in humans after burn and data from animal models pointed at histamine as an important mediator. Modern human clinical studies investigating the role of histamine as a mediator of the generalized post burn increase in vascular permeability are lacking. less thanbrgreater than less thanbrgreater thanMethod: We examined histamine turnover by measuring the urinary excretion of histamine and methyl histamine for 48 h after burns in 8 patients (mean total burn surface area 24%). less thanbrgreater than less thanbrgreater thanResults: Over time, in this time frame and compared to healthy controls we found a small increase in the excretion of histamine, but no increase of its metabolite methylhistamine. less thanbrgreater than less thanbrgreater thanConclusion: Our findings do not support that histamine is an important mediator of the increased systemic vascular permeability seen after burn.

Place, publisher, year, edition, pages
Elsevier , 2012. Vol. 38, no 7, 1005-1009 p.
Keyword [en]
Burn, Histamine, Mediator, Oedema, Vascular permeability
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-85848DOI: 10.1016/j.burns.2012.02.014ISI: 000310410300008OAI: oai:DiVA.org:liu-85848DiVA: diva2:573288
Note

Funding Agencies|Research and Development Unit, Jamtland County Council, Sweden||

Available from: 2012-11-30 Created: 2012-11-30 Last updated: 2017-12-07
In thesis
1. Function of granulocytes after burns and trauma, associations with pulmonary vascular permeability, acute respiratory distress syndrome, and immunomodulation
Open this publication in new window or tab >>Function of granulocytes after burns and trauma, associations with pulmonary vascular permeability, acute respiratory distress syndrome, and immunomodulation
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: Our innate immunesystem protects us from infections but, since its methods is not all specific for microorganisms, may also induce collateral damage.

Severe physical injury often proved deadly throughout evolution. Such injuries may induce massive collateral damage. Nowadays we can initiate advanced critical care for affected patients and save them from imminent trauma-related death. We are therefore faced with the fact that the collateral damage from the immune system may pose a major threat to the patient, the pathophysiology of which is not amenable to direct medical treatment and which leaves us with only passive supportive measures.

In this thesis we investigated the role of leucocytes under such circumstances.

Our main aim was to understand better the role of leucocytes in the development of increased vascular permeability after burns and trauma.

More specifically we investigated the impact of an injury on the function of leucocytes such as the dynamic change of certain cell-surface receptors on the leucocytes and in their numbers and immature forms. We wanted to find out if the increased pulmonary vascular permeability after a burn could be mediated through heparin binding protein (HBP) released from granuloctes, and whether HBP could be used as a biomarker for respiratory failure after trauma. We also wanted to confirm the possible role of histamine as a mediator of the systemic increase in vascular permeability after burns.

Methods: The dynamic change of cell-surface receptors was measured by flow-acquired cytometer scanning (FACS) on blood samples taken after burns. The concentrations of HBP after a burn and mechanical trauma were analysed in plasma. Pulmonary vascular permeability after a burn was assessed using transpulmonary thermodilution. The histamine turnover after a burn was assessed with high performance liquid chromatography (HPLC) for concentrations of histamine and methylhistamine in urine.

Results: We confirmed earlier investigations showing altered expression of receptors on leucocytes after a burn, receptors intimately associated with leucocyte functions (study I). In a pilot study of 10 patients we measured plasma concentrations of HBP and found them to be increased soon after a burn (study II). This finding was not confirmed in a larger, more extensive and specific study of 20 patients. We did, however, find an association between alterations in the number of leucocytes soon after a burn and pulmonary vascular permeability, indicating that they had a role in this process (study III).

In another study of trauma (non burn) we found an association between the concentration of HBP in early plasma-samples after injury and the development of ARDS, indicating that granulocytes and HBP have a role in its aetiology (study IV).

We found a small increase in urinary histamine and normal urinary methylhistamine concentrations but had anticipated a distinct increase followed by a decrease after reading the current papers on the subject. This indicates that the role of histamine as a mediator of increased vascular permeability after burns may have been exaggerated (study V).

Conclusions: We conclude that leucocytes are affected by burns and trauma, and it is likely that they contribute to the development of respiratory failure and acute respiratory distress syndrome (ARDS). HBP is a candidate biomarker for the early detection of ARDS after trauma, and the white blood count (WBC) is a useful biomarker for the detection of decreased oxygenation soon after a burn.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2013. 72 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1362
Keyword
ARDS, azurocidin, burn, CAP-37, critical care, granulocyte, HBP, histamine, intensive care, leucocyte, leukocyte, mediator, methylhistamine, MOF, oedema, neutrophil, permeability, PMN, trauma, vascular permeability
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-94513 (URN)978-91-7519-632-9 (ISBN)
Public defence
2013-09-05, Elsa Brändström salen, Campus US, Linköpings universitet, Linköping, 09:00 (Swedish)
Opponent
Supervisors
Available from: 2013-06-25 Created: 2013-06-25 Last updated: 2014-03-24Bibliographically approved

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Bäckryd, EmmanuelGranerus, GöranSjöberg, Folke
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Department of Clinical and Experimental MedicineFaculty of Health SciencesRehabilitation MedicineClinical PhysiologyDepartment of Clinical Physiology UHLBurn CenterDepartment of Plastic Surgery, Hand surgery UHLDepartment of Anaesthesiology and Surgery UHL
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