Changes in novel haematological parameters following thermal injury: A prospective observational cohort study

Dinsdale, Robert J.; Devi, Amarpreet; Hampson, Peter; Wearn, Christopher M.; Bamford, Amy; Hazeldine, Jon; Bishop, Jonathan; Ahmed, Sumiya; Watson, Chris; Lord, Janet M.; Moiemen, Naiem; Harrison, Paul

doi:10.1038/s41598-017-03222-w

Cited by 24 publications

(14 citation statements)

References 33 publications

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“…In the present study, plasma MDA levels were significantly increased, thus demonstrating severe lipid peroxidation following considerable burn injury, a finding consistent with other studies (54,55). The pathophysiological alterations are most likely a consequence of ischemia/reperfusion injury and polymorphonuclear cell activation both locally and in the systemic circulation resulting in free-radical overgeneration (56,4). On the other hand, the depletion of plasma glutathione and antioxidant enzymes has been shown as a cause for the manifestations of the systemic oxidative response and the aggravation of the pathological processes in thermal trauma (57).…”

Section: Discussionsupporting

confidence: 92%

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Melatonin attenuates oxidative stress and modulates inflammatory response after experimental burn trauma

Hristova¹,

Bekyarova²,

Atanasova³

et al. 2018

JMMS

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Introduction. Thermal injury activates an inflammatory response. Melatonin possesses antioxidant and anti-inflammatory properties. The objective of the present work was to study melatonin effects on the inflammatory response under conditions of oxidative stress during the early stage of thermal injury. Materials and methods. We used 24 white male rats of Wistar breed, randomly divided into three experimental groups. Group one was the control, group two was inflicted with burn trauma, and group three was inflicted with burn trauma, with melatonin application following the thermal injury. Melatonin was applied twice in doses of 10 g/kg b.m. immediately after the burn trauma and again at 12 hours. Plasma levels of tumor necrosis-factor-α (TNF-α), a pro-inflammatory mediator, and of interleukin-10 (Il-10), an anti-inflammatory mediator, were examined and their ratio was calculated. The levels of malondialdehyde (MDA), an oxidative stress marker, were also estimated. Results. Thermal trauma significantly increased plasma TNF-α levels (ð<0.01) and TNF-α /IL-10 ratio but did not change IL-10 ones. Plasma MDA concentrations were significantly elevated as well (ð<0.0001). Melatonin application significantly reduced TNF-α (ð<0.05), increased IL-10 (ð<0.05), down-regulated TNF-α/IL-10 ratio and changed MDA concentrations (ð<0.01). In conclusion, our results show that local alteration induces oxidative stress and inflammatory response with TNF-α /IL-10 disbalance. Melatonin modulates this response and attenuates oxidative stress in experimental burn injury.

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Section: Discussionsupporting

confidence: 92%

“…Their count in systemic circulation also increases. (4) Tumor necrosis factor-α (TNF-α) is a cytokine presenting with a variety of biological effects (11) and…”

Section: Introductionmentioning

confidence: 99%

Melatonin attenuates oxidative stress and modulates inflammatory response after experimental burn trauma

Hristova¹,

Bekyarova²,

Atanasova³

et al. 2018

JMMS

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“…Their experimental results showed that MDW has a higher diagnostic performance than white cell count (WBC) in the diagnosis of sepsis. Ayres, Cornet, and Dinsdale also found that changes in the cellular complexity and nucleic acid content of neutrophils can reflect the infection status of the body, assisting the early diagnosis of sepsis (16)(17)(18)(19)(20)(21).…”

Section: Discussionmentioning

confidence: 97%

The clinical value of hematological neutrophil and monocyte parameters in the diagnosis and identification of sepsis

Zhang¹,

Zhang²,

Pan³

et al. 2021

Ann Transl Med

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“…sGPVI discriminatory power may further increase if used in combination with other strong sepsis predictive markers such as cell-free DNA and immature granulocytes. 37,38 This inflammatory trauma cohort presumably contained an abundance of healthy people who were essentially well and unencumbered before receiving their injury. Measurement of sGPVI on day 1 could potentially enable clinicians to stratify patients based on sepsis risk and aid clinical management of patients.…”

Section: Discussionmentioning

confidence: 99%

“…Ninety-nine patients with injury afflicting up to 95% total body surface area (TBSA) were recruited to the Scientific Investigation of the Biological Pathways Following Thermal Injury Study (SIFTI: REC-12/EM/0432) at the Queen Elizabeth Hospital, Birmingham, United Kingdom. 37,38 Citrated blood was collected at intervals after injury (day [D] 1, D3, D7, D14, D21, and D28 and month 2, 3, 6, and 12 postinjury). Sepsis diagnosis was made when more than 3 American Burn Association criteria 39 were met, plus positive bacterial culture and/or evidence of antibiotic response.…”

Section: Blood Collectionmentioning

confidence: 99%

Soluble GPVI is elevated in injured patients: shedding is mediated by fibrin activation of GPVI

Montague

Delierneux

Lecut³

et al. 2018

Blood Advances

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• Soluble GPVI is elevated in patients with thermal injury with sepsis, and sGPVI levels augment severity score prediction of mortality.• The GPVI ligand, fibrin, induces GPVI shedding without requirement for platelet activation or signaling Soluble glycoprotein VI (sGPVI) is shed from the platelet surface and is a marker of platelet activation in thrombotic conditions. We assessed sGPVI levels together with patient and clinical parameters in acute and chronic inflammatory conditions, including patients with thermal injury and inflammatory bowel disease and patients admitted to the intensive care unit (ICU)for elective cardiac surgery, trauma, acute brain injury, or prolonged ventilation. Plasma sGPVI was measured by enzyme-linked immunosorbent assay and was elevated on day 14 after thermal injury, and was higher in patients who developed sepsis. sGPVI levels were associated with sepsis, and the value for predicting sepsis was increased in combination with platelet count and Abbreviated Burn Severity Index. sGPVI levels positively correlated with levels of D-dimer (a fibrin degradation product) in ICU patients and patients with thermal injury. sGPVI levels in ICU patients at admission were significantly associated with 28-and 90-day mortality independent of platelet count. sGPVI levels in patients with thermal injury were associated with 28-day mortality at days 1, 14, and 21 when adjusting for platelet count. In both cohorts, sGPVI associations with mortality were stronger than D-dimer levels. Mechanistically, release of GPVI was triggered by exposure of platelets to polymerized fibrin, but not by engagement of G protein-coupled receptors by thrombin, adenosine 59-diphosphate, or thromboxane mimetics. Enhanced fibrin production in these patients may therefore contribute to the observed elevated sGPVI levels. sGPVI is an important platelet-specific marker for platelet activation that predicts sepsis progression and mortality in injured patients.

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Changes in novel haematological parameters following thermal injury: A prospective observational cohort study

Cited by 24 publications

References 33 publications

Melatonin attenuates oxidative stress and modulates inflammatory response after experimental burn trauma

Melatonin attenuates oxidative stress and modulates inflammatory response after experimental burn trauma

The clinical value of hematological neutrophil and monocyte parameters in the diagnosis and identification of sepsis

Soluble GPVI is elevated in injured patients: shedding is mediated by fibrin activation of GPVI

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