Alcohol and drug abuse in burn injuries

Haum, A.; Perbix, Walter; Häck, H.J.; Stark, Greg; Spilker, G.; Doehn, M.

doi:10.1016/0305-4179(95)80008-c

Cited by 75 publications

(43 citation statements)

References 9 publications

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“…Nearly one million burn injuries are reported in the United States every year, and 50% of these injuries occur in individuals under the influence of alcohol/ethanol (EtOH) (4)(5)(6)(7)(8). Studies indicate that intoxicated patients have higher rates of septic complications, longer hospital stays and increased mortality compared with patients who have a similar extent of burn injury but did not consume EtOH before injury (7)(8)(9)(10)(11). There is evidence that EtOH intoxication combined with burn injury abrogates the host immune system.…”

Section: Introductionmentioning

confidence: 99%

Activation of Toll-Like Receptor 2 Prevents Suppression of T-Cell Interferon γ Production by Modulating p38/Extracellular Signal-Regulated Kinase Pathways following Alcohol and Burn Injury

Rendón

Akhtar

et al. 2012

Mol Med

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Recent studies indicate that toll-like receptors (TLRs) are expressed on T cells and that these receptors directly or indirectly activate the adaptive immune system. We have shown previously that acute alcohol/ethanol (EtOH) intoxication combined with burn injury suppresses mesenteric lymph node (MLN) T-cell interleukin-2 (IL-2) and interferon γ (IFN-γ) production. We examined whether direct stimulation of T cells with TLR2, 4, 5 and 7 agonists modulates CD3-mediated T-cell IL-2/IFN-γ release following EtOH and burn injury. Male mice were gavaged with EtOH (2.9 gm/kg) 4 h prior to receiving an ~12.5% total body surface area sham or full-thickness burn injury. Animals were killed on d 1 after injury and T cells were purified from MLN and spleens. T cells were cultured with plate-bound anti-CD3 in the presence or absence of various TLR ligands. Although TLR2, 4 and 5 agonists potentiate anti-CD3-dependent IFN-γ by T cells, the TLR2 agonist alone induced IFN-γ production independent of CD3 stimulation. Furthermore, T cells were treated with inhibitors of myeloid differentiation primary response protein 88 (MyD88), TIR domain-containing adaptor protein (TIRAP), p38 and/or extracellular signal-regulated kinase (ERK) to determine the mechanism by which TLR2 mediates IL-2/IFN-γ production. IL-2 was not influenced by TLR agonists. MyD88 and TIRAP inhibitory peptides dose-dependently diminished the ability of T cells to release IFN-γ. p38 and ERK inhibitors also abolished TLR2-mediated T-cell IFN-γ. Together, our findings suggest that TLR2 directly modulates T-cell IFN-γ production following EtOH and burn injury, independent of antigen-presenting cells. Furthermore, we demonstrated that MyD88/TIRAP-dependent p38/ERK activation is critical to TLR2-mediated T-cell IFN-γ release following EtOH and burn injury.

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Section: Introductionmentioning

confidence: 99%

Activation of Toll-Like Receptor 2 Prevents Suppression of T-Cell Interferon γ Production by Modulating p38/Extracellular Signal-Regulated Kinase Pathways following Alcohol and Burn Injury

Rendón

Akhtar

et al. 2012

Mol Med

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“…The importance of ethanol as a complicating factor regarding burn injury is underscored by the finding that nearly 50% of the patients with burn injuries have detectable levels of ethanol in their circulation at the time of admission (Haum et al, 1995;Howland and Hingson, 1983;Thal et al, 1985). In addition, patients who consume ethanol before sustaining a burn injury demonstrate increased susceptibility to bacterial infections and subsequent mortality (Brezel et al, 1998;Kelley and Lynch, 1992;McGill et al, 1995).…”

mentioning

confidence: 97%

Interleukin‐4 Treatment Restores Cellular Immunity After Ethanol Exposure and Burn Injury

Messingham

Heinrich

Schilling

et al. 2002

Alcoholism Clin & Exp Res

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“…Burns by flame were commonest (130, 47.6%), followed by scalding (96, 35.2%), contact (23,8.4%), chemical (22,8.1%), and electrical (1, 0.4%).…”

Section: Resultsmentioning

confidence: 98%

“…Fauerbach et al 16 and Dyster-Aas et al 6 report drug and alcohol use disorders within their burns patient groups in the order of 6 to 24%, and 32% to 41%, respectively; and multiple authors have reported positive blood alcohol readings on nearly half of the patients presenting with burns in the United States. [21][22][23][24][25][26][27][28][29][30][31][32] This is significant as intoxicated patients suffer delayed wound healing, longer hospital stays, higher infection rates, and higher overall mortality; when compared to their sober counterparts. 21,23-25,27-31 Choudhry and Chaudry suggest that alcohol impairs intestinal immunity, and a smaller burn combined with alcohol intoxication can cause impairments in host defence.…”

mentioning

confidence: 99%

A 365-Day View of the Difficult Patients Treated in an Australian Adult Burn Center

Alexander

Coghlan

Greenwood

2015

Journal of Burn Care & Research

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Although the effect of burns on mental health has been well examined, the aims of this study were to determine the prevalence of pre-existing mental health, drug and alcohol, and forensic problems in an Australian burn patient population; examine differences between these groups in terms of burns characteristics and healing; and also establish any patterns of presentation amongst these groups. Retrospective case notes of all the acute burn admissions, 273 patients, into a busy tertiary adults burn center in a full year were reviewed. Almost half of the patients admitted had underlying complex issues. Those with psychotic, forensic, and/or drug and alcohol problems tended to stay longer in hospital and required more procedures, despite burn sizes comparable with those in the general population. These patients also tended to sustain their burn injuries, and present to hospital, on a Saturday, Sunday, or Monday, rarely coming later in the week. Those with depression/anxiety had similar lengths of stay, number of procedures and random temporal presentations to the general burns population. Burn centers should be well staffed and educated in how to deal with patients with complex needs; this staffing should be actively structured to deal with a clear pattern of presentation over the weekend and Monday.

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Alcohol and drug abuse in burn injuries

Cited by 75 publications

References 9 publications

Activation of Toll-Like Receptor 2 Prevents Suppression of T-Cell Interferon γ Production by Modulating p38/Extracellular Signal-Regulated Kinase Pathways following Alcohol and Burn Injury

Activation of Toll-Like Receptor 2 Prevents Suppression of T-Cell Interferon γ Production by Modulating p38/Extracellular Signal-Regulated Kinase Pathways following Alcohol and Burn Injury

Interleukin‐4 Treatment Restores Cellular Immunity After Ethanol Exposure and Burn Injury

A 365-Day View of the Difficult Patients Treated in an Australian Adult Burn Center

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