Pathophysiology of polytrauma

Keel, Marius; Trentz, O.

doi:10.1016/j.injury.2004.12.037

Cited by 785 publications

(667 citation statements)

References 194 publications

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“…Superoxide anions are formed in the reperfusion phase of ischemia-reperfusion mechanism. Peroxynitrite, formed by the interaction of superoxide anion and NO, is an important free oxygen radical causing cellular damage (Laroux et al 2001;Keel and Trentz 2005). As in some other clinical trials (Prasad et al 2003), the levels of NO were found to be high especially on the postfracture 7th and 14th days in the present study.…”

Section: Discussionsupporting

confidence: 79%

“…When mechanical forces cause fractures (with local tissue damage), local and systemic host responses occur in order to protect the immune integrity and stimulate the reparative mechanisms (Rotstein 2003;Keel and Trentz 2005). Immunocompetant cells accumulate in the region of tissue damage where many local and systemic mediators are produced and released (Bone 1992;Rose and Marzi 1996).…”

Section: Discussionmentioning

confidence: 99%

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Time-Dependent Changes in Serum Nitric Oxide Levels after Long Bone Fracture

Keskin

Kızıltunç

2007

Tohoku J. Exp. Med.

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Nitric oxide (NO) is a free radical of physiological signifi cance. The changes in the production of NO during the fracture healing process are not well known. This clinical prospective study was planned to determine these changes in patients with fractured long bone(s), who underwent surgery in the 3rd week after fracture. The patients were divided into two groups: 20 patients with an isolated femoral fracture and 20 patients with multiple fractures, including a femoral fracture. Venous blood was drawn from the healthy volunteers (n = 20) once, and from the patients seven times during 21 days after fracture. NO level was measured as nitrite in each serum sample. The serum NO levels at all measurements of the patients were signifi cantly higher than those of the control subjects. The timedependent changes in the NO levels were similar in both patient groups. The serum NO levels were highest in the fi rst 6 hrs, and then decreased to the lowest level on the 3rd day. Subsequently, there was an increasing trend on the 5th, 7th and 14th days. At all times of the measurements, the NO levels were higher in patients with multiple fractures than in those with the femoral fracture, with the signifi cant difference observed at the 6 hrs and on the 7th day. The NO levels were decreased on the 21st day after surgery. The present study suggests that NO production may be increased in considerable amounts during the fi rst 2 weeks of fracture healing, particularly in the fi rst 6 hrs.human; bone; fracture; blood; nitric oxide © 2007 Tohoku University Medical PressNitric oxide (NO) is a physiological free radical, synthesized from the amino acid L-arginine by the 3 NO synthase (NOS) isoforms; neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). It functions in vascular regulation, host immune defense, neurotransmission, and other systems. While some diseases, like vascular dysfunctions, impair NO production, some diseases, like septic schock, cerebral infarction, diabetes mellitus and neurodegenerative disorders, augment NO production (Mori and Gotoh 2004). It is not clear how NO affects bone cells. Some studies show that NO has a biphasic effect on bone cell activity. It has been stated that moderate concentrations of NO produced by eNOS in the bone is necessary for normal osteoblast growth and fracture healing (Ralston 1997;Corbett et al. 1999). However, it was suggested that high concentrations of NO produced by cytokine-induced iNOS activity may inhibit the

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Time-Dependent Changes in Serum Nitric Oxide Levels after Long Bone Fracture

Keskin

Kızıltunç

2007

Tohoku J. Exp. Med.

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“…Multiple organ failure of various noninfectious causes (trauma, burn, myocardial infarction, pancreatitis) is well known to induce a rise in inflammatory cytokine levels. Therefore, it is not surprising that IL-6, IL-8, or TNF-α is not appropriate to discriminate between septic or non-septic causes of death [5,11].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of C-reactive protein, procalcitonin, tumor necrosis factor alpha, interleukin-6, and interleukin-8 as diagnostic parameters in sepsis-related fatalities

et al. 2011

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The aims of this study were to investigate the usefulness of serum C-reactive protein, procalcitonin, tumor necrosis factor alpha, interleukin-6, and interleukin-8 as postmortem markers of sepsis and to compare C-reactive protein and procalcitonin values in serum, vitreous humor, and cerebrospinal fluid in a series of sepsis cases and control subjects, in order to determine whether these measurements may be employed for the postmortem diagnosis of sepsis. Two study groups were formed, a sepsis group (eight subjects coming from the intensive care unit of two university hospitals, with a clinical diagnosis of sepsis in vivo) and control group (ten autopsy cases admitted to two university medicolegal centers, deceased from natural and unnatural causes, without elements to presume an underlying sepsis as the cause of death). Serum C-reactive protein and procalcitonin concentrations were significantly different between sepsis cases and control cases, whereas serum tumor necrosis factor alpha, interleukin-6, and interleukin-8 values were not significantly different between the two groups, suggesting that measurement of interleukin-6, interleukin-8, and tumor necrosis factor alpha is non-optimal for postmortem discrimination of cases with sepsis. In the sepsis group, vitreous procalcitonin was detectable in seven out of eight cases. In the control group, vitreous procalcitonin was clearly detectable only in one case, which also showed an increase of all markers in serum and for which the cause of death was myocardial infarction associated with multiorganic failure. According to the results of this study, the determination of vitreous procalcitonin may be an alternative to the serum procalcitonin for the postmortem diagnosis of sepsis.

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“…Postoperative host responses are therefore understood as being a balance of SIRS and CARS, but they have not been fully explored in surgery for esophageal cancer. Moreover, an imbalance between these dual immune responses, with an overwhelming release of pro-or anti-inflammatory cytokines, seems to be responsible for organ dysfunction and increased susceptibility to infections (5). Medical regulation of SIRS and CARS has been conducted to improve these adverse effects, but the most desirable means of regulation remains under investigation (6)(7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Postoperative immunosuppression cascade and immunotherapy using lymphokine-activated killer cells for patients with esophageal cancer: Possible application for compensatory anti-inflammatory response syndrome

Yamaguchi

Hihara²,

Hironaka³

et al. 2006

Oncol Rep

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Abstract.Immunological parameters were measured in order to elucidate a postoperative immunosuppression mechanism in transthoracic esophagectomy for patients with esophageal cancer. Moreover, lymphokine-activated killer (LAK) cells were transferred just after the surgery to overcome the postoperative immunosuppression. Fifteen consecutive patients who underwent transthoracic esophagectomy were subjected to the postoperative measurement of immunological parameters. Ten patients who underwent open cholecystectomy served as controls. Heparinized venous blood was obtained pre-and postoperatively, and serum levels of cytokines IL-6 and IL-10 and immunosuppressive acidic protein (IAP) were measured. Peripheral blood lymphocytes were harvested and analyzed by flow cytometry for phenotype detection and by a mixed lymphocyte reaction for detecting concanavalin (Con)-A-induced or -non-induced suppressor activity. Another 29 consecutive patients who underwent transthoracic esophagectomy were randomly enrolled in a postoperative immunotherapy trial either with or without lymphokineactivated killer cells. It was found that, in the esophagectomy group, IL-6 and IL-10 increased postoperatively and peaked on day 1, followed by an increase in IAP, peaked again on day 4, with a profound decrease in helper and cytotoxic T-cell subsets, followed by increases in Con-A-induced (on day 7 or later) and spontaneous (on day 10) suppressor activities. These changes were minimal in the cholecystectomy group. LAK cell transfer restored the postoperative decrease in the helper and cytotoxic T-cell population, and there was a trend of reduction for postoperative remote infection such as pneumonia and surgical site infection in the LAK therapy group. Taken together, we would like to propose the existence of a postoperative immunosuppression cascade consisting of increases in cytokines and immunosuppressive proteins, decreases in helper and cytotoxic T-cell populations, and the development of suppressor T-cell activities in surgery for esophageal cancer. Postoperative adoptive transfer of LAK cells may be a novel clinical application in surgery for esophageal cancer as a means of treating this postoperative immunosuppressive condition that may be identical to the status of compensatory anti-inflammatory response syndrome (CARS).

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Pathophysiology of polytrauma

Cited by 785 publications

References 194 publications

Time-Dependent Changes in Serum Nitric Oxide Levels after Long Bone Fracture

Time-Dependent Changes in Serum Nitric Oxide Levels after Long Bone Fracture

Evaluation of C-reactive protein, procalcitonin, tumor necrosis factor alpha, interleukin-6, and interleukin-8 as diagnostic parameters in sepsis-related fatalities

Postoperative immunosuppression cascade and immunotherapy using lymphokine-activated killer cells for patients with esophageal cancer: Possible application for compensatory anti-inflammatory response syndrome

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