Immunologie bei Schwerverletzten

Zusammenfassung. Der klinische Verlauf bei polytraumatisierten Patienten wird durch das h?ufige Auftreten schwerwiegender immunologischer Komplikationen beeintr?chtigt. Die Immunantwort auf schweres Trauma kann durch die vermehrte Freisetzung proinflammatorischer Mediatoren über das „systemic inflammatory response syndrome (SIRS)“ zum Mehrorganversagen [„multisystem organ failure (MOF)“] führen, welches mit einer Letalit?t von bis zu 80 % behaftet ist. Charakteristisch für die Entwicklung des Multiorganversagens ist das Auftreten des „remote organ failure (ROF)“, eine Fehlfunktion von Organen, die durch das eigentliche Trauma keinen direkten Schaden erlitten haben. Diese Arbeit gibt einen kurzen überblick über die neueren Entwicklungen auf dem Gebiet der tierexperimentell-immunologischen Traumaforschung und geht eingehend auf den aktuellen Stand der klinisch-immunologischen Traumaforschung ein. Insbesondere wird die Bedeutung der sog. pro- und antiinflammatorischen Cytokine bei der Entstehung von SIRS, MOF und ROF er?rtert. Trotz der vielen Fortschritte auf dem Gebiet der klinischen Immunologie und der vielf?ltigen Informationen über die Trauma-induzierten Immunfunktionsst?rungen müssen jedoch noch viele offene Fragen gel?st werden, bevor die immunologischen Ver?nderungen nach schwerem Trauma durch immunmodulatorische Therapieans?tze nachhaltig positiv beeinflu?t werden k?nnen.      

Surgical metabolism

Summary. Trauma, operative interventions, infection and other disturbances of homeostasis lead to a uniform reaction of the body, namely release and activation of hormones and cytokines. Profound alterations of substrate flow result, with mobilization of energy stores and degradation of structural and functional proteins of vital organs like the gut mucosa. Due to these reactions the energy demands of the organs are met and energy-consuming synthesis of substrates is indicated. Clinically, hypermetabolism, hyperglycemia, lipolysis and increased urea production with negative nitrogen balance can be observed. The metabolic reactivity is reached by an increased substrate cycling. To avoid negative consequences such as organ dysfunction, a rational situation-adapted substrate supply is warranted as well as reduction of catabolic stimuli and stimulation of anabolic factors. The metabolic care of the surgical patient is still a basic and important task.      

血清脂联素及CRP／APN比值的变化在腹部创伤患者病情监测中的意义

目的：探讨血清脂联素（ APN）及C反应蛋白（ CRP）与APN比值（ CRP／APN比值）的变化在腹部创伤患者病情监测中的意义。方法将本科室收治的80例腹部外伤患者依据AIS－ISS评分分为轻伤组及重伤组,将来本院体检的正常成年人30例作为对照组。分别于入院后即刻及第1 d、2 d、4 d、7 d共5个时间点,采用放射免疫法检测患者APN、CRP水平及CRP／APN比值,并同步进行全身炎症反应综合征（ SIRS）评分,对所得结果进行统计学分析及相关性分析。结果与对照组相比,轻伤组和重伤组患者的APN水平均明显降低（ P＜0.05）,重伤组APN水平明显低于轻伤组（ P＜0.05）;血清CRP与CRP／APN比值与SIRS评分呈正相关,相关系数分别为0.81（P＜0.05）和0.91（P＜0.05）,而APN水平与SIRS评分呈负相关（r＝－0.88,P＜0.05）。结论APN与CRP／APN比值可以作为评估腹部伤情严重程度的客观指标,有助于准确及时地评估病情。     

Procalcitonin in preoperative diagnosis of abdominal sepsis

Background and aims The present study attempted to identify the diagnostic significance of procalcitonin (PCT) in acute abdominal conditions as well as the range of concentrations relating to diagnosis of abdominal sepsis. Materials and methods This was prospective clinical study. The study included 98 consecutive patients with acute abdominal conditions, divided in sepsis and systemic inflammatory response syndrome (SIRS) group. Results PCT concentrations on admission were significantly higher in the sepsis group than in the SIRS group (median [interquartile range] 2.32 [7.41] vs 0.45 ng/ml [2.62]). A cutoff value of 1.1 ng/ml yielded 72.4% sensitivity and 62.5% specificity. In a group of patients with abdominal symptoms lasting for more than 24 h, a cut-off value of 1.1 ng/ml yielded higher sensitivity (82.9%) and higher specificity (77.3%). Conclusion Our results suggest that PCT measurements may be useful for early, preoperative diagnosis of abdominal sepsis.     

腹部外科SIRS患者下丘脑-垂体-甲状腺轴的功能改变及机制探讨

目的：研究SIRS状态下下丘脑-垂体-甲状腺轴的功能改变并探讨其机制。方法：应用放射免疫分析方法测定25例病人的血清T3、T4、rT3、TSH、TRH水平,并与20例正常对照进行比较。结果：SIRS病人血清T3、T4水平低于对照组。TSH和TRH水平观察组高于对照组。结论：SIRS病人下丘脑-垂体-甲状腺轴的功能出现紊乱,其可能的机制是由于甲状腺本身的功能受到抑制以及应激刺激作用的结果。     

MK2 plays an important role for the increased vascular permeability that follows thermal injury

We previously reported Rho kinase is involved in vessel hyper-permeability caused by burns. Here we further explore the Rho kinase downstream signaling, it is found that its specific inhibitor Y27632 significantly diminishes the activation of JNK and p38 MAPKs but not ERK that induced by serum from burned rats (burn-serum). JNK activation was found involved in the expression of HUVEC adhesion molecules following thermal injury, although not in the process of stress fiber formation. Inhibition of various MAPKs by specific inhibitors showed that SB203580 (inhibitor of p38), but neither SP600125 (inhibitor of JNK) nor PD98059 (inhibitor of ERK), abolish activation of the p38 downstream kinase MK2. Demonstration of stress fibers by fluorescent-labeled phalloidin showed that inhibition of MK2, either by its specific inhibitor or by dominant negative adeno-viral-carried constructs, significantly reduced burn-serum-induced HUVEC stress-fiber formation, while inhibition of another downstream p38 MAPK kinase, PRAK, had no such effects. Transfection of dominant negative adeno-viral MK2 (Ad-MK2(A)) significantly inhibited thermal injury-induced blood vessel hyper-permeability in rats and, moreover, prolonged the survival of burned rats beyond 72 h following thermal injury. One of the mechanisms behind these phenomena is that Ad-MK2(A) causes a significant depression of burn-serum-induced HSP27-phosphorylation, while the adeno-viral transported dominant negative PRAK (Ad-PRAK(A)) does not block. Although the effect of blockade of MK2 through its adeno-viral approach requires further study and investigation of alternatives to know for sure, we may have found a new pathway behind thermal-injury-induced blood vessel hyper-permeability, namely: Rho kinase > p38 > MK2 > HSP27.     

生态免疫肠内营养保护肠屏障功能的研究

目的探讨生态免疫肠内营养对全身炎症反应综合征(SIRS)大鼠肠屏障功能的保护作用。方法通过尾静脉注射脂多糖(LPS)建立SIRS大鼠模型,60只雄性SD大鼠随机分为4组(标准营养组、免疫增强组、生态营养组、生态免疫组),分别给予不同构成的肠内营养剂7d,观察各组大鼠血浆D-乳酸、二胺氧化酶(DAO)以及尿乳果糖/甘露醇(L/M)比值的动态变化。结果治疗7d后,生态营养组大鼠血浆D-乳酸水平明显低于标准营养组和免疫增强组(P<0.05),但这3组均高于生态免疫组3倍或以上(P<0.01)。血浆DAO水平标准营养组显著高于其他3组(P<0.01)。注射LPS后第1天起,各组大鼠尿液L/M比值均有大幅升高,至第6天回落到注射前水平。第1天时生态免疫组尿L/M比值低于其他3组(P<0.05),第3天时标准营养组尿L/M比值显著高于另外3组(P<0.01),至第6天各组已无明显差异。结论联合应用免疫增强营养素和生态制剂的生态免疫肠内营养能更有效地保护肠屏障功能。