Similar articles

Abstract: Objective: The aim of the present study was to examine dynamic changes in serum cholinesterase (ChE) activity during early-stage severe trauma and the clinical significance of these changes. Methods: This prospective, observational study included 81 patients with severe trauma who were treated between October 2011 and April 2013 in the emergency intensive care unit (EICU) of a university-affiliated, tertiary-care, grade A general hospital in China. Serum ChE activity was measured on Days 1, 3, and 7 post-injury. The correlation of dynamic changes in serum ChE activity with trauma severity and prognosis was assessed. Correlations between changes in serum ChE activity after injury and albumin (ALB), prealbumin (PAB), transferrin (TRF), and C-reactive protein (CRP) levels were also analyzed. Results: Serum ChE activity in trauma patients was 42.3%–50.2% lower on Days 1, 3, and 7 compared with the control (P<0.001 for all time points), and it continued to decrease after Day 7 in both the survival and death subgroups. In the subgroup with an injury severity score (ISS) of ≤25, serum ChE activity initially decreased, but eventually increased. However, activity decreased continuously in the ISS>25 subgroup. ChE activity was significantly lower in both the death and the ISS>25 subgroups than in the survival and ISS≤25 subgroups on Days 1, 3, and 7 after injury. Activity was negatively correlated with ISS and acute physiology and chronic health evaluation III (APACHE III) at all time points. When comparing the receiver operating characteristic (ROC) curves for predicting prognosis, the area under the curve (AUC) in the plot of serum ChE was similar to the AUCs in plots of ISS and APACHE III, but significantly smaller than the AUC in the plot of the trauma and injury severity score (TRISS). Serum ChE activity was positively correlated with ALB, PAB, and TRF at all time points post-injury. Activity was not significantly correlated with CRP on Day 1, but was significantly and negatively correlated with CRP on Days 3 and 7. Conclusions: There is a significant decrease in serum ChE activity after severe trauma. Serum ChE may be regarded as a negative acute phase protein (APP) and the dynamic changes in serum ChE may be useful as an auxiliary indicator for evaluating trauma severity and predicting prognosis.

严重创伤后血清胆碱酯酶活性的动态变化

探讨严重创伤患者早期血清胆碱酯酶（ChE）活性的动态变化规律与临床意义。 阐明了在严重创伤后早期血清ChE动态的变化规律，为评估创伤的严重程度和预后判断提供新的参考辅助指标。 前瞻性观察研究：分析81例严重创伤患者伤后第1、3、7天血清ChE活性的动态变化，通过亚组（不同预后、不同伤情严重程度）间变化比较及与损伤严重度评分（ISS）、急性生理和慢性健康评分III（APACHEIII）和创伤严重程度评分（TRISS）进行比较，评估其反映病情严重程度和预后的价值；同时分析伤后血清ChE活性与急性期蛋白（APP），如白蛋白（ALB）、前白蛋白（PAB）、转铁蛋白（TRF）和C反应蛋白（CRP）浓度变化的关系。 血清ChE活性在严重创伤后显著降低，持续下降的幅度越大，则提示损伤越重，预后可能越差，而且血清ChE或可视为负急性期蛋白的一种，血清ChE作为严重创伤伤情和预后评估的简单辅助指标具有一定的可靠性。
多发性创伤；血清胆碱酯酶；急性期蛋白

[1] Bernik, T.R., Friedman, S.G., Ochani, M., 2002. Pharmacological stimulation of the cholinergic antiinflammatory pathway. J Exp Med, 195(6):781-788. 

[2] Borovikova, L.V., Ivanova, S., Zhang, M., 2000. Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. Nature, 405(6785):458-462. 

[3] Chiarla, C., Giovannini, I., Giuliante, F., 2011. Plasma cholinesterase correlations in acute surgical and critical illness. Minerva Chir, 66(4):323-327. 

[4] Chougule, A., Hussain, S., Agarwal, D.P., 2008. Prognostic and diagnostic value of serum pseudocholinesterase, serum aspartate transaminase, and serum alinine transaminase in malignancies treated by radiotherapy. J Cancer Res Ther, 4(1):21-25. 

[5] Cowan, J.A., Dubosh, N., Hadley, C., 2009. Seatbelt and helmet depiction on the big screen blockbuster injury prevention messages. J Trauma Inj Infect Crit Care, 66(3):912-917. 

[6] Evans, J.A., van Wessem, K.J., Mcdougall, D., 2010. Epidemiology of traumatic deaths: comprehensive population-based assessment. World J Surg, 34(1):158-163. 

[7] Gabay, C., Kushner, I., 1999. Acute-phase proteins and other systemic responses to inflammation. N Engl J Med, 340(6):448-454. 

[8] Hofer, S., Eisenbach, C., Lukic, I.K., 2008. Pharmacologic cholinesterase inhibition improves survival in experimental sepsis. Crit Care Med, 36(2):404-408. 

[9] Jin, Q.H., He, X.J., Li, T.L., 2011. Predictive value of serum cholinesterase for the prognosis of aged patients with systemic inflammatory response syndrome. Chin Med J, (in Chinese),124(17):2692-2695. 

[10] Kaibori, M., Matsui, K., Saito, T., 2008. Risk factors for early death due to recurrence after resection of large hepatocellular carcinomas. Hepatogastroenterology, 55(88):2151-2156. 

[11] Kamolz, L.P., Andel, H., Greher, M., 2002. Serum cholinesterase activity in patients with burns. Clin Chem Lab Med, 40(1):60-64. 

[12] Kamolz, L.P., Andel, H., Greher, M., 2002. Serum cholinesterase activity reflects morbidity in burned patients. Burns, 28(2):147-150. 

[13] Kassab, A.S., Vijayakumar, E., 1995. Profile of serum cholinesterase in systemic sepsis syndrome (septic shock) in intensive care unit patients. Eur J Clin Chem Clin Biochem, 33(1):11-14. 

[14] Keel, M., Trentz, O., 2005. Pathophysiology of polytrauma. Injury, 36(6):691-709. 

[15] Lampn, N., Hermida-Cadahia, E.F., Riveiro, A., 2012. Association between butyrylcholinesterase activity and low-grade systemic inflammation. Ann Hepatol, 11(3):356-363. 

[16] Libert, C., 2003. Inflammation: a nervous connection. Nature, 421(6921):328-329. 

[17] Lo, W.K., 2006. Serum parameters, inflammation, renal function and patient outcome.  Peritoneal Dialysis: A Clinical Update. Contrib Nephrol,Basel, Karger Vol.150:152-155. 

[18] Murdock, D., 2008. Trauma: when there’s no time to count. AORN J, 87(2):322-328. 

[19] Nzegwu, M.A., Banjo, A.A., Akhiwu, W., 2008. Morbidity and mortality among road users in Benin-City, Nigeria. Ann Afr Med, 7(3):102-106. 

[20] Paleari, L., Grozio, A., Cesario, A., 2008. The cholinergic system and cancer. Semin Cancer Biol, 18(3):211-217. 

[21] Paraoanu, L.E., Steinert, G., Koehler, A., 2007. Expression and possible functions of the cholinergic system in a murine embryonic stem cell line. Life Sci, 80(24-25):2375-2379. 

[22] Pavlov, V.A., Tracey, K.J., 2004. Neural regulators of innate immune responses and inflammation. Cell Mol Life Sci, 61(18):2322-2331. 

[23] Pavlov, V.A., Ochani, M., Yang, L.H., 2007. Selective α7-nicotinic acetylcholine receptor agonist GTS-21 improves survival in murine endotoxemia and severe sepsis. Crit Care Med, 35(4):1139-1144. 

[24] Rehiman, S., Lohani, S.P., Bhattarai, M.C., 2008. Correlation of serum cholinesterase level, clinical score at presentation and severity of organophosphorous poisoning. J Nepal Med Assoc, 47(170):47-52. 

[25] Rodriguez, J.A., Buzaleh, A.M., Fossati, M., 2002. The effects of some porphyrinogenic drugs on the brain cholinergic system. Cell Mol Biol, 48(1):103-110. 

[26] Santarpia, L., Grandone, I., Contaldo, F., 2013. Butyrylcholinesterase as a prognostic marker: a review of the literature. J Cachexia Sarcopenia Muscle, 4(1):31-39. 

[27] Wang, H., Yu, M., Ochani, M., 2003. Nicotinic acetylcholine receptor α7 subunit is an essential regulator of inflammation. Nature, 421(6921):384-388. 

[28] Yoshiba, M., Sekiyama, K., Inoue, K., 2002. Accurate prediction of fulminant hepatic failure in severe acute viral hepatitis: multicenter study. J Gastroenterol, 37(11):916-921.