多发伤并发持续炎症-免疫抑制-分解代谢综合征患者的临床特征及预后分析

目的:研究多发伤并发持续炎症-免疫抑制-分解代谢综合征(persistent inflammation, immunosuppression and catabolism syndrome, PICS)患者的临床特征及预后。方法:分析2019年1月至2020年7月间收治于同济医院创伤外科的1 083例多发伤患者的临床资...     

严重创伤进展为持续炎症-免疫抑制-分解代谢综合征的影响因素分析

目的:研究严重创伤进展为持续炎症-免疫抑制-分解代谢综合征(persistent inflammation, immunosuppression and catabolism syndrome, PICS)的影响因素，并构建PICS发生风险的列线图预测模型并评估其预测效果。方法:收集新疆医科大学第一附属医院TICU 2017年6月—2023年5月收治的169例严重创伤患者资料。根据ICU住院第14天的C反应蛋白、淋巴细胞计数和白蛋白水平将患者分为PICS组(78例)和非PICS组(91例)。收集了患者的入院初次诊断指标、血栓弹力图、血小板指标及生化指标，使用独立样本t检验、Mann-Whitney U检验和χ²检验进行单因素分析，再进行多因素logistic分析确定严重创伤并发PICS的危险因素；使用R软件建立列线图预测模型，通过受试者工作特征曲线下面积(area under curve, AUC)和拟合度检验评估模型预测效果。结果:在169例严重创伤患者中，78例发展为PICS,91例未发展为PICS。两组在年龄、年龄评分、最大振幅(maximum amplit...     

重症急性胰腺炎并持续性炎症-免疫抑制-分解代谢综合征研究进展

重症急性胰腺炎起病急、病情进展迅速,部分患者在病程后期合并持续性炎症-免疫抑制-分解代谢综合征,可致患者全身多器官衰竭,病死率高。本文就重症急性胰腺炎并持续性炎症-免疫抑制-分解代谢综合征的病理改变及临床表现、发病机制、诊断标准及治疗等研究进展作一综述。     

严重多发伤患者并发持续炎症-免疫抑制-分解代谢综合征的早期警示因子北大核心CSCD

目的通过回顾性分析, 研究严重多发伤患者伤后并发持续炎症-免疫抑制-分解代谢综合征(persistent inflammation, immunosuppression and catabolism syndrome, PICS)的早期警示因子, 以期加深对严重创伤后慢性危重症病理变化的认识。方法收集2019年3月至2020年12月间收治于同济医院创伤外科严重多发伤患者276例。入选标准:创伤严重度评分(injury severity score, ISS)≥27分, 年龄≥18岁, 住院时间>15 d。排除标准:既往有恶性肿瘤、免疫性、消耗性、代谢性疾病史的患者。收集患者的临床资料、ISS、格拉斯哥昏迷评分(Glasgow coma scale, GCS)、序贯器官衰竭评分、APACHE Ⅱ评分, 以及伤后第3天的营养及免疫指标等资料, 通过t检验、χ^(2)检验或Mann-WhitneyU检验比较组间差异, Logistic回归分析并发PICS的早期警示因子。结果并发PICS患者为PICS组(102例), 不伴PICS的患者为N-PICS组(174例)。PICS组与N-PICS组相比, 年龄偏大, 伴发颅脑与胸部损伤多。在伤后第3天, PICS组IL-6、IL-10水平更高, Treg细胞比率更高, NK细胞计数和分类以及活化T淋巴细胞比率更低(P<0.05)。Logistic回归分析提示, 年龄>65岁(OR=2.375, 95%CI: 1.442~4.531)、同时伴有颅脑及胸部创伤(OR=2.846, 95%CI: 1.522~5.361)、GCS≤8分(OR=3.431, 95%CI: 1.843~8.512)、伤后早期IL-10>10 pg/mL(OR=2.173, 95%CI: 1.751~5.614)、Treg细胞比率>7%(OR=3.871, 95%CI: 1.723~6.312)是严重多发伤后并发PICS的早期独立危险因素。结论年龄>65岁、同时伴有颅脑及胸部创伤、GCS评分、伤后早期IL-10和Treg细胞比率可作为多发伤后并发PICS的早期警示因子。早期警示因子的发现将为早期甄别严重多发伤后潜在并发PICS的高危患者及早期采取干预措施创造可能。     

ICU滞留患者的临床特征及预后分析

目的 探讨ICU滞留患者的临床特征及预后.方法 回顾性分析2018年1月至2019年12月间入住ICU病房滞留时间≥8 d的112例患者.依据慢性危重病(CCI)及持续性炎症-免疫抑制-分解代谢综合征(PICS)诊断标准将所有患者分成4组:PICS组(27例)、CCI组(30例)、PICS合并CCI组(30例)及非PI...     

炎症因子与代谢综合征相关性研究的进展

代谢综合征是指人体的蛋白质、脂肪、碳水化合物等物质发生代谢紊乱的病理状态,是一组复杂的代谢紊乱症候群。代谢综合征患者发生心脑血管疾病、2型糖尿病等疾病的风险更高,其基本病因和发病机制目前尚未完全阐明。研究证实炎症参与代谢综合征的发生发展过程,不同的炎症因子标记物作用于代谢综合征的不同阶段,包括肿瘤坏死因子-α、C反应蛋白、白细胞介素、脂肪因子等。本文就部分炎症因子与代谢综合征相关性做一综述。     

《SHOCK》2021年第6期新观点

脓毒症仍然是一种死亡率很高的疾病,本期《休克》杂志中的脓毒症相关文章重点关注了先天免疫.创伤和脓毒症是导致持续炎症、免疫抑制和分解代谢综合征(PICS)的疾病状态,虽然已经深入研究了脓毒症和创伤后的急性炎症反应,但长期免疫抑制的机制尚不清楚. Bergmann等对淋巴细胞在 PICS 发展中的作用进行综述,认为调节性T...     

炎症、炎症介质和代谢综合征

代谢综合征是多种代谢紊乱在同一个体身上聚集的一种病理状态.目前认为亚临床炎症在代谢综合征的发生发展中起着重要的作用,甚至从某种意义上来说,代谢综合征本身是一种低度全身性炎症状态.作者主要介绍炎症、炎症介质在代谢综合征发生发展中的作用.     

HMGB1早期预测重症急性胰腺炎患者发生PICS的价值研究

目的:探讨血清高迁移率族蛋白B1(HMGB1)预测重症急性胰腺炎(SAP)患者发生持续炎症反应-免疫抑制-分解代谢综合征(PICS)的价值。方法:选取2018年1月—2020年12月内蒙古自治区人民医院收治的SAP患者141例,根据是否发生PICS将患者分为PICS组(n=39)和无PICS组(n=102)。酶联免疫吸附试验检测入院24 h、48 h、7 d、14 d时血清HMGB1表达水平。PICS影响因素分析采用logistic多因素分析;采用受试者工作特征曲线(ROC)分析HMGB1预测PICS的价值,计算曲线下面积(AUC)、灵敏度和特异度。结果:PICS组患者入院24 h、48 h、7 d、14 d时血清HMGB1表达水平均高于无PICS组(P<0.05)。logistic多因素分析结果显示,APACHEⅡ评分、C-反应蛋白水平、HMGB1入院24 h水平、HMGB1入院48 h水平为SAP患者发生PICS的独立影响因素(P<0.05)。HMGB1入院24 h水平预测SAP患者发生PICS的AUC为0.940,灵敏度为92.05%、特异度为91.47%;HMGB1...     

慢性炎症在肥胖和代谢综合征中的重要意义

肥胖尤其是内脏肥胖,是代谢综合征中最为主要的症状,并在其中扮演了重要角色。研究发现在代谢综合征患者机体的许多器官或组织内,常出现炎性细胞浸润等炎症反应;但是,关于组织的炎症反应及其与肥胖和代谢综合征之间的因果关系,目前仍不十分清楚。     

Persistent inflammation and immunosuppression: a common syndrome and new horizon for surgical intensive care

Surgical intensive care unit (ICU) stay of longer than 10 days is often described by the experienced intensivist as a "complicated clinical course" and is frequently attributed to persistent immune dysfunction. "Systemic inflammatory response syndrome" (SIRS) followed by "compensatory anti-inflammatory response syndrome" (CARS) is a conceptual framework to explain the immunologic trajectory that ICU patients with severe sepsis, trauma, or emergency surgery for abdominal infection often traverse, but the causes, mechanisms, and reasons for persistent immune dysfunction remain unexplained. Often involving multiple-organ failure (MOF) and death, improvements in surgical intensive care have altered its incidence, phenotype, and frequency and have increased the number of patients who survive initial sepsis or surgical events and progress to a persistent inflammation, immunosuppression, and catabolism syndrome (PICS). Often observed, but rarely reversible, these patients may survive to transfer to a long-term care facility only to return to the ICU, but rarely to self-sufficiency. We propose that PICS is the dominant pathophysiology and phenotype that has replaced late MOF and prolongs surgical ICU stay, usually with poor outcome. This review details the evolving epidemiology of MOF, the clinical presentation of PICS, and our understanding of how persistent inflammation and immunosuppression define the pathobiology of prolonged intensive care. Therapy for PICS will involve innovative interventions for immune system rebalance and nutritional support to regain physical function and well-being.     

Changes in serum and urine lysozyme activity after kidney transplantation: influence of graft function and therapy with azathioprine.

We investigated changes in lysozyme activity in serum and urine of kidney-transplant patients, and found that the production and catabolism of lysozyme in such patients differs markedly from that in normal subjects. Resumption of graft function decreases the high serum lysozyme activity by increasing the rate of catabolism in the transplant; at the same time, however, the production is inhibited by therapy with azathioprine. Changes in serum lysozyme activity correlate well with leukocyte count; thus its determination might be useful in monitoring immunosuppression. The urinary excretion of the enzyme, although not specific to rejection, is a good index of the degree of tubular damage.     

Immunomodulatory treatment strategies in inflammatory cardiomyopathy: current status and future perspectives

Chronic autoimmunity and viral persistence constitute prognostic factors for adverse outcome in dilated cardiomyopathy patients. Inflammatory cardiomyopathy is a specific cardiomyopathy entity diagnosed in approximately 50% of dilated cardiopmyopathy patients by immunohistological quantification of immunocompetent infiltrates and cell adhesion molecule abundance. Patients with autoimmune inflammatory cardiomyopathy benefit from immunosuppressive treatment and immunoadsorption by improvement of left ventricular ejection fraction and heart failure symptoms, paralleled by a significant suppression of intramyocardial inflammation. However, dilated cardiomyopathy patients with viral persistence do not respond favorably to immunosuppression.     

Central nervous system inflammation induces muscle atrophy via activation of the hypothalamic-pituitary-adrenal axis

Skeletal muscle catabolism is a co-morbidity of many chronic diseases and is the result of systemic inflammation. Although direct inflammatory cytokine action on muscle promotes atrophy, nonmuscle sites of action for inflammatory mediators are less well described. We demonstrate that central nervous system (CNS)-delimited interleukin 1β (IL-1β) signaling alone can evoke a catabolic program in muscle, rapidly inducing atrophy. This effect is dependent on hypothalamic-pituitary-adrenal (HPA) axis activation, as CNS IL-1β-induced atrophy is abrogated by adrenalectomy. Furthermore, we identified a glucocorticoid-responsive gene expression pattern conserved in models of acute and chronic inflammatory muscle atrophy. In contrast with studies suggesting that the direct action of inflammatory cytokines on muscle is sufficient to induce catabolism, adrenalectomy also blocks the atrophy program in response to systemic inflammation, demonstrating that glucocorticoids are requisite for this process. Additionally, circulating levels of glucocorticoids equivalent to those produced under inflammatory conditions are sufficient to cause profound muscle wasting. Together, these data suggest that a significant component of inflammation-induced muscle catabolism occurs indirectly via a relay in the CNS.     

Modulation of prostaglandin activity,part 1: Prostaglandin inhibition in the management of nonrheumatologic diseases: Immunologic and hematologic aspects

Prostaglandins (PGs) are active biologic substances that are involved in a wide range of physiologic processes; when their production is out of balance, they are factors in the pathogenesis of illness. Modulation of PGs by inhibition or stimulation is promising for the management of various conditions. PG inhibitors are widely used to relieve pain and inflammation in patients with rheumatologic disease. Interest in the use of PG inhibitors to prevent cancer and cardiovascular events is growing. More than 27 y ago, investigators found that PG depresses antibody production in vivo; reduces serum iron, hemoglobin, and leukoid series in bone marrow during acute and chronic blood loss; reduces albumin during antigenic stimulation; suppresses hypercalcemia after bleeding; and reduces fasting blood sugar and hyperglycemia after ether anesthesia and bleeding. Chronic conditions that produce large quantities of PGs are associated with immunosuppression and secondary anemia. Investigators in the present study hypothesized (1) that the overproduction of PGs is responsible for immunosuppression and secondary anemia in conditions associated with increased PG synthesis, such as pathologic inflammation, malignancy, trauma, and injury, and (2) that PG inhibitors reverse immunosuppression and secondary anemia, thereby enhancing the immune response. This is supported by many reports that show the immunosuppressive effects of PGs and their role in the immunosuppression associated with pathologic inflammation, burns, trauma, and tumors. Inhibition of PGs can be achieved through the use of synthetic medicines and natural products. This article reviews the effects of PGs and inhibition of increased synthesis of PGs on the lymphoid system, hematologic indices, and bone marrow elements in trauma, injury, burns, and tumors. The Medline database (1966–2006) was used in this study. Investigators in the present study and others have provided evidence that shows the involvement of PGs in immunosuppression and secondary anemia, as well as the efficacy of inhibited overproduction of PGs in many pathologic conditions other than rheumatologic disease.     

Admission en réanimation

Although mechanical ventilation is an essential support in patients admitted to the intensive care unit, clinical and experimental studies have shown that it could be harmful and could induce lung injury. Pulmonary and immune cells can convert mechanical stimuli into biological signals that will lead to inflammation. This sterile inflammation both locally and systemically will cause immunosuppression.     

Synthesis rates of total liver protein and albumin are both increased in patients with an acute inflammatory response

The general perception that catabolism and inflammation are associated with a high synthesis rate of total liver protein and a low albumin synthesis rate has been challenged in recent years by several studies in man, indicating that the synthesis rate of albumin in response to a catabolic insult is increased rather than decreased. Thus changes in liver protein synthesis rates in conjunction with catabolism and acute inflammation in man need to be characterized better. The aim of the present study was to measure protein synthesis rates of total liver protein and albumin during a state of acute inflammation. Patients (n = 10) undergoing acute laparoscopic cholecystectomy due to acute cholecystitis were investigated. FSRs (fractional synthesis rates) of total liver protein (liver biopsy specimens) and albumin (plasma samples) were investigated as early as possible during the surgical procedure, using a flooding dose of L-[2H5]phenylalanine. The results were compared with a reference group of patients without cholecystitis undergoing elective laparoscopic cholecystectomy (n = 17). FSR of total liver protein was 60% higher (P < 0.001) and the FSR of albumin was 45% higher (P < 0.01) in the cholecystitis patients compared with the control group. In conclusion, the synthesis rates of total liver protein and albumin are both increased in patients with an acute general inflammatory reaction undergoing laparoscopic cholecystectomy.     

Immunomodulatory effects of agents of plant origin.

The immunomodulatory properties of amla (Emblica officinalis) and shankhpushpi (Evolvulus alsinoides) were evaluated in adjuvant induced arthritic (AIA) rat model. Injecting Complete Freund's Adjuvant (CFA) in right hind paw of the animals induced inflammation. The crude extracts of both the herbs were administered intraperitonially following a repeated treatment profile. The anti-inflammatory response of both the extracts was determined by lymphocyte proliferation activity and histopathological severity of synovial hyperplasia. Both the extracts showed a marked reduction in inflammation and edema. At cellular level immunosuppression occurred during the early phase of the disease. There was mild synovial hyperplasia and infiltration of few mononuclear cells in amla or shankhpushpi treated animals. The induction of nitric oxide synthase (NOS) was significantly decreased in treated animals as compared to controls. These observations suggest that both the herbal extracts caused immunosuppression in AIA rats, indicating that they may provide an alternative approach to the treatment of arthritis.     

Immunologic alterations following excisional wounding and immediate repair with syngeneic or allogeneic skin grafts

Immunosuppression and its associated infectious complications have long been recognized as consequences of major thermal trauma, though the factors that mediate this suppression remain unclear. A murine split-thickness skin graft model was developed to investigate the role of a large surface area wound in the initiation of immunosuppression in the absence of burn injury. Significant T cell-mediated immunosuppression was demonstrated following wounding and immediate repair with either syngeneic or allogeneic split-thickness skin grafts. These results are consistent with previous experiments in a murine burn model treated by escharectomy and resurfacing with syngeneic composite full-thickness skin. Data also supports the concept that mediators of inflammation at the wound site play an important role in postburn immunosuppression. Furthermore, these results suggest that the use of skin allografts during the early postburn period does not adversely affect cell-mediated immunity in any way that could be abrogated by primary autografting.     

Nutritional considerations in heart failure

There are a number of factors related to heart failure pathophysiology and treatment that influence nutrient requirements for patients. These include catabolism, inflammation, oxidative stress, diuretic use, and presence of comorbidities. On the other hand, there is evidence that specific nutrients can alter heart failure pathophysiology. This article reviews the current evidence for nutritional recommendations regarding sodium and fluid restriction, macro- and micronutrient intake, and dietary changes required by the presence of common comorbidities.