Periplaneta americana extract used in patients with systemic inflammatory response syndrome

BACKGROUND:Periplaneta americana extract is recognized to have a positive effect on gastrointestinal mucosa.This study aimed to investigate the effects of periplaneta americana extract on immune function,nutrition status and gastrointestinal complications of early enteral nutrition patients with systemic inflammatory response syndrome(SIRS).METHODS:Patients with SIRS were randomly divided into two groups:treatment and control groups.All patients in the two groups received conventional therapy including enteral nutrition,but periplaneta americana extract,an additional Chinese medicine,was given to the patients in the treatment group.At the beginning of treatment(0 day)and 1,3,and 7 days after treatment,the levels of immunoglobulin(Ig A),total lymphocyte count(TLC),total protein(TP)and prealbumin(PA)were respectively tested in patients'venous blood.The incidences of bloating,diarrhea,aspiration pneumonia and high blood sugar at 7 days after treatment were recorded.The mortality of the patients in 28 days was recorded.RESULTS:At 3 and 7 days after treatment,the levels of Ig A and TLC in the treatment group were higher than those in the control group(P<0.05).At 7 days after treatment,the levels of TP and PA in the treatment group were higher than those in the control group(P<0.05).The incidences of bloating and diarrhea in the treatment group were lower than those in the control group,the differences were significant(P<0.05).The mortality of treatment group was lower than that of the control group(P>0.05).CONCLUSION:Periplaneta americana extract could reduce gastrointestinal complications and improve immune function and nutritional status in patients with systemic inflammatory response syndrome.

Prognostic significance of urokinase-type plasminogen activator and its receptor in patients with systemic inflammatory response syndrome

BACKGROUND： This study aimed to determine the plasma levels of urokinase-type plasminogen activator （uPA）, urokinase-type plasminogen activator receptor （uPAR）, D-dimer, IL-6 and TNF-α, and observe the relations among uPA, uPAR, D-dimer, IL-6 and TNF-α in patients with systemic inflammatory response syndrome （SIRS）.METHODS： A prospective, clinical case-control study was conducted in patients with SIRS at age of more than 55 years old treated during 2008-2010 at Wuhan Central Hospital. Venous blood samples were collected by routine venipuncture. Eighty-five patients were divided into two groups according to diagnostic criteria of SIRS： SIRS patients from intensive care units （n=50）, and non- SIRS patients from medical wards （n=35）. Thirty healthy blood donors who visited the General Health Check-up Division at Wuhan Central Hospital served as controls. Excluded from the study were （1） those patients with pregnancy; （2） those with cancer; （3） those died after admission into the ICU in 7 days; （4） those received cardiopulmonary resuscitation; （5） those who had previous blood system diseases; and （6） those with SIRS before admission into the ICU. The levels of uPA, uPAR, D-D, IL-6 and TNF-a in blood were detected by commercial enzyme-linked immunosorbent assay （ELISA） kit. The data were analyzed using SPSS version 17.0 and expressed as mean ＋ standard. Student＇s t test and the Mann-Whitney U test were used in the analysis. The relations of uPA, uPAR and D-dimer, IL-6 TNF-α levels were analyzed using Spearman＇s rank-order correlation coefficient test. RESULTS： The plasma levels of uPA, uPAR, D-dimer, lL-6 and TNF-α in the patients with SIRS were obviously higher than those in the non-SIRS patients and controls （P〈0.001）. Correlation analysis showed a positive correlation between uPAR and IL-6 levels （r=0.395, P=0.004） and between uPAR and TNF-a levels （r=0.606, P〈0.001）, but no correlation between uPAR and D-dimer levels （r=0.069, P=0.632）. No correlation was observed between uPA, D-dimer, IL-6 and TNF-α levels （P〉0.05）. The establishment of ROC curve was based on the levels of uPAR, D-dimer, IL-6 and TNF-α in 24 hours for the diagnosis of multiple organ dysfunction syndrome （MODS）, and the ROC areas under the curve were 0.76, 0.58, 0.86 and 0.83, respectively. CONCLUSIONS：uPA and uPAR play a major role in patients with SIRS in the process of coagulation disorder, but the mechanism of SIRS is not the same. uPAR may play a central role in the development of SIRS to MODS.

Expression and Significance of Toll-like Receptor 2,4 of Peripheral Blood Mononuclear Cells in Acute Abdomen Patients Associated with Systemic Inflammatory Response Syndrome

The changes of Toll-like receptor （TLR） 2, 4 of peripheral blood mononuclear cells （PBMCs） in the acute abdomen patients associated with systemic inflammatory response syndrome （SIRS） and their potential significance were explored. A clinical study was performed on 103 acute abdomen patients in whom 65 were associated with SIRS. Forty healthy individuals served as normal controls. The mRNA expression of TLR2, 4 was detected by RT-PCR, and the expression of TNF-α and IL-6 by ELISA. The level of plasma endotoxin, hospital stay and mortality were measured. It was found that the endotoxin level was increased to varying degrees in all the acute abdomen patients, and the endotoxin level was and hospital stay longer in SIRS group than in non-SIRS group （P〈0.01）. TLR2 mRNA, TLR4 mRNA, IL-6 and TNF-ct could be detected with low value in normal controls, but they were up-regulated markedly on the 1 st day after admission. Then TLR4 mRNA, IL-6 and TNF-α were decreased gradually, but TLR2 mRNA maintained at a high level till the 5th day. These indexes above in SIRS group were higher than those in non-SIRS group （P〈0.01）. The results of correlation analysis revealed the expression of TLR2, 4 mRNA was positively correlated with the levels of TNF-α and IL-6, and the hospital stay, The results of Logistic regression demonstrated that overexpression of TLR2, 4 mRNA might result in higher risk of multiple organ dysfunction syndrome （MODS）. It was concluded that in the acute abdomen patients associated with SIRS, the expression of TLR2, 4 in PBMCs was increased markedly, suggesting that TLR might play an important role in the pathogenesis of acute abdomen associated with SIRS.

Urokinase-type plasminogen activator receptor as a predictor of poor outcome in patients with systemic inflammatory response syndrome

BACKGROUND:Urokinase-type plasminogen activator(uPA) and urokinase-type plasminogen activator receptor(uPAR) are known as important factors,which mediate a variety of functions in terms of vascular homeostasis,inflammation and tissue repair.However,their role in systemic inflammatory response syndrome(SIRS) has been less well studied.This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the patients with SIRS.We therefore analyzed their role and clinicopathological significance in patients with SIRS.METHODS:A case-control study was conducted with 85 patients who were divided into two groups according to the diagnostic criteria of SIRS:SIRS group(n=50) and non-SIRS group(/7=35).The SIRS group was divided into MODS group(n=26) and non-MODS group(n=24) by their severity,and survival group(n=35) and non-survival group(n=15) by their prognosis.Another 30 healthy adults served as normal controls.uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay(ELISA) kits.RESULTS:The plasma level of uPA was lower in the SIRS group than in the non-SIRS group and controls(P<0.001 and P<0.001).It was lower in sepsis patients and the MODS group than in the non-sepsis patients and the non-MODS patients(all P<0.05).However,there was no difference in uPA level between survivors and non-survivors(P>0.05).The plasma level of uPAR increased in the SIRS group compared with the non-SIRS group and controls(P<0.001 and P<0.001).There was a significant elevation of uPAR in sepsis patients,MODS patients and non-survivors as compared with non-sepsis patients,non-MODS patients and survivors respectively(all P<0.05).Plasma uPAR levels were positively correlated with APACHE Ⅱ score(r=0.575,P<0.001) and SOFA score(r=0.349,P=0.013).AUCs for the prediction of SIRS mortality were 0.67 and 0.51,respectively,for uPA and uPAR.CONCLUSION:uPAR could be a predictor of poor outcome in patients with SIRS.

Effects of internal iliac artery embolization on systemic inflammatory response syndrome in dogs with simulatedpelvic-fracture combined with massive bleeding

Background: Pelvic fracture combined with massive bleeding(PFCMB) is a complex issue in clinical practice. Currently, the use of angiography and embolization for the treatment of PFCMB obtains good results. The aim of this study is to observe the effects of early internal iliac artery embolization on the systemic inflammatory response syndrome(SIRS) in dogs with simulated-pelvic-fracture combined with massive bleeding.Methods: Twenty adult dogs were randomly divided into an embolization group(EG) and a control group(CG). For the two groups, heart rate, respiratory rate and body temperature and other physiological variables were measured, and IL-6, TNF-α and arterial blood gas levels were monitored. These variables were assayed every 30 min until death in the CG, while dogs in the EG underwent arterial angiography after 60 min of modeling. The internal iliac artery was embolized on the injured side.Results: The average time to SIRS in the CG was 3.56 h, occurring at a rate of 90%(9/10) within 24 h, with a mortality rate of 50%(5/10); the average time to SIRS for the EG was 5.33 h, occurring at a rate of 30%(3/10) within 24 h, with a mortality rate of 10%(1/10). When SIRS occurred in the EG, the mean plasma IL-6 level was 52.66±7.38pg/ml and the TNF-ps, tα level was 11.45±2.72ng/ml, showing a significant difference with those of the CG(P<0.05). In the two grouhe respiratory rate and leukocyte levels were higher at each monitored time after modeling than those before modeling; the mean arterial pressure, levels of hemoglobin and oxygen partial pressure were significantly lower at each time point after modeling than those before modeling except for the mean arterial pressure at 0h in EG; the platelet levels at 4 and 8h were higher than those before modeling; and the differences were statistically significant(P<0.05). In the EG, the mean arterial pressure, heart rate, respiratory rate and hemoglobin levels at 2, 4 and 8h were lower than those at 0h; the levels of leukocytes, platelets and carbon dioxide partial pressure at 4 and 8h after modeling were higher than those at 0h, and the differences were statistically significant(P<0.05, P<0.01); in the CG after modeling, the mean arterial pressure, levels of hemoglobin and carbon dioxide partial pressure at 2, 4 and 8h were lower than those at 0h; the levels of heart rate and leukocytes were higher than those before modeling; the respiratory rate and platelet levels at 4 and 8h were higher than those at 0h; and the differences were statistically significant(P<0.05). The levels of the mean arterial pressure and hemoglobin at 4 and 8h and the p H values at 8h after modeling in the EG were significantly higher than those in the CG, while the heart rate and respiratory rate at 4 and 8h were significantly lower than those in the CG. The p H values at 8h after modeling were significantly lower than those of the other monitored times in the CG(P<0.05, P<0.01). The two groups had elevated levels of alkaline phosphatase after injury induction.Conclusion: Through the use of an on-spot interventional treatment cabin, early internal iliac artery embolization can control bleeding associated with pelvic fractures, delay the occurrence of SIRS, and improve the success rate of the treatment of pelvic fracture combined with bleeding.

Integrated systemic inflammatory response syndrome epidemic model in scale-free networks

Based on the scale-free network, an integrated systemic inflammatory response syndrome model with artificial immunity, a feedback mechanism, crowd density and the moving activities of an individual can be built. The effects of these factors on the spreading process are investigated through the model. The research results show that the artificial immunity can reduce the stable infection ratio and enhance the spreading threshold of the system. The feedback mechanism can only reduce the stable infection ratio of system, but cannot affect the spreading threshold of the system. The bigger the crowd density is, the higher the infection ratio of the system is and the smaller the spreading threshold is. In addition, the simulations show that the individual movement can enhance the stable infection ratio of the system only under the condition that the spreading rate is high, however, individual movement will reduce the stable infection ratio of the system.

Role of E. coli DNA in systemic inflammatory response syndrome

Objective: To investigate whether bacterial DNA involving in the pathogenesis of systemic inflammatory response syndrome (SIRS) and possible mechanism. Methods: Escherichia coli DNA (EC DNA) was extracted from Escherichia coli 25922 with alkaline lysis method. The mice mortality was observed after EC DNA was injected into mice via caudal vein. The changes of serum TNF-α and IL-6 levels in rats were measured with ELISA after rats were given EC DNA. Calf thymus DNA and lipopolysaccharide (LPS) were used as the control, respectively. Results: EC DNA led mice to death with notable dose-effect relationship (LD50=11.51 mg/kg), but CT DNA didn't. The peak level of TNF-αwas lower in EC DNA group than in LPS group (P＜0. 05), though the former reaching the peak I h earlier than the latter. However, they had coordinate ability to induce IL-6 release in rats, and no significant difference was seen in serum IL-6 peak level between 2 groups. Conclusion: EC DNA leads mice to death, and induces the increases of serum TNF-αand IL-6 levels in rats. EC DNA has the effect equal to LPS in inducing SIRS by triggering cytokines cascade.

Expression and significance of toll-like receptor 2,4 in peripheral blood mononuclear cells in patients with systemic inflammatory response syndrome

To explore changes of toll-like receptor (TLR) 2,4 in peripheral blood mononuclear cells (PBMC) in acute abdomen patients with systemic inflammatory response syndrome (SIRS) and their significance.Methods A clinical study was done on 103 patients of which 65 were with SIRS.The mRNA expression of TLR2,4 were detected by RT-PCR;the expression of TNF-α and IL-6 were observed by ELISA;the correlation between TLR2,4 mRNA,the level of TNF-α and IL-6,and the clinical course was evaluated.Results TLR2 mRNA ,TNF-α and IL-6 were upregulated markedly on the first day of hospitalization,then decreased gradually;TLR2 mRNA maintained on high level till the 5th day.The expression of TLR2,4 mRNA was positive correlated with the level of TNF-α and IL-6,and the length of stay.TLR2,4 mRNA expression increased in patients with multiple organ failure.Conclusion In actue abdomen patients with SIRS,the expression of TLR2,4 of PBMC increased markedly,indicating its improtant role in the pathogenesis of SIRS.4 refs,2 figs,2 tabs.

Predictive value of serum cholinesterase for the prognosis of aged patients with systemic inflammatory response syndrome

Background Some studies found that cholinesterase （ChE） can be an independent risk factor for patients with multiple organ dysfunction syndrome. To assess aged patients with systemic inflammatory response syndrome （SIRS） early and predict their prognosis, the predictive value of ChE for the prognosis of aged patients with SIRS was analyzed. Methods From September 2009 to September 2010, all aged patients with SIRS in the ICU of the Second Affiliated Hospital of Zhejiang University School of Medicine were retrospectively analyzed if they met inclusion criteria： patients aged 〉65 years and met American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference criteria for SIRS. Serum ChE, albumin, D-dimer, lactic acid and C-reactive protein （CRP） were measured, and the Acute Physiology and Chronic Health Evaluation （APACHE） II and Glasgow Coma Scale （GCS） scores were evaluated within the first 24 hours in the ICU. Fisher＇s exact test was used for comparison of the primary disease between the deceased group and surviving group. For comparison of study variables between the two groups, the Student＇s t test or Mann-Whitney U test was used. Multivariate significance was tested with binary Logistic regression analysis. Results The clinical data of 124 aged patients with SIRS were collected and analyzed. Sixty-six patients （46 male, 20 female, mean age （78.70±8.08） years） who died were included in the deceased group and 58 patients （34 male, 24 female, mean age （76.02±6.57） years） who survived were included in the surviving group. There were no significant differences in age, gender, APACHE II score and GCS score between the deceased group and surviving group （all P 〉0.05）, but there were significant differences in lactic acid （P=0.011）, D-dimer （P=0.011）, albumin （P=0.007）, CRP （P=0.008）, and ChE （P 〈0.0001）. The correlation analysis showed that the APACHE II score and CRP were not correlated with ChE （both P 〈0.05）. D-dimer and albumin were correlated with ChE （Spearman＇s rho correlation coefficients were -0.206 and 0.324, the corresponding P values were 0.022 and 〈0.0001）. Multiple Logistic regression analysis showed that age, gender, lactic acid, D-dimer, albumin, CRP, APACHE II score, and GCS score were not independent risk factors for prognosis of aged patients with SIRS, but that ChE was （P 〈0.0001）. The receiver operating characteristic curve of ChE had an area under the curve of 0.797 （standard error=0.04; P 〈0.0001）, and a ChE of 103.00 U/L was the cut-off value with sensitivity=0.793, specificity=0.742. Conclusion Serum ChE might be a predictive marker for the prognosis of aged patients with SIRS, with low serum ChE levels indicating poor prognosis.

Role of Shenfu Injection(参附注射液) in Rats with Systemic Inflammatory Response Syndrome

Objective： To investigate the role of Shenfu Injection （参附注射液, SFI） in rats with systemic inflammatory response syndrome （SIRS）. Methods： The SIRS rat model was induced by the intravenous injection of lipopolysaccharide （LPS）. Forty-five male Wistar rats were randomly divided into 3 groups, the sham operative control group （control group, n=5）, the SIRS model group （model group, n=20） and the SFI treatment group （SFI group, n=20）. LPS was injected through the external jugular vein （12 mg/kg, 6 mg/mL） to all rats except for those in the control group, and SFI （10 mL/kg） was given to those in the SF group only once through intraperitoneal injection, while the normal saline （10 mL/kg） was given to those in the model group. For those in the control group, normal saline was given through the external jugular vein （2 mL/kg） and intraperitoneal injection （10 mL/kg）. Then, rats in the model group and SFI group were divided into 4 subgroups according to the time points, i.e., 1 h, 2 h, 4 h and 6 h subgroups, 5 rats in each group. The activity of nuclear factor of κB （NF-κB） of in blood mononuclear cells and the plasma levels of tumor necrosis factor- α （TNF- α ） and interleukin 6-（IL-6） were determined using enzyme-linked immunoabsordent assay （ELISA） at 1 h, 2 h, 4 h and 6 h after modeling. Histopathologic changes of the lung and liver were observed under a light microscope. Results： Compared with the control group, the activity of NF-κB in mononuclear cells and the plasma level of TNF-α were obviously increased at each time points （all P〈0.01）, reaching the peaks at 2 h after modeling. The plasma level of IL-6 increased gradually as time went by in the model group （P〈0.01）. Pathological examination showed pulmonary alveoli hemorrhage, edema and inflammatory cell infiltration in the lung tissue, and angiotelectasis, congestion, and local necrosis in the liver tissue in the model group. Compared with the model group, the activity of NF- κB and the levels of TNF-α and IL-6 in plasma decreased significantly in the SFI group （P〈0.01）, and the pathological injury in the lungs and liver was significantly alleviated. Conclusion： SFI plays a protective role by inhibiting the activity of NF-κB, and reducing the expressions of TNF-α and IL-6 in SIRS rats.

Changes in phospholipase D activity of leukocytes during human systemic inflammatory response syndrome induced by cardiopulmonary bypass

Objective To investigate the fluctuations in arterial leukocyte phospholipase D (PLD) activity during the perioperative period of open heart surgery under cardiopulmonary bypass ( CPB), and the relationship between PLD activity and systemic inflammatory response induced by CPB.Methods Arterial blood was obtained from 26 patients undergoing open heart surgery at 8 different time points during the perioperative period, from which leukocytes were isolated for determination of PLD activity, CD11b expression and myeloperoxidase (MPO) activity. Plasma IL-6, IL-8 and C-reactive protein were also determined. The 26 cases were retrospectively divided into 3 groups according to perfusion time in order to detect the possible influences of CPB on PLD activity and IL-6 and IL-8 levels.Results When the ascending aorta was declamped, average arterial leukocyte PLD activity was 0. 305±0.132 nmol choline·min-1·mg-1, 5. 0 times higher of the pre-CPB value, and remained (5. 4 times higher of the pre-CPB level) at 72 hours after CPB. Leukocyte CD11 b expression and plasma IL-6 and IL-8 levels increased significantly at the end of CPB, while MPO activity and C-reactive protein concentration reached their peaks at 1 and 24 hours, respectively, after CPB. At the end of CPB, the arterial leukocyte PLD activity of patients whose CPB duration was longer than 90 minutes were 1. 82- and 1. 74-fold that of the other two groups with CPB lasting between 90 and 60 minutes and less than 60 minutes.Conclusions Arterial leukocyte PLD activity rises significantly in CPB and its elevation is earlier and more persistent than other inflammation-related indicators tested; longer CPB duration leads to higher leukocyte PLD activity at the end of CPB. These results imply that PLD could be a new target for prevention of systemic inflammatory response induced by CPB.

Relation or Influence of RVOTO in the Inflammatory Response to Reoxygenation in Patients with Tetralogy of Fallot

Background:This study evaluated differential inflammatory response to cardiopulmonary bypass reoxygenation in tetralogy of Fallot repair.Methods:We performed a retrospective study at a cardiovascular center from 2012 to 2018,including 500 patients aged 1 week–18 years who received complete repair of tetralogy of Fallot.Patients were grouped according to tertiles of preoperative RVOT gradient on echocardiography into mild,moderate,and severe stenosis.We measured the highest perfusate oxygenation(PpO_(2))during aortic occlusion as independent variable.Primary outcome was systemic inflammatory response syndrome(SIRS)within 7 days postoperatively or the time of death or discharge.Results:Overall,rate of SIRS was 24.2% without significant differences among three groups(P>0.05).Older age,male,and smaller indexed left ventricular end-diastolic volume is independent risk factor of SIRS.There were significant interactions between RVOT stenosis and PpO2 on SIRS(P interaction=0.011):higher PpO_(2) was associated with a greater SIRS risk among combined moderate and severe stenotic children(OR 1.46395%CI[1.080,1.981]per-SD increase,P=0.014)but not among mild stenotic children(OR 0.900[0.608,1.333]per-SD increase;P=0.600),independent of covariates.Conclusion:The association of PpO_(2) with SIRS was modified by RVOT obstruction severity in tetralogy of Fallot repair.

Early selective enteral feeding in treatment of acute pancreatitis: A case report

BACKGROUND Early initiation of enteral feeding is recognized to play a crucial role in improving the outcomes of treatment of acute pancreatitis.However,the method of adminis-tration of enteral nutrition remains debatable.We present the experience of treating a patient with moderate-severe acute pancreatitis,at high risk of progressing to a severe or fatal condition,using a novel method of selective feeding with duodenal isolation.CASE SUMMARY A 27-year-old female patient presented to the emergency unit of the hospital with a typical manifestation of acute pancreatitis.Despite a conventional treatment,the patient’s condition deteriorated by day 2 of hospitalization.Using an endoscopic approach,a novel catheter PandiCathffwas placed to the duodenum of the patient,isolating its segment between the duodenal bulb and the ligament of Treitz.In the isolated area created,a negative pressure was applied,followed by introduction of early selective enteral feeding.The patient’s condition subsequently improved in a rapid manner,and no complications often associated with moderate-to-severe acute pancreatitis developed.CONCLUSION Within 48 h of starting treatment with the novel method,it can prevent the development of multiple organ failure and,when combined with minimally invasive drainage methods,help prevent infection.

MiR-30a-5p alleviates LPS-induced HPMEC injury through regulation of autophagy via Beclin-1

Background:Sepsis,a type of systemic disease,can impact nearly all organs,tissues and cells.Among them,endothelial cells are amongst thefirst to be affected and respond to the insult.In this study,we investigated the protective effects of microRNA-30a-5p(miR-30a-5p)on human pulmonary microvascular endothelial cells(HPMECs)treated with lipolysaccharide(LPS).Methods:An in vitro model of sepsis was established in HPMECs with the use of LPS.Transfecting with different tools(mimetic and inhibitor)to modify miR-30a-5p expression.Cell viability,proliferation and apoptosis were detected by the CCK-8 assay,the EdU kit andfluorescence staining,respectively.The autophagy-related protein and mRNA expression,the number of autophagosomes were separately examined through Western blot analysis,qPT-PCR and confocal microscopy.TargetScan and the luciferase reporter assays were used to probe target genes interacting with miR-30a-5p.Results:LPS caused a reduction in the viability and proliferation of HPMECs,as well as an elevation in the number of apoptotic cells.Subsequently,we observed that miR-30a-5p might play a role in preventing LPS-induced inhibition of cell damage and decreasing HPMEC apoptosis,suggesting the potential function of miR-30a-5p in this injury process.Finally,we confirmed that miR-30a-5p exerts its protective effect by regulating cell autophagy,possibly by targeting Beclin-1.Conclusion:Our study provided evidence that autophagy is a crucial aspect in the protective role of miR-30a-5p against LPS-induced HPMEC injury,identifying a promising target for sepsis-related endothelial cell injury.

Effect of flurbiprofen combined with prednisolone on interleukin-6 in elderly surgery patients

Objective: To determine the effect of flurbiprofen combined with prednisolone on interleukin-6 in elderly surgery patients. Methods: In this double-blind randomized controlled study, patients aged 65 to 80 who were undergoing spinal fusion surgery for disc herniation were administered flurbiprofen 100 mg (P group, flurbiprofen group), prednisolone 0.6 mg/kg (D group, prednisolone group), prednisolone 0.6 mg/kg plus flurbiprofen 100 mg (P + D group, flurbiprofen + prednisolone group) or normal saline (S group, saline group) 15 minutes before the induction of anesthesia. Plasma samples were collected before surgery (T0) and on day 1 (T1), day 2 (T2) and day 3 (T3) following surgery. At the same time, systemic inflammatory response syndrome (SIRS) was assessed by SIRS criteria. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP) for collected samples were measured. Results: Other groups had significantly lower levels of IL-6, CRP and occurrence of SIRS than S group (p < 0.05). Compared to groups P and D, the levels of IL-6 and CRP in P + D group were significantly lower on T1 (p < 0.05). Peak levels of IL-6 in all groups were presented on T1 (p 0.05). The levels of CRP within three days were significantly different but did not show peak levels (p > 0.05). Conclusion: Compared to prednisolone or flurbiprofen, combining flurbiprofen with prednisolone in elderly surgery patients led to an increased suppression of IL-6.

Application of bedside continuous blood purification in patients with multiple organ dysfunction syndromes

BACKGROUND:The complications of systemic inflammatory response syndrome(SIRS)include acute lung injury,acute kidney injury,shock,and multiple organ dysfunction syndrome(MODS).In recent years,how to clear inflammatory mediators has become a hot topic in critical care medicine.Researchers hypothesize that continuous blood purification(CBP) can effectively eliminate a variety of inflammatory mediators which participate in the occurrence of MODS and adjust the immune imbalance.This study aimed to observe the effects of CBP in MODS patients.METHODS:In this retrospective clinical study,a total of 38 MODS patients,18 males and 20 females,were enrolled.After conventional therapy,all the patients received CBP.Biochemistry,blood gas analysis,oxygenation index,mean arterial blood pressure(MAP),acute physiology and chronic health evaluation(APACHE) II scores were monitored.RESULTS:After CBP,the vital signs of patients were rapidly stable,and electrolyte disorders and acid-base imbalance were corrected.Renal function,blood gas,oxygenation index were all improved.MAP was increased,and APACHE II score was significantly decreased.All patients had good tolerance,stable hemodynamics,and no obvious adverse reaction on CBP compared with pre-CBP.CONCLUSION:CBP can effectively clean toxins,correct electrolyte acid-base balance,and improve systemic inflammatory response syndrome and the organ function of MODS patients.

Acute pancreatitis at the beginning of the 21st century: The state of the art

Acute pancreatitis is an acute inflammatory disease of the pancreas which can lead to a systemic inflammatory response syndrome with significant morbidity and mortality in 20% of patients. Gallstones and alcohol consumption are the most frequent causes of pancreatitis in adults. The treatment of mild acute pancreatitis is conservative and supportive; however severe episodes characterized by necrosis of the pancreatic tissue may require surgical intervention. Advanced understanding of the pathology, and increased interest in assessment of disease severity are the cornerstones of future management strategies of this complex and heterogeneous disease in the 21st century.

Pharmacologic therapy for acute pancreatitis

While conservative management such as fluid,bowel rest,and antibiotics is the mainstay of current acute pancreatitis management,there is a lot of promise in pharmacologic therapies that target various aspects of the pathogenesis of pancreatitis.Extensive review of preclinical studies,which include assessment of therapies such as anti-secretory agents,protease inhibitors,anti-inflammatory agents,and anti-oxidants are discussed.Many of these studies have shown therapeutic benefit and improved survival in experimental models.Based on available preclinical studies,we discuss potential novel targeted pharmacologic approaches that may offer promise in the treatment of acute pancreatitis.To date a variety of clinical studies have assessed the translational potential of animal model effective experimental therapies and have shown either failure or mixed results in human studies.Despite these discouraging clinical studies,there is a great clinical need and there exist several preclinical effective therapies that await investigation in patients.Better understanding of acute pancreatitis pathophysiology and lessons learnedfrom past clinical studies are likely to offer a great foundation upon which to expand future therapies in acute pancreatitis.

Immunomodulatory therapies for acute pancreatitis

It is currently difficult for conventional treatments of acute pancreatitis (AP), which primarily consist of anti-inflammatory therapies, to prevent the progression of AP or to improve its outcome. This may be because the occurrence and progression of AP, which involves various inflammatory cells and cytokines, includes a series of complex immune events. Considering the complex immune system alterations during the course of AP, it is necessary to monitor the indicators related to immune cells and inflammatory mediators and to develop more individualized interventions for AP patients using immunomodulatory therapy. This review discusses the recent advances in immunomodulatory therapies. It has been suggested that overactive inflammatory responses should be inhibited and excessive immunosuppression should be avoided in the early stages of AP. The optimal duration of anti-inflammatory therapy may be shorter than previously expected (< 24 h), and appropriate immunostimulatory therapies should be administered during the period from the 3rd d to the 14th d in the course of AP. A combination therapy of anti-inflammatory and immune-stimulating drugs would hopefully constitute an alternative to anti-inflammatory drug monotherapy. Additionally, the detection of the genotypes of critical inflammatory mediators may be useful for screening populations of AP patients at high risk of severe infections to enable the administration of early interventions to improve their prognosis. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.

Immune-modulating therapy in acute pancreatitis:Fact or fiction

Acute pancreatitis(AP) is one of the most common diseases of the gastrointestinal tract,bearing significant morbidity and mortality worldwide.Current treatment of AP remains unspecific and supportive and is mainly targeted to aggressively prevent systemic complications and organ failure by intensive care.As acute pancreatitis shares an indistinguishable profile of inflammation with sepsis,therapeutic approaches have turned towards modulating the systemic inflammatory response.Targets,among others,have included pro- and antiinflammatory modulators,cytokines,chemokines,immune cells,adhesive molecules and platelets.Even though,initial results in experimental models have been encouraging,clinical implementation of immuneregulating therapies in acute pancreatitis has had a slow progress.Main reasons include difficulty in clinical translation of experimental data,poor understanding of inflammatory response time-course,flaws in experimental designs,need for multimodal approaches and commercial drawbacks.Whether immune-modulation in acute pancreatitis remains a fact or just fiction remains to be seen in the future.