Humans ; Meningeal Neoplasms/surgery* ; Meningioma/surgery* ; Neurosurgical Procedures ; Pneumonia/etiology* ; Postoperative Complications ; Retrospective Studies ; Systemic Inflammatory Response Syndrome

The aim of this study was to explore the effects of parenteral supplementation with omega-3 fish oil emulsion (Omegaven) on systemic inflammatory response syndrome (SIRS) during the initial stage of severe acute pancreatitis (SAP). In a prospective, randomized and controlled trial, 60 patients with SAP were randomized either to treat with conventional therapy (Con group, n=30) or conventional therapy plus intravenous supplementation with omega-3 fish oil emulsion 0.2 g/kg every day (FO group, n=30). The effects were analyzed by the SIRS-related indexes. The results showed that APACHE-II scores in FO group were significantly lower, and the gap increased much farther after the 4th day than those in Con group (P<0.05). Fluid equilibrium time became shorter markedly in FO group than in Con group (5.1+/-2.2 days vs 8.4+/-2.3 days). In FO group, SIRS scores were markedly decreased and the SIRS state vanished after the 4th day; Plasma level of TNF-alpha was significantly reduced, while IL-10 decreased markedly, most prominently between the 4th and 7th day, and the ratio of IL-10/TNF-alpha raised as compared with Con group (P<0.05). During the initial stage of SAP, parenteral supplementation with omega-3 fish oil emulsion could efficiently lower the magnitude and persistence time of the SIRS, markedly retrieve the unbalance of the pro-/anti-inflammatory cytokines, improve severe condition of illness and may provide a new way to regulate the SIRS.
Dietary Supplements ; Emulsions ; Fatty Acids, Omega-3/*administration & dosage ; Fish Oils/*administration & dosage ; Pancreatitis, Acute Necrotizing/complications ; Pancreatitis, Acute Necrotizing/*therapy ; Parenteral Nutrition/methods ; Prospective Studies ; Systemic Inflammatory Response Syndrome/etiology ; Systemic Inflammatory Response Syndrome/*therapy ; Young Adult

Acute Disease ; Dexamethasone ; therapeutic use ; Glucocorticoids ; therapeutic use ; Humans ; Pancreatitis ; complications ; therapy ; Respiratory Distress Syndrome, Adult ; etiology ; prevention & control ; Systemic Inflammatory Response Syndrome ; etiology ; prevention & control

OBJECTIVETo investigate the effects of lipopolysaccharide (LPS) and heat co-exposure on serum urea and creatinine (Cr) concentrations in rats.

METHODSMale Wistar rats were randomized into normothermic saline injection control group (group C), heat exposure saline injection group (group H), normothermic LPS injection group (group L), and heat exposure LPS injection group (group HL). The rats in groups H and HL were exposed to heat in a chamber at an dry bulb temperature (Tdb) of 35.0-/+0.5 degrees Celsius, and those in groups C and L were kept in a chamber at Tdb of 26-/+0.5 degrees Celsius. LPS (8 mg/kg) was injected via the tail vein in the rats in groups L and HL to induce endotoxemia, while those in groups C and H were given normal saline injection (8 ml/kg) via the tail vein. The serum levels of urea and Cr were determined at the time points of 0, 40, 80, and 120 min after the injections.

RESULTSNo significant difference was found in serum Cr level at any level of the main effects of time, drug, or Tdb (P>0.05), but serum urea level varied significantly between the different time points, different levels of Tdb, and the drug injections (P<0.01). Significant interactions were identified between the time after injection, injected agents, and Tdb (P<0.01). Except for those in the group C, all rats showed elevated serum urea levels 40 min after the injection, particularly those in group HL. The serum urea levels were positively correlated to the level of tumor necrosis factor-alpha (P<0.01).

CONCLUSIONCo-exposure to LPS and heat in rats may elicit and worsen systemic inflammatory response syndrome and kidney injury.

Animals ; Creatinine ; blood ; Hot Temperature ; Lipopolysaccharides ; toxicity ; Male ; Random Allocation ; Rats ; Rats, Wistar ; Shock, Septic ; blood ; etiology ; Systemic Inflammatory Response Syndrome ; blood ; etiology ; Urea ; blood

BACKGROUNDIn patients suffering from acute pancreatitis, the pathogenesis is not completely understood, and several recent studies in vitro suggested that heat shock proteins might play an important role in cell signaling. To investigate the possible role of extracellular heat shock protein 70 (Hsp70) in pancreatitis, toll-like receptor-4 (TLR4)-deficient and wild-type mice were administered with exogenous Hsp70 during the course of cerulein-induced pancreatitis (CIP).

METHODSAcute pancreatitis was induced by 5 intraperitoneal injections of cerulein at hourly intervals, and then treated with recombinant Hsp70 through the caudal vein 4 hours after the start of cerulein injections. Subsequently serum amylase and serum cytokines levels were detected. Histologic alteration of the pancreas was evaluated. Tumor necrosis factor alpha (TNF-alpha) concentrations and myeloperoxidase (MPO) activity in both pancreas and lungs were analyzed. The nuclear factor kappa B (NF-kappaB) activation in pancreatic tissue was measured using a sensitive RelA enzyme-linked immunosorbent assay.

RESULTSTreatment with recombinant Hsp70 to wild-type mice in CIP resulted in significant aggravation of inflammation in pancreas, elevated levels of serum cytokines, up-regulation of pulmonary MPO activity and increase of lung tissues TNF-alpha concentrations. In contrast, treatment with Hsp70 to TLR4-deficient mice had little effect on serum cytokines levels, pancreatic inflammation, pulmonary MPO activity and TNF-alpha concentrations.

CONCLUSIONSThe results suggest that extracellular Hsp70 might induce systemic inflammatory response syndrome (SIRS)-like response in vivo and TLR4 might be involved in the Hsp70-mediated activation of inflammatory reaction in the progression of CIP without infection.

Acute Disease ; Animals ; Ceruletide ; toxicity ; Female ; HSP70 Heat-Shock Proteins ; physiology ; Male ; Mice ; Mice, Inbred C57BL ; Pancreatitis ; etiology ; Systemic Inflammatory Response Syndrome ; etiology ; Toll-Like Receptor 4 ; physiology

OBJECTIVETo study the risks on acute cerebral stroke (ACS) inducing systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS).

METHODSData from 1751 patients with acute cerebral stroke were studied by prospective analysis.

RESULTSIn all of the ACS patients,the incidence rate (IR) of SIRS was 36.50% with 205 patients having ACS inducing MODS, to which the IR was 11.71%, and 93 deaths. The case fatality ratio (CFR) was 45.37%. The pathogeneses condition of patients and the MR after the occurrence of MODS had positive correlation with the numbers of dysfunction organs. Study on single factor analysis revealed that the incidence of MODS had some related risk factors in the ACS inducing MODS, including age, diseased region close to the mean line, GCS, level of blood sugar, blood white cell count and the chronic disease history etc. The IR of ACS inducing SIRS and MODS was much higher in the condition of the diseased region near the mean line and the ACS of the basilar artery system.

CONCLUSIONSIRS seemed the base for MODS while the probability and the development degree were not only involved ACS but also SIRS. MODS induced by ACS could be reduced through the second grade program of disease precaution. The detection of those risk factors in the early period of the ACS course could provide some prediction of the prognosis and turnover, thus some early use of intervention methods might be helpful in the treatment of the disease.

Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Male ; Middle Aged ; Multiple Organ Failure ; epidemiology ; etiology ; Prospective Studies ; Risk Factors ; Stroke ; complications ; epidemiology ; Systemic Inflammatory Response Syndrome ; epidemiology ; etiology

PURPOSE: Due to the seroepidemiological shift in hepatitis A (HA), its severity, mortality, and complications have increased in recent years. Thus, the aim of this study was to identify predictive factors associated with poor prognosis among patients with HA. MATERIALS AND METHODS: A total of 304 patients with HA admitted to our institution between July 2009 and June 2011 were enrolled consecutively. Patients with complications defined as acute liver failure (ALF) were evaluated, and mortality was defined as death or liver transplantation. RESULTS: The mean age of patients (204 males, 100 females) was 32 years. Eighteen (5.9%) patients had progressed to ALF. Of the patients with ALF, 10 patients (3.3%) showed spontaneous survival while 8 (2.6%) died or underwent liver transplantation. Multivariate regression analysis showed that Model for End-Stage Liver Disease (MELD) and systemic inflammatory response syndrome (SIRS) scores were significant predictive factors of ALF. Based on receiver operating characteristics (ROC) analysis, a MELD > or =23.5 was significantly more predictive than a SIRS score > or =3 (area under the ROC: 0.940 vs. 0.742, respectively). In addition, of patients with a MELD score > or =23.5, King's College Hospital criteria (KCC) and SIRS scores were predictive factors associated with death/transplantation in multivariate analysis. CONCLUSION: MELD and SIRS scores > or =23.5 and > or =3, respectively, appeared to be related to ALF development. In addition, KCC and SIRS scores > or =3 were valuable in predicting mortality of patients with a MELD > or =23.5.
Adult ; Female ; Hepatitis A/*complications ; Humans ; Liver Failure, Acute/*etiology/*mortality/pathology ; Male ; Multivariate Analysis ; Prognosis ; Prospective Studies ; ROC Curve ; Systemic Inflammatory Response Syndrome/complications

OBJECTIVETo explore the relationship between systemic inflammatory response syndrome(SIRS) and severity of acute pancreatitis combined with plateau erythrocythemia in the high altitude.

METHODSA retrospective analysis on the clinical data which involved acute pancreatitis combined with plateau erythrocythemia (n = 40) and without plateau erythrocythemia (n = 40) admitted from September 2006 to September 2009 was conducted. According to the unified standards, these cases were divided into plateau erythrocythemia group and no plateau erythrocythemia group. The patients in plateau erythrocythemia group were further divided into severe group and mild group according to scores of APACHEII. The data was analyzed according to the patient with (or without) SIRS, SIRS's standard indicators, diagnostic parameter and relation of severity and duration of SIRS in acute pancreatitis combined with plateau erythrocythemia.

RESULTSThere was significantly discrepancy between plateau erythrocythemia group and no plateau erythrocythemia group not only in the incidence of patients who developed SIRS, but also in two items of patients fulfilling or not fulfilling diagnostic criteria of SIRS (P < 0.05). There was significant statistical difference in three items of diagnostic parameter of SIRS between plateau erythrocythemia group and no plateau erythrocythemia group (P < 0.05). Significant difference in two and three diagnostic parameter was found on severity of SIRS in acute pancreatitis combined with plateau erythrocythemia (P < 0.05). The more severity acute pancreatitis combined with plateau erythrocythemia was, the longer duration of SIRS was.

CONCLUSIONSIRS is highly correlated with the severity of SIRS in acute pancreatitis combined with plateau erythrocythemia in the high altitude.

APACHE ; Acute Disease ; Adult ; Aged ; Altitude ; Female ; Humans ; Male ; Middle Aged ; Pancreatitis ; complications ; Polycythemia ; complications ; Retrospective Studies ; Systemic Inflammatory Response Syndrome ; etiology

OBJECTIVETo investigate the relationship between phospholipase D (PLD) activation and neutrophil priming induced by cardiopulmonary bypass (CPB), and try to clarify whether CPB-induced systemic inflammatory response can be attenuated by inhibiting neutrophilic PLD activation.

METHODSNeutrophils were isolated from arterial blood of 8 patients undergoing valve replacement before operation and 30 min after initiation of CPB respectively. Both the preoperative and CPB-stirred neutrophils were subdivided into 5 groups by receiving different experimental interventions: (1) bacterial lipopolysaccharide (LPS, 10 ng x ml(-1)), (2) N-formylmethionylphenylalanine (fMLP, 1 micromol x L(-1)), (3) LPS+fMLP, (4) 1-butanol (0.5%)+LPS+fMLP, (5) vehicle. Elastase and myeloperoxidase (MPO) release was measured for the parameters of neutrophil activation, neutrophil PLD activity was determined by quantitation of choline produced from the stable product of phosphatidylcholine catalyzed by PLD.

RESULTS(1) Preoperative neutrophils treated with LPS+fMLP presented significantly higher PLD activity (13.48+/-2.61 nmol choline x h(-1) x mg(-1)) and released more elastase and MPO than cells treated with vehicle (PLD activity 3.70+/-0.49 nmol choline x h(-1) x mg(-1)), P<0.01), LPS (P<0.01) and fMLP respectively. In 1-butanol+LPS+fMLP group, PLD activity of preoperative neutrophils was lower than that in LPS+fMLP group (P<0.01), besides the release of elastase and MPO decreased sharply below both LPS+fMLP and fMLP groups (P<0.01). In LPS group, PLD activity was higher (P<0.01), while elastase and MPO release did not differ from control. fMLP group presented PLD activity, elastase and MPO release higher than control (P<0.01); nevertheless, lower than LPS+fMLP group (P<0.01). (2) CPB-stirred neutrophils presented prominent PLD activity increment, and even the control level was 3.59-fold of the pre-operative control (P<0.01). PLD activity in LPS+fMLP group was higher than that in other groups. Notably, PLD activity was even nonstatistically lower in 1-butanol+LPS+fMLP group than that in LPS or fMLP group. CPB-stirred neutrophils in LPS+fMLP group released more elastase and MPO than control, LPS, and 1-butanol+LPS+fMLP groups did (P<0.01); however, neither of the release was statistically different from that of fMLP group.

CONCLUSIONSCardiopulmonary bypass enables neutrophil priming accompanied with significant increase in PLD activity. Inhibition of neutrophil PLD activation attenuates its priming and may alleviate CPB-induced systemic inflammatory reaction.

Adolescent ; Adult ; Cardiopulmonary Bypass ; adverse effects ; Female ; Humans ; Male ; Middle Aged ; Neutrophil Activation ; physiology ; Phospholipase D ; pharmacology ; Systemic Inflammatory Response Syndrome ; etiology ; physiopathology

OBJECTIVETo evaluate the clinical efficacy of continuous venous-venous hemofiltration (CVVH) combined with coupled plasma filtration adsorption (CPFA) in the management of systemic inflammation response syndrome (SIRS) complicated by acute renal failure (ARF).

METHODSThirty patients with SIRS complicated by ARF (including 25 with severe acute pancreatitis, 2 with colonic perforation with infection, and 3 with acute infective endocarditis) were randomly divided into CVVH plus CPFA group (n=14) and CVVH alone group (n=16). The APACHE II score, mean arterial pressure, PaO2/FiO2, TNF-alpha and IL-10 were detected prior to or after the intervention. The feasibility and tolerance of CVVH plus CPFA and the therapy-related adverse reactions were evaluated.

RESULTSThe two groups showed no significant differences in the baseline clinical characteristics (P>0.05). The mean arterial pressure and PaO2/FiO2 increased significantly after treatment as compared with the control (P<0.05), with TNF-alpha being reduced and IL-10 elevated. In CVVH plus CPFA group, APACHEII score improved significantly after 10 days (P<0.05). No therapy-related adverse reactions were noted, suggesting good tolerance of CVVH plus CPFA.

CONCLUSIONCVVH combined with CPFA is an effective and safe method for improving the clinical outcome of patients with SIRS and ARF.

Acute Kidney Injury ; etiology ; therapy ; Adult ; Female ; Hemofiltration ; methods ; Humans ; Male ; Middle Aged ; Systemic Inflammatory Response Syndrome ; complications ; therapy ; Treatment Outcome