Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-one routine clinical and laboratory data in 161 patients with necrotizing pancreatitis (NP) undergoing surgical treatment were analyzed. The necrotic tissue at operation was bacterially infected in 41% of the patients. The goal of the study was to evaluate whether there was any special clinical feature in cases of an infection. The parameters were recorded during 48 h after admission as well as during 48 h before operation, and the frequencies submitted to both a univariate and a multivariate analysis (logistic regression model). In the period after admission, patients with infected necrosis significantly more often had a rectal temperature greater than 38.5 degrees C (p = 0.001). Before operation (i.e., after maximum conservative treatment), four findings were significantly related to an infection: rectal temperature greater than 38.5 degrees C, base excess greater than -4 mmol/L, hematocrit less than 35% (all p = 0.0001), and paO2 less than 60 mm Hg (p = 0.001). The multivariate analysis, which calculates and quantifies the mutual influence of factors, showed a combination of three findings (rectal temperature greater than 38.5 degrees C, base excess greater than -4 mmol/L, and hematocrit less than 35%) to be related to necrosis infection before operation. All three criteria in a patient imply a probability of infection of 83%. It is noteworthy that the sepsis indicators were equally distributed in patients with focal, extended, or subtotal/total infected necrosis, but correlated with the necrosis extent in sterile necrotizing pancreatitis. Moreover, all parameters not related to the pancreatic infection [e.g., hyperglycemia, hypocalcemia, rise of lactic dehydrogenase (LDH), and the white blood cell count] correlated with the three necrosis categories.
Pancreas 1987
PMID:Sepsis indicators in acute pancreatitis. 367 46

Cardiac output (CO) and the distribution of blood flow were studied in chronically catheterized conscious rats during sustained (4 days) sepsis. Septicemia was induced by intraperitoneal administration of a pooled fecal inoculum, and tissue blood flow and CO were determined daily with 15-micron radioactive microspheres. Mean arterial blood pressure (MABP, 113 +/- 2 mmHg), CO (244.5 +/- 11.4 ml X min-1 X kg-1), and total peripheral resistance (TPR, 1.36 +/- 0.07 mmHg X ml-1 X min) were stable in control rats over the 4 days postinoculation. Septic animals showed a consistent tachycardia with MABP significantly reduced only on days 3 and 4 (86 +/- 4 mmHg). A hyperdynamic response to sepsis was indicated by an elevated CO (27%) and similarly reduced TPR on day 2. The calculated stroke volume averaged 0.22 +/- 0.01 ml/beat and did not vary over time or between the two groups. There was a 40-70% increase in blood flow to the heart, spleen, adrenal glands, and small intestine, and a greater than sixfold increase in hepatic arterial blood flow. The sustained elevation of coronary blood flow, observed in septic animals, was independent of myocardial work and is consistent with impaired myocardial function. Pancreas, stomach, and skeletal muscle blood flow was consistently compromised (24, 39, and 52%, respectively) during sepsis. Blood flow in other organs remained unchanged over time. Sepsis-induced changes in the fractional distribution of blood flow to various organs were similar to those described for absolute flow. (ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cardiac output and redistribution of organ blood flow in hypermetabolic sepsis. 670 86

The decision between a simultaneous pancreas-kidney (SPK) or kidney-alone (KA) transplant for the treatment of diabetic end-stage renal disease depends on the risk-versus-benefit of each procedure. In this study we compared the mortality, morbidity, graft function and acute rejection after 88 SPK and 65 KA transplants. All acute rejection episodes were biopsy-proven. Patient survival was higher in the KA group (KA 92%, SPK 83%) at 1 year, but similar in both groups at 5 years (SPK 78%, KA 71%). Whereas myocardial infarction accounted for a similar proportion of deaths in both groups, sepsis and surgical complications were more common causes of death in the SPK group. The majority of cardiovascular deaths occurred early in the SPK group compared to the KA group. Kidney graft survival was similar at 1 year (SPK 79%, KA 81%) and 5 years (SPK 66%, KA 59%). Pancreas graft survival at 1 and 5 years was 75% and 60% respectively. Biopsy-proven acute rejection occurred more frequently in the SPK group (SPK 63%, KA 46%). Morbidity was greater in the SPK group and included vascular (SPK 19%, KA 3%), non-infectious urologic (SPK 23%, KA 3%) and infectious complications (SPK 86%, KA 33%). The majority of complications in the SPK group were related to the pancreas allograft. In summary, SPK transplants were associated with an increased risk of early cardiovascular death, greater morbidity and more frequent biopsy-proven acute rejection episodes. However, kidney graft survival was not affected by the addition of the pancreas allograft.
 ...
PMID:Simultaneous pancreas-kidney versus kidney-alone transplants in diabetics: increased risk of early cardiac death and acute rejection following pancreas transplants. 806 63

Bacterial infection increases mortality and morbidity in acute pancreatitis. The aim of the present study was to analyze possible mechanisms by which bacterial infectious complications may worsen the course of the disease. Systemic arterial pressure, mucosal microcirculation, and intestinal, peritoneal, and pulmonary permeability of 125I-labeled human serum albumin were measured 3, 6, 12, 24, 48, and 72 h after sham operation, induction of pancreatitis (AP), abdominal sepsis (AS), or AP+AS. The mortality rate at 48 and 72 h was 33% in AS and 58 and 75%, respectively, in AP+AS, whereas there were no deaths in the AP or sham-operated groups. The systemic arterial pressure and intestinal blood flow decreased early in all study groups, with the lowest values for AP+AS. Bacterial infection aggravated the increase in intestinal, peritoneal, and pulmonary permeability to labeled albumin in pancreatitis. This was true for both intestinal endothelial permeability (blood to tissue) and mucosal barrier permeability (blood to lumen). The findings demonstrate the occurrence of circulatory failure and changes of the capillary barrier in multiple organs in acute pancreatitis. Moreover, the changes were aggravated by an intraabdominal septic challenge. The observations imply that bacterial infection may play a role in the development of multiple organ failure in acute pancreatitis, tentatively by aggravating alterations in tissue barrier function.
Pancreas 1995 Nov
PMID:The influence of abdominal sepsis on acute pancreatitis in rats: a study on mortality, permeability, arterial pressure, and intestinal blood flow. 853 53

Clinical and laboratory data or imaging results cannot provide a positive diagnosis of septic complications of pancreatic and peripancreatic necrosis in patients with acute pancreatitis. Confirmation can be obtained only after percutaneous computed tomography (CT)-guided aspiration of the necrotic tissues or fluid collection; although the important role of 99Tc(m)-HMPAO-labeled granulocyte scintigraphy has been recently emphasized. The aim of this study was to determine the sensitivity and specificity of 99m-technetium-hexamethylpropyleneamine oxime (99Tc(m)-HMPAO)- or 111In-oxine-labeled granulocyte scintigraphy for the diagnosis of infection in pancreatic or peripancreatic necrosis to define the ideal label for diagnosis. Thirty-six scintigraphic examinations were performed in 34 consecutive patients (mean age, 58 +/- 2 years) 20 +/- 2 days after the onset of acute pancreatitis (Balthazar classes A-C, n = 7; classes D and E, n = 29). The scintigraphic study included scintigraphic tomography and static acquisition 1 and 3 h, respectively, after reinjection of the autologous 99Tc(m)-labeled granulocytes and static images 3-4 and 24 h after the simultaneous reinjection of 111In-oxine-labeled autologous granulocytes. The diagnosis of infected pancreatic or peripancreatic necrosis was confirmed with percutaneous CT-guided aspiration (14 positive aspirates among 20 performed) and sterile necrosis after negative aspiration (6 negative aspirates) or after a 6 +/- 1-month follow-up free of clinical or biological signs of ongoing sepsis. The sensitivity and specificity were 86 and 73%, respectively, for scintigraphic tomography, 100 and 55% for 3-h 111In images, 93 and 68% for 3-4-h 111In images, and 100 and 64% for 24-h 111In images. The fall in splenic activity between the 3-4 and the 24-h 111In images was 26 +/- 3% in patients with septic pancreatic and peripancreatic necrosis (n = 14) and 16 +/- 3% in those with sterile necrosis (n = 22) (p < 0.01). Labeled granulocyte scintigraphy was thus shown to be an effective tool for the diagnosis of infection in pancreatic and/or peripancreatic necrosis due to acute pancreatitis, especially when the scintiscans are performed early after injection of 99Tc(m) or when the fall in splenic activity over the 24 h following reinjection of 111In is measured in particularly difficult cases. These promising preliminary results should be confirmed by a prospective study.
Pancreas 1996 May
PMID:Labeled granulocyte scanning for the diagnosis of infected necrosis in acute pancreatitis: what kind of labeling should be used? 874 Apr 6

Infectious complications currently account for 80% of deaths from acute pancreatitis. The aim of this study was to evaluate the necessity for prophylactic antibiotics in patients with severe acute pancreatitis. Twenty-three consecutive patients suffering from acute alcoholic pancreatitis with computed tomography demonstrating two or more fluid collections were randomly assigned to one of two groups receiving either nonantibiotic treatment or prophylactic antibiotics (ceftazidime, amikacine, and metronidazole for 10 days). Sepsis was always diagnosed by positive cultures. Seven episodes of severe sepsis occurred (pancreatic infection and septic shock) in the nonantibiotic group, and no infection occurred in the prophylactic antibiotic group (p < 0.03). In conclusion, the use of prophylactic antibiotics in severe alcoholic acute pancreatitis significantly reduces the incidence of severe infection.
Pancreas 1996 Aug
PMID:Prophylactic antibiotics in treatment of severe acute alcoholic pancreatitis. 882 89

Serum levels of human hepatocyte growth factor (HGF) were determined in 38 patients with acute pancreatitis by an enzyme-linked immunosorbent assay. The mean value of serum HGF levels on admission in the 38 patients was 1.69 +/- 0.40 (SEM) ng/ml. In 35 patients, serum HGF levels were found to be positive (> 0.39 ng/ml), with an incidence of 92.1%. In 17 patients, they were > 1.0 ng/ml, which was the cutoff value for fulminant hepatic failure. Serum HGF levels in the patients with severe acute pancreatitis (2.30 +/- 0.61 ng/ml; mean +/- SEM) were significantly higher than those in the patients with mild and moderate acute pancreatitis (0.63 +/- 0.06 ng/ml). Sixteen of seventeen patients whose serum HGF levels were > 1.0 ng/ml were evaluated as severe acute pancreatitis. Serum HGF levels were significantly elevated in the patients with higher Ranson scores, higher APACHE II scores, or higher computed tomography grades. Serum HGF levels in the patients with organ dysfunction (liver, kidney, or lung) were significantly higher than those in the patients without organ dysfunction. Moreover, serum HGF levels on admission in the nonsurvivors (3.17 +/- 1.30 ng/ml) were significantly higher than those in the survivors (1.22 +/- 0.33 ng/ml). The mortality rate of the patients showing serum HGF levels > 2.0 ng/ml on admission was 50%. In the patients with a lethal outcome, the mean serum HGF level remained constantly > 2.50 ng/ml during hospitalization. The serum HGF level reflected the clinical course of the disease rapidly and distinctly. Serum HGF levels increased with complications such as organ failure, infected pancreatic necrosis, and sepsis and decreased with successful intensive and surgical treatments. These results suggest that serum human HGF levels may reflect the severity, organ dysfunction, and prognosis in acute pancreatitis.
Pancreas 1996 Jan
PMID:Significant elevation of serum human hepatocyte growth factor levels in patients with acute pancreatitis. 892 23

Platelet-activating factor (PAF) may play a critical and primary role in the pathogenesis of acute pancreatitis and pancreatitis-associated distant organ injury. The present study evaluated the effect of a PAF antagonist, lexipafant (an (S)-4-methyl-2[methyl-imidazo[4,5-c]pyridin-1-ylmethyl)-benzene sulphonyl]-amino]pentanoic acid ethyl ester, BB-882; British Biotech Ltd.), on the potential prevention of gut barrier dysfunction, by measuring gut origin sepsis, bidirectional permeability of the intestinal barrier, and pancreatic capillary endothelial barrier integrity, in acute pancreatitis induced by intraductal infusion of 5% sodium taurodeoxycholate. Pancreatic endothelial permeability significantly increased in animals with acute pancreatitis, whereas pretreatment with lexipafant had a preventive effect (p < 0.05 vs. pancreatitis with saline). Similarly, alterations noted in hematocrit and plasma levels of lipase and calcium were counteracted by the PAF antagonist. It also prevented the increase in albumin leakage from blood to the mucosal interstitium and from blood to the intestinal lumen in acute pancreatitis. Albumin passage from the gut lumen to blood in animals with pancreatitis pretreated with saline increased from 3 h and on, and lexipafant prevented alterations in mucosal epithelial permeability. Bacterial translocation was commonly seen in pancreatitis, whereas only a few positive cultures were observed in pancreatitis animals given lexipafant. Microthrombosis in intestinal villi seemed less frequent after lexipafant pretreatment. We conclude that (a) PAF may play a role in the pathogenesis of pancreatitis-associated intestinal dysfunction, (b) PAF may be involved in the development of distant organ dysfunction by triggering endothelial barrier dysfunction, and (c) PAF antagonists may provide potential agents for preventing pancreatitis-associated gut barrier dysfunction.
Pancreas 1998 Aug
PMID:Effect of a platelet-activating factor antagonist on pancreatitis-associated gut barrier dysfunction in rats. 970 Sep 40

We investigated the role of platelet-activating factor (PAF) as a priming signal for cytokine-induced neutrophil chemoattractant (CINC) expression by bronchoalveolar macrophages in acute pancreatitis. Pancreatitis was induced by four intramuscular injections of cerulein (50 micrograms/kg at 1-h intervals) in Wistar rats. The animals were injected intraperitoneally with 10 micrograms/kg of lipopolysaccharide (LPS) as a septic challenge. Pancreatitis rats were treated with a bolus intravenous injection of TCV-309 (3 or 30 micrograms/kg) 30 min before the septic challenge. Intense mononuclear cell infiltration and lung hemorrhage occurred in pancreatitis rats complicated with sepsis but were not seen in pancreatitis rats receiving a bolus TCV-309. Pancreatitis rats treated with TCV-309 had lower serum concentrations of CINC after septic challenge and lower levels of CINC messenger RNA (mRNA) in the lung, as well as fewer pulmonary infiltrates immunoreactive for CINC or Mac-1 (CD11b/CD18). In vitro CINC production in response to LPS by bronchoalveolar macrophages obtained from pancreatitis rats 6 h after the first cerulein injection, immediately before septic challenge, was enhanced but was significantly reduced in a TCV-309-sensitive manner. LPS-stimulated in vitro CINC production by naive bronchoalveolar macrophages was significantly enhanced by pretreatment with PAF. TMB-8 (an inhibitor of calcium release from endoplasmic reticulum) or W7 (calmodulin antagonist) completely abrogated the chemoattractant production by bronchoalveolar macrophages pretreated with PAF after LPS stimulation. Altered intracellular calcium, due to Ca2+ efflux from intracellular stores, may be involved in the "priming" of bronchoalveolar macrophages to release CINC after triggering with LPS during acute cerulein-induced pancreatitis. The PAF antagonist TCV-309 effectively prevented hyperactivity of bronchoalveolar macrophages and pancreatitis-associated lung injury after the septic challenge.
Pancreas 1999 May
PMID:Platelet-activating factor antagonist (TCV-309) attenuates the priming effects of bronchoalveolar macrophages in cerulein-induced pancreatitis rats. 1023 40

The pathophysiology of severe acute pancreatitis (AP) resembles other conditions with systemic inflammatory response syndrome (SIRS) such as sepsis predisposing to remote organ failure. Because extracellular phospholipases A2 (PLA2) have been implicated in AP, their serum concentrations were analyzed with respect to SIRS and systemic complications in patients with severe AP. The serum samples were collected daily for 12 days in 57 patients with severe AP. SIRS, early organ complications, local complications, and outcome of AP were recorded. Time-resolved fluoroimmunoassays were used for group I and group II PLA2 measurements. Thirty-nine (68.4%) patients fulfilled the criteria of SIRS within 12 days from admission. Pancreatic necrosis was detected in 43 (75.4%) patients. Infected necrosis was found preoperatively or at operation in five (8.8%) patients. Twenty-six (45.6%) and eight (14.0%) patients had respiratory or renal failure, respectively. Seven (12.3%) patients died of their disease. All patients with systemic complications fulfilled the criteria of SIRS. The increasing number of positive SIRS criteria was associated with increased frequency of systemic complications. Pancreatic necrosis was not significantly associated with SIRS. The serum concentration of group II PLA2 was significantly higher in patients with SIRS (p < 0.05) compared with patients without from day 7 onward. The concentration of group II PLA2 increased (p < 0.01) in patients with SIRS but decreased in patients without. The serum concentration of group II PLA2 did not differ significantly with respect to systemic complications. The concentration of group I PLA2 decreased (p < 0.05) similarly in patients with and without SIRS or systemic complications during follow-up, respectively. Early systemic complications of severe AP are associated with SIRS with increasing frequency as the number of positive SIRS criteria increases. Group II PLA2 but not group I PLA2 may have pathophysiologic importance in severe AP-associated SIRS. Increasing serum concentration of group II PLA2 seems to reflect the ongoing systemic inflammation in severe AP-associated SIRS.
Pancreas 1999 May
PMID:Extracellular phospholipases A2 in relation to systemic inflammatory response syndrome (SIRS) and systemic complications in severe acute pancreatitis. 1023 44


1 2 Next >>