UMLS:C0036690 - FACTA Search

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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neutrophil function was assessed in patients undergoing anesthesia and surgery using a chemiluminescence (CL) assay. With the anesthetic agents enflurane and nitrous oxide, peroperative CL (99.1 mV; 13.8 SEM: postinduction but prior to surgery) was significantly lower than the preoperative value (146.5 mV; 14.1 SEM) with a mean fall of 30% (P less than 0.001). CL measurements taken 24 hr postoperatively were significantly increased (193.9 mV; 16.4 SEM) over the pre- and peroperative values, showing mean increases of 32 and 96%, respectively (P less than 0.001 in both cases). The inhibitory influence on CL appeared to be due to serum factors since peroperative patients' sera inhibited control neutrophils. Significantly depressed levels of the complement component C3 and IgG detected during the peroperative period (P less than 0.05) may explain this phenomenon. Postoperatively, C3 and IgG levels returned to normal. The transient decrease in peroperative neutrophil function may be a contributory factor to the establishment of postoperative sepsis in surgical patients.
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PMID:Impaired neutrophil function during anesthesia and surgery is due to serum factors. 368 4

The immune response of 22 morbidly obese patients was measured before and 6 months after gastric bypass. In-vivo skin testing was carried out using five recall antigens. In-vitro response assessed the ability of isolated lymphocytes to take up radioactive thymidine after culture with the same antigens. The mean (+/- SD) preoperative weight of the patients of 122 +/- 14 kg declined by 33.5 +/- 8 kg after 6 months. The number of positive skin tests increased from a mean (+/- SEM) of 1.8 +/- 0.17 to 2.1 +/- 0.17 (p = 0.2). Mean (+/- SEM) induration of the skin-test response assessed at 24 hours after antigen injection increased from 4.7 +/- 0.6 mm to 5.5 +/- 0.6 mm (p = 0.35) and at 48 hours from 5.4 +/- 0.7 mm to 6.9 +/- 0.9 mm (p = 0.05). One patient who was anergic before gastroplasty responded normally 6 months later after substantial weight loss. In-vitro response, expressed as a stimulation index (+/- SEM), increased from 4.71 +/- 0.65 to 7.95 +/- 1.56 (p = 0.06) for the average of all antigens and from 12.85 +/- 2.05 to 15.79 +/- 2.84 (p = 0.2) for the largest response. The authors conclude that the response to test antigens in vitro and in vivo is not reduced significantly 6 months after gastric bypass and profound weight loss. Patients with severe vomiting, rapid weight loss or sepsis may respond differently and require individual assessment.
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PMID:Immune response after gastric bypass and weight loss. 373 Sep 74

The increased susceptibility of severely injured patients to infection and death from sepsis has been attributed to abnormalities in cell-mediated immunity. The authors therefore assessed the relative number of peripheral blood T helper cells and T suppressor/cytotoxic cells and total T lymphocytes identified by the monoclonal antibodies (McA) OKT4, OKT8, and OKT3, respectively, in 25 patients with burns from 5 to 85% total body surface area (TBSA) (mean: 40%) and 21 patients with nonthermal injuries (mean Injury Severity Score (ISS): 21.4). Patients were compared to 21 healthy controls. Cells reacting with the McA were detected by flow cytometry, which enabled the examination of a population of cells the size of T lymphocytes, excluding larger contaminating cells that might bind the McA. Patients with burns of 30% TBSA or greater had a significant reduction (p less than or equal to 0.05) in OKT3+ cells up to 50 days post-burn. Both septic and nonseptic burn patients had reduced numbers of OKT3+ cells, as did patients after nonthermal injury, suggesting that this reduction was due to the injury itself. Patients with smaller burns (less than 30% TBSA) as a group did not have reduced OKT4+ cells, whereas those with larger burns showed significant reductions in OKT4+ cells (P less than or equal to 0.05) at 0 to 5, 6 to 10, 11 to 20, 21 to 30, and 41 to 50 days post-burn. Seven burn patients who became septic 10 days post-burn or later had significantly lower OKT4+ cells within 10 days of injury (mean: 33.75% +/- 7.4 SEM) than 10 patients who remained free of sepsis (mean: 42.2% +/- 5.4, p = 0.004). Patients with uncomplicated nonthermal injuries failed to show any significant reduction in OKT4+ cells. Following thermal injury, a reduction in OKT8+ cells was observed up to 10 days in patients with burns less than 30% TBSA, and up to 20 days in patients with larger burns. In both groups, at no time were increased OKT8+ cells found to correlate with clinical events. In patients with nonthermal injury, OKT8+ cells generally remained near the normal range.
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PMID:Changes in T lymphocyte subsets following injury. Assessment by flow cytometry and relationship to sepsis. 387 11

Sepsis remains the major cause of postresuscitation death after hemorrhage and trauma. The high incidence of infection in this setting has been attributed to host defense abnormalities, including dysfunction in cell-mediated immunity. To elucidate the interaction between injury and host defense mechanisms, we measured interleukin 2 (IL 2) production by peripheral blood mononuclear cells in 21 patients immediately after unanesthetized, accidental hemorrhage or trauma. Interleukin 2 production in minimally injured patients (0.63 +/- 0.14 [SEM] units) was similar to that found in control, uninjured subjects (0.68 +/- 0.17 units). Compared with control patients, IL 2 production was reduced 56% in patients with moderate injury and 85% in patients with severe injury. There was significant correlation between the severity of injury and the reduction in IL 2 production. Lymphocyte proliferative response to phytohemagglutinin was reduced in patients with moderate and severe injury, and the reduction in proliferative response was significantly correlated with injury severity. These results indicate that marked abnormalities in cell-mediated immune function, as determined by IL 2 production, occur immediately after hemorrhage and accidental injury.
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PMID:The effects of hemorrhage and trauma on interleukin 2 production. 387 97

A new quantitative method for measuring the prognosis and severity of illness in terms of probability of survival was developed from 224 studies in an index population of 220 critically ill surgical patients. Patients were selected preoperatively to eliminate pre-existing cardiac disease, cirrhosis, nutritional debility, shock or sepsis, in order to evaluate the physiologic relationships of surgical trauma to outcome free of confounding associated medical disorders. The empirically derived numeric severity index was calculated from the probability of survival for each of 28 hemodynamic and oxygen transport variables at each time period after surgery. The score correctly indicated patient outcome in 96% of the index population and 94% of an independent, prospective population. The survivors' score consistently predicted survival within 21.6 +/- 4.4 (SEM) h after the end of surgery. The severity score of those who died consistently predicted nonsurvival within 37 +/- 11 (SEM) h after the end of surgery. We conclude that the score provides a useful, objective, physiologic measure of the severity of illness and prognosis.
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PMID:Probability of survival as a prognostic and severity of illness score in critically ill surgical patients. 396 10

We studied the relationship between serum antibodies to the cross-reactive endotoxin core of Escherichia coli and survival following Pseudomonas aeruginosa septicemia. Core glycolipid was purified from the outer cell membrane of a uridine diphosphate galactose 4-epimerase-deficient rough mutant E. coli (J5 strain), characterized, and used as the antigen in a quantitative enzyme-linked immunosorbent assay (ELISA) to measure core-specific IgG and IgM antibodies. 43 patients with Pseudomonas septicemia, among whom there was a mortality of 42%, were evaluated. Core-specific antibody concentrations in acute sera ranged from 1 to 49 micrograms/ml in the case of IgG and from 1 to 200 micrograms/ml for IgM. Core-specific antibodies of both isotypes were higher in patients who survived compared with those who succumbed to their septicemias (mean, microgram/ml +/- SEM, 26 +/- 3 vs. 14 +/- 4, P = 0.005 for IgG, and 55 +/- 12 vs. 18 +/- 5, P = 0.009 for IgM). Although total IgG levels were also higher in acute sera from survivors compared with nonsurvivors (mean, mg/dl +/- SEM, 1,120 +/- 99 vs. 694 +/- 119, P = 0.004), total IgM levels were virtually identical in the two groups (146 +/- 23 vs. 148 +/- 48, P = 0.52). Conversely, patients with core-specific IgG levels greater than 10 micrograms/ml at the onset of septicemia had better survival than those with levels less than 10 micrograms/ml (79 vs. 14%, P less than 0.001), and patients with core-specific IgM levels greater than 30 micrograms/ml had better survival than those with levels less than 30 micrograms/ml (81 vs. 44%, P = 0.01). In comparison, patients with total IgG levels greater than 1,000 mg/dl also had better survival than those with levels less than 1,000 mg/dl (82 vs. 42%, P = 0.01), while those with total IgM levels greater than 150 mg/dl showed somewhat less improvement in survival compared with those with levels less than 150 mg/dl (71 vs. 50%, P = 0.12). Core-specific IgM was highly correlated with core-specific IgG (r = 0.52), but not with type-specific anti-lipopolysaccharide (r = 0.13) or anti-toxin A (r = 0.12) antibodies, or with total IgG (r = 0.28) or IgM (r = 0.31). In contrast, core-specific IgG correlated somewhat more closely with type-specific antibodies (r = 0.36), and with total IgG (r = 0.51) and IgM (r = 0.52). Stepwise linear discriminant analysis indicated that type-specific antibody levels were the best predictor of outcome, among those antibodies examined, followed by anti-core IgM. Although anti-core IgG, anti-toxin A, and total IgG levels all correlated individually with survival, none augmented the prognostic power of type-specific antibodies in combination with anti-core IgM, which together predicted outcome accurately 73.5% of the time. Host factors not significantly associated with anti-core antibody levels included rapidly fatal underlying disease, age, sex, leukopenia, and prior treatment with cytotoxic drugs. In contrast, prior steroid therapy was associated with low levels of both core-specific IgG and IgM (P < 0.05). These data suggest cross-protective activity against P. aeruginosa septicemia of naturally occurring antibodies to the endotoxin core of E. coli. Anti-core antibodies, particularly of the IgM isotype appear to augment the more specific protective immunity engendered by antibodies to the O-specific side chains of Pseudomonas lipopolysaccharides. This cross-protective immunity likely applies to other Gram-negative pathogens as well.
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PMID:Enhanced survival in Pseudomonas aeruginosa septicemia associated with high levels of circulating antibody to Escherichia coli endotoxin core. 635 57

Sepsis remains the most common associated factor in acute respiratory failure (ARF). Endogenous opiates are known to have both respiratory and cardiovascular depressant effects. Because there is a high level of circulating endogenous opiates in sepsis, the possible role of opioids in the ARF syndrome seen in sepsis was studied. Sixteen piglets were infused with an LD100 dose (7.5 X 10(10) organisms/kg) of live Escherichia coli (Type 09-41). The pigs were hemodynamically monitored. Serial blood samples were taken for arterial blood gases and lactate. Serial lung biopsies were taken for determining wet/dry lung weight ratios and for histology. Group I (n = 8): septic shock controls without naloxone; group II (n = 8): naloxone treated, given as 2 mg/kg/hr intravenous boluses, starting within 1 min of E. coli infusion. All animals died of septic shock. Survivors at 150 min in group II had a higher blood pressure than group I (67.7 +/- 5.33 SEM vs 39.0 +/- 9.39) and cardiac output was also greater (1.07 +/- 0.23 vs 0.25 +/- 0.25). By 210 min, group I had no survivors (0/8) while 3/8 in group II survived. Pulmonary vascular resistance in group II at 90 and 120 min (870.8 +/- 274.1 and 942.5 +/- 12.9, respectively) was lower than in group I (2868.3 +/- 843.6 and 4156 +/- 1067). The PO2 was markedly better in group II and at 90 min; controls had a PO2 70.7 +/- 13.0, while group II had a PO2 111.4 +/- 8.4 (P less than 0.05). PCO2 levels showed a progressive rise in group I from 39.25 +/- 1.4 to 49.4 +/- 8.57.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pulmonary effects of opiate blockade in septic shock. 637 93

Acute respiratory failure in humans often follows extrathoracic sepsis. The purpose of this study was to determine the effect of repeated episodes of intra-abdominal sepsis over several weeks on the structure and function of rat lung. Intermittent peritonitis and a bacteremia of Escherichia coli and Bacteroides fragilis were produced by weekly intra-abdominal implants of gelatin capsules containing these organisms (3.0 +/- 1.0 X 10(7) and 5.0 +/- 1.0 X 10(7) colony-forming units/ml, respectively; mean +/- SEM). After 4 weeks alveolar walls were thickened and cellular with focal areas of alveolar space consolidation: circulating polymorphonuclear leukocytes were increased (12.2 +/- 1.2 to 19.9 +/- 2.0 X 10(3)/mm3; p less than 0.05), as were plasma levels of 6-keto-PGF1 alpha (0.56 +/- 0.08 to 1.02 +/- 0.18 ng/ml; p less than 0.01). After 8 weeks the capillary bed was dilated and the alveolar walls and ducts appeared less cellular but showed fibrosis: The WBC count had increased to 25.5 +/- 1.0 X 10(3) (p less than 0.01). After 4 or 8 weeks of intermittent sepsis there was no increase in the pulmonary artery pressure or vascular resistance or any change in arterial oxygen tension, plasma thromboxane beta 2 level, or platelet count. We conclude that repeated bouts of sepsis and bacteremia in the rat cause progressive injury to lung alveoli without evidence of altered blood gas tensions or pulmonary hemodynamics.
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PMID:The development of a model of subacute lung injury after intra-abdominal infection. 637 62

The severely burned patient responds differently to starvation ketosis in the early stage of injury as compared to the normal individual. A similar response has been observed in the patient after skeletal trauma and sepsis. In order to determine the extent of muscle protein contribution and the mechanism(s) involved, 11 burn patients with 35% to 80% BSA burn were resuscitated using carbohydrate-free solutions for 3 days followed by unrestricted intake. Blood was drawn daily and 24-hour urinary nitrogens were determined. Controls consisted of 10 preoperative elective surgical patients and two normal volunteers. The burned patients lost a mean +/- SEM of 17.1 +/- 1.72 g nitrogen per day on the third day. The mean +/- SEM ketone body response on the third day for burned patients was 385 +/- 77 mumol/l compared to 727 +/- 81 mumol/l for control patients. The mean +/- SEM 3-methylhistidine loss for burned patients on the third day was 9.83 +/- 0.82 mumol/kg compared to 3.6 mol/kg for control patients. Insulin levels on the third day of fast were three times the normal group. This insulin increase may be the modulating factor that suppresses excessive fat mobilization. This metabolic response causes a lower plasma ketone level, which may then necessitate the need for continued protein catabolism for glucose production for certain tissues. The protein contribution to the hypercatabolic response as assessed by increased urinary nitrogen losses is in part supported by an increased muscle protein breakdown as indicated by increased 3-methylhistidine excretion.
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PMID:The effect of major thermal injury and carbohydrate-free intake on serum triglycerides, insulin, and 3-methylhistidine excretion. 638 84

An early event in the evolution of acute respiratory failure (ARF) is thought to be the activation of platelets, their pulmonary entrapment and subsequent release of the smooth muscle constrictor serotonin (5HT). This study tests the thesis that inhibition of 5HT will improve lung function. The etiology of ARF in the 18 study patients was sepsis (N = 10), aspiration (N = 3), pancreatitis (N = 1), embolism (N = 2), and abdominal aortic aneurysm surgery (N = 2). Patients were divided into two groups determined by whether their period of endotracheal intubation was less than or equal to 4 days (early ARF, N = 12) or greater than 4 days (late ARF, N = 6). Transpulmonary platelet counts in the early group showed entrapment of 26,300 +/- 5900 platelets/mm3 in contrast to the late group where there was no entrapment (p less than 0.05). The platelet 5HT levels in the early group were 55 +/- 5 ng/10(9) platelets, values lower than 95 +/- 15 ng/10(9) platelets in the late ARF group (p less than 0.05), and 290 +/- 70 ng/10(9) platelets in normals. The selective 5HT receptor antagonist, ketanserin was given as an intravenous bolus over 3 minutes in a dose of 0.1 mg/kg, followed by a 30-minute infusion of 0.08 mg/kg. During this period mean arterial pressure (MAP) fell from 87 +/- 5 to 74 +/- 6 mmHg (mean +/- SEM) (p less than 0.05). One and one-half hours following the start of therapy, MAP returned to baseline. At this time, patients with early ARF showed decreases in: physiologic shunt (Qs/QT) from 26 +/- 3 to 19 +/- 3 (p less than 0.05); peak inspiratory pressure from 35 +/- 2 to 32 +/- 2 cmH2O (p less than 0.05) and in mean pulmonary arterial pressure from 32 +/- 2 to 29 +/- 1 mmHg (p less than 0.05). At 4 hours all changes returned to baseline levels. In early ARF ketanserin did not alter pretreatment values of: pulmonary arterial wedge pressure, 17 +/- 3 mmHg; cardiac index, 2.8 +/- 0.3 L/min X m2; platelet count, 219,000 +/- 45,000/mm3; platelet 5HT, 55 +/- 5 ng/10(9) platelets; plasma 5HT, 142 +/- 21 ng/ml; plasma thromboxane B2, 190 +/- 30 pg/ml; or plasma 6-keto-PGF1 alpha, 40 +/- 10 pg/ml. Ketanserin infusion in patients with late ARF yielded no benefit. In both ARF groups the decreases in QS/QT were inversely related to the duration of intubation (r = 0.70; p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of serotonin in patients with acute respiratory failure. 654 16

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