Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

Escherichia coli hemolysin has been implicated as a pathogenicity factor in extraintestinal E. coli infections including sepsis. In the present study the effects of intravascular administration of hemolysin were investigated in isolated blood-free perfused rabbit lungs. Low concentrations of the toxin in the perfusate (0.05-5 hemolytic units/ml, corresponding to approximately 5-500 ng/ml), caused a dose- and time-dependent release of potassium, thromboxane A2, and prostaglandin I2, but not of lactate dehydrogenase, into the recirculating medium, as well as a dose-dependent liberation of the prostanoids into the bronchoalveolar space. These events were paralleled by a dose-dependent pulmonary hypertension, and studies with different inhibitors collectively indicated that the vasoconstrictor response was mediated predominantly by pulmonary thromboxane generation. In addition, E. coli hemolysin elicited a protracted, dose-dependent increase in the lung capillary filtration coefficient, which was independent of the prostanoid-mediated pressor response and resulted in severe pulmonary edema formation. We conclude that E. coli hemolysin can elicit thromboxane-mediated pulmonary hypertension combined with severe vascular leakage in isolated lungs in the absence of circulating inflammatory cells and humoral mediator systems, mimicking the key events in the development of acute respiratory failure in states of septicemia.
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PMID:Thromboxane-mediated hypertension and vascular leakage evoked by low doses of Escherichia coli hemolysin in rabbit lungs. 250 Apr 55

Rhabdomyolysis was evaluated by measurement of total creatine kinase (CK) and lactic dehydrogenase (LDH) in 19 patients with severe sepsis; 12 developed acute renal failure (Group B) and 7 did not (Group A). Results were compared to 7 patients with trauma (Group C) and 6 patients with chronic renal failure and minor infections (Group D). CK was higher (p less than 0.005) in Group B than in A. Results in Group C were similar to those in A. Elevation of CK correlated to increases in creatinine (r = 0.655, p less than 0.005). CK levels of Group D patients were lower than those of Group B. Blood pressure, lactate and pO2 were similar in both groups but thrombopenia was noted in Group B patients. Our results suggest that rhabdomyolysis and thrombopenia play a role in the development of renal failure in patients with severe sepsis.
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PMID:[Rhabdomyolysis caused by severe sepsis: discussion on its role in the development of acute renal failure]. 251 72

Previous investigation has demonstrated that in vivo complement activation can produce acute lung injury. Complement component C5a has been implicated as a key factor in this damage. In addition, C5a is thought to play a central role in mediating polymorphonuclear leukocyte (PMN) function. Studies suggest that administering antibodies to C5a might play a role in attenuating lung injury in animal models of sepsis. To evaluate further the effects of anti-C5a antibodies, we compared the effects of anti-human C5a des-Arg monoclonal (MAb) and polyclonal (PAb) antibodies on PMN functions including chemotaxis, chemiluminescence, and lysosomal release. PMN chemotaxis was assayed in Boyden chambers using 0.5% zymosan-activated serum (ZAS) as a source of C5a and 0.5% normal human serum (NHS) as a control. PMN chemiluminescence was measured by scintillation counting using ZAS as a stimulant and NHS as control. In addition, the lysosomal marker enzyme beta-D-glucuronidase was spectrophotometrically determined to assess lysosomal release. The PMN chemotactic response to ZAS was completely abolished with MAb and PAb anti-C5a antibodies (p less than 0.01). Control antibodies had no effect on ZAS-stimulated chemotaxis. The anti-C5a MAb markedly inhibited PMN chemotaxis at concentrations ranging from 20 to 0.2 microgram/ml, and was approximately 30 times more potent than the PAb. ZAS-stimulated PMN chemiluminescence was markedly decreased in response to monoclonal antibodies to C5a. In contrast, the control antibody did not inhibit ZAS-stimulated PMN chemiluminescence. Anti-C5a antibodies also significantly attenuated the release of the lysosomal enzyme beta-D-glucuronidase from ZAS-stimulated PMN. Anti-C5a antibody treatment did not cause a significant lytic effect when incubated with PMN, as demonstrated by the absence of the cytoplasmic marker lactate dehydrogenase in the supernatant. These studies suggest that in states of complement activation, MAbs and PAbs may decrease PMN functions including chemotaxis, chemiluminescence, and lysosomal enzyme release.
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PMID:Effects of anti-C5a antibodies on human polymorphonuclear leukocyte function: chemotaxis, chemiluminescence, and lysosomal enzyme release. 260 Jun 3

The most important diagnostic step in the management of patients with severe acute pancreatitis is the discrimination between acute interstitial and necrotizing pancreatitis. Measurement of C-reactive protein, lactic acid dehydrogenase, alpha-1-antitrypsin, and alpha-2-macroglobulin and contrast-enhanced CT are useful in detecting the necrotizing course of acute pancreatitis. C-reactive protein, lactic acid dehydrogenase, and contrast-enhanced CT offer detection rates of 85 per cent to more than 90 per cent for pancreatic necrosis. Surgical decision-making in necrotizing pancreatitis should be based on clinical, morphologic, and bacteriologic data. Patients with focal pancreatic necrosis, in general, respond well to medical treatment and do not need surgery. Extended (50 per cent or more) pancreatic necroses, infected necroses, and intrapancreatic parenchymal necroses plus extrapancreatic fatty tissue necroses are indicators for surgical management. The decision for the timing of operation in patients with proved necrotizing pancreatitis should be based on clinical criteria: the development of an acute surgical abdomen, generalized sepsis, shock, persisting or increasing organ dysfunction, or some combination thereof despite maximum intensive care treatment for at least 3 days. Major pancreatic resection for the treatment of necrotizing pancreatitis appears disadvantageous. Necrosectomy and continuous local lavage allow debridement of devitalized tissue and preservation of vital pancreatic tissue. Postoperative local lavage thus results in an atraumatic evacuation of necrotic tissue, the bacterial material, and biologically active substances. The hospital mortality rate of patients treated with necrosectomy and continuous local lavage (the Ulm protocol) is below 10 per cent. Nevertheless, controlled prospective clinical trials should be performed in order to bring more precision to our clinical decisions in respect to the role of surgery for this disease.
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PMID:Surgical management of necrotizing pancreatitis. 265 62

Serum samples from patients receiving intravenous streptokinase were examined for evidence of interaction in vivo between streptokinase and lactate dehydrogenase (EC 1.1.1.27; LD). We found that this treatment produced a band of LD activity that remained at the electrophoretic origin of LD isoenzyme analysis. Treatment with tissue plasminogen activator produced no such band. The streptokinase-LD complex could be removed from serum by ultracentrifugation. It remained in the circulation for as long as 48 h after streptokinase infusion. A similar phenomenon was observed in a case of pneumococcal sepsis. Examination of supernates from both cultures of several species of Gram-positive cocci revealed interactions between human LD and Streptococcus groups A and C and also Streptococcus pneumoniae. Evidently streptokinase can form complexes with LD in vivo after either streptokinase therapy or infection, with consequent alteration of the LD isoenzyme pattern.
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PMID:Alterations in lactate dehydrogenase isoenzyme patterns after therapy with streptokinase or streptococcal infection. 275 47

Based on remarkable activity in refractory lymphomas, a combination of etoposide, cisplatin (both administered by 4-day continuous infusions), cytarabine (Ara-C), and dexamethasone (EDAP) was evaluated in 20 patients with advanced myeloma refractory to standard melphalan and prednisone (MP) and/or vincristine, Adriamycin (doxorubicin; Adria Laboratories, Columbus, OH), and dexamethasone (VAD) and even to high doses of melphalan (HDM) (seven patients). Forty percent of patients responded regardless of previously recognized risk factors (eg, duration of drug resistance, tumor mass, and serum lactic dehydrogenase [LDH] level). While the median survival was only 4.5 months, patients with good performance (Zubrod less than 2) and low or intermediate tumor stage survived more than 14 months compared with only 2 months for the remaining group. EDAP could be readily administered in the outpatient clinic, but neutropenic fever prompted hospital admission in 80% of patients, half of whom developed penumonia and sepsis, a fatal outcome in four patients. Severe myelosuppression was of short duration, so that subsequent cycles could be administered every 3 to 4 weeks. No serious extramedullary toxicity, including renal toxicity, was encountered. Marrow toxicity and hence infectious complications may be reduced by elimination of Ara-C without compromising treatment efficacy. We conclude that the lack of cross-resistance with VAD and even HDM makes EDAP or a similar combination an attractive regiment to be formally explored in an alternating sequence with VAD in high-risk myeloma.
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PMID:Etoposide, dexamethasone, cytarabine, and cisplatin in vincristine, doxorubicin, and dexamethasone-refractory myeloma. 277 81

The effects of Pseudomonas aeruginosa cytotoxin on the pulmonary microvasculature were studied in blood-free, perfused, isolated rabbit lungs. Cytotoxin was administered to the recirculating Krebs Henseleit albumin (1%) buffer during two consecutive 30-min-perfusion phases (phases 1 and 2) at a concentration of 13 micrograms/ml, followed by a third perfusion phase (phase 3) without toxin. After perfusion phases 2 and 3, the capillary filtration coefficient (Kf,c) and vascular compliance were determined gravimetrically from two-step microvascular pressure increments under zero-flow conditions. Cytotoxin caused a continuous release of K+ and lactate dehydrogenase, which started within the first 5 min and amounted to about 50% of the total lung cellular K+ and 5 to 7% of the total lactate dehydrogenase by the end of the experiment. The toxin caused the continuous generation of prostaglandin I2, which was detectable in the perfusates of all perfusion phases at maximum values five times above the control values and which was measured in the bronchoalveolar lavage fluid at the end of the experiment. Thromboxane generation in toxin-treated lungs did not significantly exceed that of control lungs or of lungs with mechanically induced edema. Cytotoxin caused a gradual increase in pulmonary vascular resistance, to maximum values 2.5 times above the control, starting within 1 min; the increase was partially reversible after washout of the toxin. After a lag period of 20 to 30 min, the lungs gained weight, amounting to a mean gain of 9.1 g at the end of the experiments. After perfusion phases 2 and 3, an almost fourfold increase in Kf,c, which was not reversible after washout of the toxin, was measured, whereas the values of vascular compliance were not altered. We conclude that pseudomonal cytotoxin may be an important factor in the pathogenesis of prolonged microvascular injury, encountered in states of P. aeruginosa sepsis or acute lung failure with secondarily acquired P. aeruginosa pneumonia.
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PMID:Pulmonary microvascular injury induced by Pseudomonas aeruginosa cytotoxin in isolated rabbit lungs. 351 62

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.
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PMID:Sepsis indicators in acute pancreatitis. 367 46

The purpose of this study is to elucidate the pathophysiology of the acute pancreatitis and set up the criteria for assessing the severity of this disease. One hundred and fifty seven cases of acute pancreatitis were treated at the First Surgical Department of Tokyo University Hospital and its affiliated hospitals. They consisted of 24 severe cases, 76 moderate cases, and 57 mild cases according to our classification. In early stage ten parameters, namely, abnormalities of white cell count, platelet count, hematocrit, lactic acid dehydrogenase, blood urea nitrogen, serum calcium, base excess, PaCO2 and fasting blood glucose and age within 24 hours after admission and X-ray CT scan within 48 hours as early prognostic signs, enabled us to predict severe, moderate, or mild pancreatitis. More than 4 weeks later than the onset of acute pancreatitis, X-ray CT scan, white blood cell count, elevation of serum FDP level, endotoxemia and fall of plasma opsonic index served as good indicators to evaluate the severity of abdominal sepsis. In experimental pancreatitis, CH50 and opsonic index were remarkably decreased at 6 and 12 hours after induction of acute pancreatitis. As the above results, determination of early prognostic signs immediately after onset and late prognostic signs 3-4 weeks after onset is very important to evaluate and manage the acute pancreatitis patients.
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PMID:[Pathophysiology and prognosis of acute pancreatitis--early and late prognostic signs]. 408 48

We report nine patients with a sixth band, migrating cathodic to lactate dehydrogenase 5, appearing on routine electrophoresis for serum lactate dehydrogenase (LD, EC 1.1.1.27). Eight of these patients died during their hospitalization. Acidosis, hypotension, and sepsis were the common clinical conditions preceding the band's appearance. In several cases the band appeared transiently. We examined tissue samples from two of the cases, finding LD-6 in liver and skeletal muscle but not in heart. In randomly selected autopsy tissues, LD-6 was detected consistently in liver and skeletal muscle, sometimes in spleen, kidney, and adrenal tissue, but never in heart. Biochemical studies indicate that the LD-6 isoenzyme is not an artifact or an immunoglobulin complex, is larger than the other LD isoenzymes, contains an M-subunit but not an H-subunit, has an isoelectric point in the pH range of 9.0-9.6, and is more heat stable than LD-5.
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PMID:Clinical significance and partial biochemical characterization of lactate dehydrogenase isoenzyme 6. 669 Jan 51


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