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

Impaired mental status is a poorly understood manifestation of sepsis and may be associated with altered permeability of the blood-brain barrier. To examine the possibility that sepsis affects permeability of the blood-brain barrier, rats were infected with a peritoneal implant consisting of sterilized feces, barium sulfate, and 10(8) colony forming units (CFU) of Escherichia coli. Using this model, reproducible episodes of peritonitis with bacteremia resulted. Rats were sacrificed hourly after 5 min circulation of 100 mg horseradish peroxidase. Animals were perfused-fixed and the brains removed. Representative coronal sections were stained for peroxidase reaction product and cerebral blood vessels were examined microscopically for evidence of HRP staining and extravasation. The number of stained cerebral vessels from infected rats was increased at all times compared to uninfected control rats. Extravasation of horseradish peroxide within neuropil was significantly higher in hours 1, 4 and 5 as compared to controls. The lack of significant increase in hours 2 and 3 may suggest transient closing or repair of the tight junctions. We conclude that peritonitis and bacteremia are associated with increased permeability of the blood-brain barrier.
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PMID:E. coli peritonitis and bacteremia cause increased blood-brain barrier permeability. 241 52

A 88-year-old man was admitted because of the left chest pain due to herpes zoster for 1 week. Blood analyses and immunoelectrophoresis revealed anemia, severe neutropenia, rouleaux formation and IgM, lambda-type monoclonal gammopathy. The HE staining and peroxidase-anti-peroxidase staining of biopsy specimens of the cervical lymph node swelling appeared from the fifth hospital day, revealed an increase in atypical lymphocytes bearing IgM, lambda-type immunoglobulin. Then a diagnosis of primary macroglobulinemia was made. Although the patient's clinical findings transiently improved after chemotherapy with prednisolone and vindesine, he died of a septic shock which appeared after klebsiella pneumonia and sepsis. We reported an unusual case of primary macroglobulinemia with severe neutropenia, leading to a rapid development of septic shock after the chemotherapy.
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PMID:[Primary macroglobulinemia with severe neutropenia, leading to a rapid development of septic shock]. 249 64

The myeloperoxidase-hydrogen peroxide-chloride (MPO-H2O2-Cl) system is an antimicrobial system of polymorphonuclear leukocytes. We demonstrated that the MPO-H2O2-Cl system is fungicidal for Trichophyton rubrum. Fungal growth of a synchronous cell culture of T. rubrum germlings was assayed by measuring the uptake of tritiated N-acetyl-D-glucosamine, and the viability of the fungi was assayed by counting colony-forming units. Cytotoxins produced by the interaction of myeloperoxidase with hydrogen peroxide and chloride ion were fungicidal for T. rubrum. Growth inhibition was abolished in the presence of catalase or L-methionine. Polymorphonuclear leukocytes through the MPO-H2O2-Cl system may prevent invasion and sepsis by dermatophytes even in the absence of specific immunity.
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PMID:Inhibition of growth of Trichophyton rubrum by the myeloperoxidase-hydrogen peroxide-chloride system. 253 15

A spontaneous complete remission of 5 month's duration was observed in a 70 year-old man with acute myeloblastic leukemia complicated with severe pneumonia. The remission occurred after severe pancytopenia. He was treated only with antibiotics and blood transfusions. On admission, the leukocyte count was 6.4 x 10(3)/microliters with 98% myeloblasts. The hemoglobin level was 9.9 g/dl and platelet count was 1.5 x 10(4)/microliters. Marrow aspirate was hypercellular with 98.5% myeloblasts, which weakly showed Ia like antigen and myeloid related antigen. On relapse after five weeks' complete remission, leukemic cells were more immature, peroxidase negative and showed no surface markers. Chromosomal abnormalities were detected. During remission induction therapy he died of severe bacterial and fungal sepsis. Such cases of spontaneous complete remission have been rarely reported, previous adult cases were summarized and the role of etiologic factors were discussed.
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PMID:[Spontaneous complete remission in a 70 year-old man with acute myeloblastic leukemia with severe pneumonia]. 268 8

Roxithromycin (RU 28965) a new semisynthetic macrolide has been reported to display an antibacterial spectrum and activity in vitro similar to those of others macrolides. However, roxithromycin seems more efficient than erythromycin in in vivo experimental infections (mice). We have previously reported that roxithromycin increases the ability of human neutrophils (PMN) for bactericidal activity (S. aureus) or phagocytosis (K. pneumoniae) in vitro without altering other PMN functional parameters. In this study, roxithromycin (single dose-300 mg) was given to 6 human volunteers. The neutrophils collected 90 min after ingestion display a significant increased ability to phagocytose and kill S. aureus and K. pneumoniae. Furthermore chemotaxis, oxidative burst and myeloperoxidase activity of the PMN after roxithromycin ingestion were enhanced compared to those of PMN before ingestion. This discrepancy between immunomodulating effect of roxithromycin in vitro and in vivo outlines the complexity of in vivo experimental models and requires further studies in vivo in particular in patients suffering from sepsis.
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PMID:[Interaction of roxithromycin with human polymorphonuclear neutrophils in vitro and ex vivo]. 284 6

Degradation of structural elements and excessive consumption of humoral factors, especially of plasma proteinase inhibitors, by proteolysis and/or oxidation is a major cause of multiple organ failure in sepsis or septic shock. Such pathobiochemical reactions seem to be induced primarily by extracellularly liberated lysosomal proteins from PMN granulocytes (e.g. elastase, cathepsin G, myeloperoxidase, lactoferrin) as well as oxygen radicals produced during extensive phagocytosis. In clinical studies on septicemia and septic shock the consumption of plasma proteins including proteinase inhibitors was inversely correlated to the liberation of lysosomal factors, especially the granulocytic elastase. Administration of relatively specific elastase-cathepsin G-inhibitors (Bowman-Birk inhibitor, eglin) in experimental septicemia proved to be a promising therapeutic approach to reduce consumption of plasma proteinase inhibitors and development of interstitial lung edema in severe inflammation.
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PMID:Pathobiochemistry of sepsis: role of proteinases, proteinase inhibitors and oxidizing agents. 352 75

The effects of intragastric prostaglandin E2 (PGE2) on the occurrence of acute GI hemorrhage in intensive care patients were investigated in a prospective, double-blind, placebo-controlled study. Ninety patients with two or more risk factors (major surgery, multiple trauma, respiratory insufficiency, renal insufficiency, jaundice, hypotension, peritonitis, sepsis) were randomized for treatment with either PGE2 (0.5 mg) or placebo, administered every 4 h via a nasogastric tube. Blood loss in gastric aspirates was measured by 51Cr-erythrocyte labeling and a peroxidase test (orthotolidine). Of 57 patients who could be evaluated, 29 received PGE2 and 28 received placebo. Hemorrhage occurred in nine PGE2 patients and 13 placebo-treated patients, not a significant difference. The occurrence of hemorrhage was related to the number of risk factors, and GI hemorrhage was rarely the major factor determining mortality. Results of the orthotolidine test were not positively correlated with those of erythrocyte labeling, indicating that peroxidase tests should not be relied upon to detect blood in gastric aspirates.
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PMID:Intragastric prostaglandin E2 and the prevention of gastrointestinal hemorrhage in ICU patients. 390 62

Burns wound sepsis is not only the most common but also the most severe complication following extensive thermal injury. One conceivable explanation of this problem is a reduced capacity of the polymorphonuclear neutrophil leucocytes of these patients to combat the invading microbes. Fifty patients (42 male and 8 female) with deep dermal burns, covering 20-90 per cent of the total body surface area, were investigated from immediately after the injury until death or until healing of the wounds. The following functions of the neutrophil granulocytes were studied: chemotaxis and random migration utilizing a modified Boyden chamber technique, phagocytosis of Staph. aureus and IgG-coated latex particles, bactericidal capacity, e.g. killing of Staph. aureus and the neutrophil granulocyte content of: myeloperoxidase, lactoferrin, and chymotrypsin-like cationic protein. The presence of stimulators and inhibitors of the granulocyte functions was studied using gel filtration of the patient's serum on Sephacryl gel columns. Sera from all patients obtained within the first 1-3 days post-burn contained significantly increased amounts of heat-labile chemokinetic stimulating activity. Sera obtained between days 4 and 10 after injury contained significantly decreased amounts of heat-stable chemokinetic stimulating activity. Reduced chemokinetic activity was found during the third and fourth weeks following major burns (greater than or equal to 40 per cent) due to the presence of one or both heat-stable chemokinetic inhibitory activities. During the second week post-burn patients with burns larger than 40 per cent of the body surface area who showed an inhibition of chemotaxis, also had defects in phagocytosis, and often impaired bactericidal capacity concomitant with lower contents than normal of the granular enzymes. A hyaluronic acid preparation in low concentrations was found to counteract the migration inhibitory effect demonstrated in vitro in sera from patients with severe burns. Based upon these results a series of patients with severe burns and impaired functions of the neutrophil granulocytes have been treated with small amounts of this hyaluronic acid preparation subcutaneously. Very promising results have been noticed, similar to those found in vitro.
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PMID:Neutrophil granulocyte functions in severely burned patients. 402 46

A 52 yr old Caucasian female (F. E.) had hemolytic anemia, a leukemoid reaction, and fatal sepsis due to Escherichia coli. Her leukocytes ingested bacteria normally but did not kill catalase positive Staphylococcus aureus, Escherichia coli, and Serratia marcescens. An H(2)O(2)-producing bacterium, Streptococcus faecalis, was killed normally. Granule myeloperoxidase, acid and alkaline phosphatase, and beta glucuronidase activities were normal, and these enzymes shifted normally to the phagocyte vacuole (light and electron microscopy). Intravacuolar reduction of nitroblue tetrazolium did not occur. Moreover, only minimal quantities of H(2)O(2) were generated, and the hexose monophosphate shunt (HMPS) was not stimulated during phagocytosis. These observations suggested the diagnosis of chronic granulomatous disease. However, in contrast to control and chronic granulomatous disease leukocytes, glucose-6-phosphate dehydrogenase activity was completely absent in F. E. leukocytes whereas NADH oxidase and NADPH oxidase activities were both normal. Unlike chronic granulomatous disease, methylene blue did not stimulate the hexose monophosphate shunt in F. E. cells. Thus, F. E. and chronic granulomatous disease leukocytes appear to share certain metabolic and bactericidal defects, but the metabolic basis of the abnormality differs. Chronic granulomatous disease cells lack oxidase activity which produces H(2)O(2); F. E. cells had normal levels of oxidase activity but failed to produce NADPH due to complete glucose-6-phosphate dehydrogenase deficiency. These data indicate that a complete absence of leukocyte glucose-6-phosphate dehydrogenase with defective hexose monophosphate shunt activity is associated with low H(2)O(2) production and inadequate bactericidal activity, and further suggest an important role for NADPH in the production of H(2)O(2) in human granulocytes.
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PMID:Complete deficiency of leukocyte glucose-6-phosphate dehydrogenase with defective bactericidal activity. 440 Dec 71

Sepsis, abscess formation or development of purulent exudates in closed cavities expresses insufficient host defense against pyogenic infections. An attempt is made to analyse the reasons for diminished host resistance and/or increased virulence of the invading microbes. While the role of cellular defense mechanisms is not considered, a number of humoral components, such as lysozymes glycolipids, lactoperoxidase, fibronectin, esterases and haptoglobin, participate in efficient defense. Special emphasis is placed on serum complement, both with regard to its unspecific but nevertheless efficient alternative pathway, and with respect to its phylogenetically much more recent classical pathway. Recognition of bacteria by either mechanism of complement activation leads to C3b deposition on the microbial surface for efficient opsonization, while the juxtaposition of at least two molecules of antibodies contained in the immunoglobulin fraction of plasma safely leads to complement activation via the classical pathway. Therefore, specific recognition of bacteria by immunoglobulin-antibodies remains the core of anamnestic antimicrobial defense, the more so since some antibodies may also confer on the bacterial surface the capacity to activate the alternative pathway. The recent description of monoclonal antibody directed at bacteria relevant in sepsis opens perspectives in the near future when such components will eventually be used for therapeutic purposes, along with antibodies also directed towards the pathogenetic bacterial products endo- and exotoxin.
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PMID:[The role of complement and specific antibodies in the development and defense mechanism of sepsis and septic shock]. 662 30


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