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

The authors studied a possibility of obtaining experimental meningococcus sepsis model on mice. The use of cyclophosphane, iron compounds, yolk medium produced no significant organism. When 4--5% mucine was injected intraperitoneally together with meningococcus culture mice died with sepsis phenomena. Differences were revealed in the sensitivity of linear and mongrel mice to meningococcus infection--AKR mice proved to be more sensitive. At the same time it was found that mongrel mice weighing from 10 to 12 g could be used to induce meningococcus sepsis.
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PMID:[Model of meningococcal sepsis in mice]. 10 42

Plasma proteins, triglyceridemia, body composition and delayed hypersensitivity were determined in 154 critically ill patients after admission. Plasma proteins levels were significantly increased in patients that were subsequently discharged vs. those that died: albumin: 33 +/- 6 g/l vs 28 +/- 6 g/l (p < 10(-6)); transferrin 2,18 +/- 0,65 g/l vs. 1,54 +/0 0,55 g/l (p < 10(-7)); prealbumin: 14,32 +/- 7,79 mg/100 ml vs. 7,28 +/-5,36 mg/100 ml (p < 10(-7)) and triglyceridemia was decreased: 1,07 +/- 0,38 g/l vs. 1,66 +/- 1,12 g/l (p not equal to 10(-3)). Body weight, fat weight and lead body mass were not correlated to subsequent mortality. Muscle cell mass was decreased (-17%, p < 10(-2)) and extracellular water was increased (+14%, p < 10(-4)), in patients who subsequently died. Total body water and visceral cell mass did not change. Initial anergy (tested with 3 antigens: candidin, tuberculin, varidase) did correlate with mortality: 35/62 died when delayed hypersensitivity was negative vs. 13/71 when it was positive (p < 10(-4)). Mortality was associated with decreased total lymphocyte count: 884 +/- 1025 vs. 1270 +/- 870 (p < 0,02) and serum iron: 51 +/- 40 micrograms/100 ml vs. 74 +/- 45 micrograms/100 ml (p < 10(-2)). Sepsis correlated with mortality (p < 10(-3)) and could produce these changes. These results suggest that critically ill paients have a protein-calorie malnutrition syndrom marktly different from that observed in simple starvation. Nutritional therapy must be, in this group of patients, adapted to this concept.
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PMID:[Nutritional status in critically ill patients. Relationship with mortality (author's transl)]. 12 28

An increased incidence of E. coli sepsis has been observed in neonates given intramuscular iron-dextran for prevention of iron deficiency. Mechanisms for this apparent effect on susceptibility to infection were investigated by comparing phagocytic and antibacterial functions in paired samples of venous blood from 7 infants, median age 5 days, before and after iron-dextran. Post-treatment sera had increased inhibitory effects on leucocyte chemotaxis and markedly reduced bacteriostatic effects agaainst E. coli. The clinical relevance of the effects on chemotaxis is uncertain. The reduction in serum bacteriostasis is similar to that observed in other forms of hyperferraemia not associated with saturation of transferrin, and is a likely cause of the increased susceptibility to infection in vivo. We consider that prophylactic treatment with parenteral iron-dextran is contraindicated in early infancy.
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PMID:Intramuscular iron-dextran and susceptibility of neonates to bacterial infections. In vitro studies. 33 10

During a five-year period the incidence of neonatal sepsis was 20 times higher in Polynesian newborns compared with European newborns (11 per 1,000 vs. 0.6 per 1,000 total births). This high incidence in Polynesians was confined to a period when the infants were being given intramuscular iron dextran. When the iron administration was stopped the incidence of disease in Polynesians decreased from 17 per 1,000 to 2.7 per 1,000 total births. An analysis of the Polynesian iron-treated and non-iron-treated groups showed a statistically significant difference in the incidence of sepsis, the type of causative organism, and mortality. The data suggest that the iron dextran injections have impaired the immunity of the treated infants, making them more susceptible to Escherichia coli sepsis.
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PMID:Increased incidence of gram-negative neonatal sepsis with intramuscula iron administration. 60 Jun 3

Complications after heart valve replacement remain a substantial source of morbidity and mortality despite continuing advances in surgical care and prosthetic design. Infectious endocarditis occurs in about 4 percent of patients and may appear early (within 60 days) or late after operation. Endocarditis of early onset is commonly due to staphylococcal, fungal or gram-negative organisms and is fatal in 70 percent or more of cases. Infection of late onset is more often of streptococcal origin and the mortality rate is lower, about 35 percent. With either type, prompt recognition, vigorous and appropriate antimicrobial therapy and early consideration of surgical intervention are crucial. The postperfusion and postpericardiotomy syndromes are relatively common and relatively benign syndromes associated with postoperative fever. Their recognition is important to prevent confusion with endocarditis or sepsis and thus to reassure the patient and physician. Treatment is primarily symptomatic. Intravascular hemolysis occurs with most prosthetic heart valves but is more common with certain prostheses and with paraprosthetic valve regurgitation, with significant hemolytic anemia in 5 to 15 percent. Oral iron replacement therapy is effective in the majority of patients, but occasionally blood transfusion or reoperation for leak around the prosthesis is necessary. Prosthesis dysfunction due to thrombus may be recognized clinically by recurrence of heart failure, syncope, cardiomegaly and altered prosthetic valve sounds or new murmurs. Hemodynamic studies verify the diagnosis, and prompt reoperation is indicated for this potentially lethal problem. Systemic embolization has decreased markedly with the introduction of cloth-covered prostheses and is frequently related to erratic or ineffective anticoagulant therapy. We continue to recommend anticoagulant therapy for all patients with prosthetic heart valves unless there is a major contraindication.
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PMID:Diagnosis and management of complications of prosthetic heart valves. 109 75

This report describes a case of septicemia and meningitis secondary to dog bites by two different dogs on two consecutive days. The case is noteworthy because of the unusual characteristics of the etiologic agent and the inability to place the etiologic agent into any currently defined genus or to identify it by the existing systems of classification. The organism is a small, thin, Gram-negative bacillus after 24 hours of incubation on blood agar; after prolonged incubation, it becomes filamentous. The organism is catalase- and oxidase-positive, hydrolyzes esculin, and forms acid in glucose, xylose, and maltose after 21 days' incubation. The organism does not manifest lysis on sheep blood agar, and does not grow on MacConkey, Salmonella-Shigella, Centrimide, nutrient, or Kligler iron agars. The tests for urea, nitrate reduction, and indol are negative. The unidentified Gram-negative bacillus showed susceptibility to all antimicrobials tested except gentamicin.
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PMID:A previously undescribed gram-negative bacillus causing septicemia and meningitis. 126 16

At the site of local reaction to infection the interleukin-1 (1L-1) is released signaling to distant tissues the presence of infection and attempting to strengthen the host's defenses and inhibit the bacterial growth. This phenomenon is accompanied by anorexia and fever. The muscle-protein breakdown is sustained and the released amino acids are taken up by the liver and other RE structures where they are used as substrates for energy and for synthesis of defense-related proteins. The metabolic adaptations to sepsis include hyperthermia, increased synthesis of hepatic globulins, development of granulopoiesis and neutrophilia and redistribution of serum iron and trace minerals.
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PMID:[Host metabolic reaction to infection]. 134 May 82

The paramagnetic molecule nitric oxide (NO), produced from L-arginine by a specific enzyme (NO synthase), has been shown to be involved in a surprising variety of mammalian cellular responses, including the regulation of T cell immunity to alloantigens in vitro. In cytotoxic activated macrophages, NO production results in a characteristic pattern of alteration of iron-containing enzyme function that is mimicked by exposure to NO. Electron paramagnetic resonance (EPR) studies have shown the formation of iron-nitrosyl species during macrophage activation and also during sepsis, indicating that alteration of iron-containing protein function may be the result of the well-documented tendency of NO to bind to metal ions. We have recently shown that the NO synthesis induced during alloantigenic activation of rat splenocytes inhibits lymphocyte proliferation and cytotoxic T-lymphocyte generation. This report demonstrates that iron-nitrosyl EPR signals similar to those observed in macrophages and during sepsis are present in the blood and in the grafted tissue of rats during the rejection of allogeneic (but not syngeneic) heart grafts. These signals are found in the blood and at the site of allograft rejection, but are not found in other tissues (such as spleen and lung), and are obliterated by administration of the immunosuppressant FK506. These results directly demonstrate the formation of iron-nitrosyl complexes during vascularized allograft rejection and suggest that consequent destruction of iron-containing protein function plays an important role in the rejection response.
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PMID:EPR detection of heme and nonheme iron-containing protein nitrosylation by nitric oxide during rejection of rat heart allograft. 137 34

The relative roles of hydroxyl radical and neutrophils in the pathogenesis of shock-induced mucosal injury and gut origin infection (GOI) were determined. The incidence of GOI was higher in the shocked rats (30 mmHg for 30 min) than the sham-shock controls (87% vs 12.5%; P less than 0.01). Administration of the hydroxyl radical scavenger, dimethyl sulfoxide (DMSO) or iron chelator and deferoxamine reduced the incidence of GOI from 87% to 20% and 40% respectively (P less than 0.05). DMSO and deferoxamine appeared to prevent shock-induced GOI by blunting the magnitude of shock-induced mucosal injury. In contrast, neutrophil depletion did not prevent GOI or protect the intestinal mucosal in the shocked rats. Instead, the incidence of systemic spread of bacteria past the mesenteric lymph nodes to the livers and spleens of the shocked rats was higher in the neutrophil depleted rats (56%) than any other group (7%) (P less than 0.01). Thus, shock-induced GOI and intestinal injury appears to be mediated by xanthine oxidase generated oxidants such as hydroxyl radical rather than neutrophil-generated factors. In addition, neutrophil depletion may be clinically deleterious, since it promotes systemic sepsis rather than preventing shock-induced GOI.
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PMID:[Role of neutrophil and hydroxyl radical in shock-induced gut origin infection]. 149 30

Thirteen patients with Stage III (3 patients) or Stage IV (10 patients) neuroblastoma were treated with a new iron chelation-cytotoxic therapy regimen. Deferoxamine given for five consecutive days followed by 3 days of cyclophosphamide, etoposide, carboplatin, and thiotepa (D-CECaT) caused moderate to severe myelotoxicity. In 39 courses there were four episodes of sepsis; platelet and packed red blood cell transfusions were required in 72% and 82% of courses, respectively. Mild nausea and vomiting occurred in 52% of courses. Objective responses after two courses were observed in 12 of 13 patients. Three of four partial responses were achieved in previously treated relapsed patients, and seven of eight complete responses (four of which were surgically documented) were achieved in previously untreated patients. This cytoreduction regimen appears to be an improvement over other initial induction regimens and may be worth testing in larger populations.
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PMID:Deferoxamine, cyclophosphamide, etoposide, carboplatin, and thiotepa (D-CECaT): a new cytoreductive chelation-chemotherapy regimen in patients with advanced neuroblastoma. 151 28


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