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

Eighty-five trauma patients between the ages of 18 and 55, with American College of Surgeon's (ACOS) trauma scores greater than or equal to 7 were entered into a double-blind, randomized, placebo-controlled study to assess the efficacy of prophylactic fibronectin (Fn) administration on clinical course, sepsis development, and septic mortality. Patients were randomized on admission to receive purified human virus-inactivated Fn or placebo control (human serum albumin, HSA). Fn or HSA was administered on a daily basis if and when the patient was Fn deficient (less than 75% normal). When a Fn deficiency was not evident, the patient received saline. Seventy one patients developed Fn deficiencies during their initial clinical course: 36 received Fn, 35 received HSA. Fourteen patients did not develop a Fn deficiency after trauma and thus received only saline. Analysis of admission data demonstrated no significant differences between the three groups with respect to extent of injury (injury severity score, ACOS trauma score) or physiologic assessments of organ function (serum creatinine, bilirubin, lactic acid). On day 1 after trauma, Fn levels were shown to correlate with other plasma proteins and cellular components (range of r values, 0.24 to 0.75; all p less than 0.05), but not with organ function parameters. Eighteen of 85 patients became septic as judged by clinical criteria. Ten of these patients had received Fn (10 of 36), five had received HSA (5 of 35), and three had received only saline (3 of 14) before the development of sepsis (differences not significant). When septic, nine of 17 patients developed Fn deficiencies. Six patients received Fn while septic, three received albumin, and eight received saline. Seven patients died: 5 of 6 Fn patients, 1 saline, and 1 HSA recipient. Our data suggest that exogenous Fn repletion in states of deficiency does not alter clinical course, the development of sepsis, or septic mortality.
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PMID:The influence of fibronectin administration on the incidence of sepsis and septic mortality in severely injured patients. The Medical College of Georgia Fibronectin Research Group. 250 98

A survey is given of the occurrence, the biochemical qualities and the various functions of macrophages. By binding of gamma-interferon and of waste products of bacteria they are activated and increasedly give off interleukin 1 and other compounds, which play a part in the evocation of the immune reaction and the inflammatory processes. The interleukin 1 causes the evocation of fever, an increase of the secretion of corticoliberin and of ACTH, an increase of the formation of the proteins which are increasedly effective in the acute phase of the inflammation as well as an activation of B- and T-lymphocytes. For the phagocytosis, among others, the fibronectin is of importance, the content of which in the blood plasma is greatly reduced in sepsis and after severe burns. In macrophages an elaboration of numerous antigens takes place which are then transferred into the membrane and under participation of glycoproteins of MCH II cause an activation of T-lymphocytes.
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PMID:[Some recent facts on the function of macrophages and their modification]. 265 17

The lung is the target organ most frequently involved in the early phase of multiple organ failure. Microembolisation of the pulmonary vasculature by bacterial and non-bacterial particles and debris with failure of the clearance mechanism of the reticuloendothelial system (RES) and depletion of plasma fibronectin have been implicated in the pathogenesis. The present study examined the concurrent changes in plasma fibronectin, RES phagocytic function, organ localisation of bacterial and non-bacterial particles and the levels of circulating endotoxin and fibrin degradation products in a clinically relevant murine model of severe intra-abdominal infection. Progressive sepsis was associated with deteriorating RES phagocytic function to 45% of control values within 48 h of sepsis induction. There was decreased hepatosplenic uptake and increased pulmonary localisation of bacterial and lipid emulsion particles. Plasma fibronectin increased in septic animals within 48 h suggesting increased fibronectin production. These changes would support the hypothesis that altered RES function may facilitate pulmonary microembolisation in the pathogenesis of septic multiple organ failure.
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PMID:Reticuloendothelial function and plasma fibronectin in a murine model of intra-abdominal sepsis. 269 66

Severe sepsis leads to depression of the reticuloendothelial (RE) system with delayed bloodstream clearance of particulate matter and bacteria. Fibronectin may be an important opsonin of the RE system and low fibronectin levels often accompany severe sepsis in man. We have investigated the effect of prolonged intra-abdominal sepsis on plasma fibronectin concentrations and RE function. Serial plasma fibronectin concentrations were determined in rabbits for 2 weeks after either the induction of sepsis (appendix abscess) (n = 6) or laparotomy only (n = 6). RE function was measured at 2 weeks by determining the clearance kinetics and organ distribution of low dose technetium tin colloid (TTC). There was an early transient depression in plasma fibronectin values followed by elevated concentrations at 48-72 h which were more marked in the sepsis group. There was a delay in the blood clearance with reduced hepatic and increased bone uptake of TTC. We conclude that depletion of opsonic fibronectin is unlikely to be an important factor contributing to the impairment of RE function associated with intra-abdominal sepsis and that RE depression in septic animals is due to intrinsic Kupffer cell dysfunction.
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PMID:Reticuloendothelial failure in chronic intra-abdominal sepsis: the role of opsonic fibronectin. 270 51

A new born infant who died when he was 40 days old, after urinary infection, septicemia and disseminated intravascular coagulation (DIC) is reported. The concentration of fibronectin (FN) was undetectable (less than 1.1 mg/dl). His mother and one sister had also decreased levels (19 and 19.5 mg/dl), although inside normal limits, when they were compared to simultaneously studied normal controls (27 +/- 8). There were not infections, coagulation disturbs neither keloid scars in the family. A patient cousin also died at the first days of life. The deficiency of our case was much more important that FN levels found in 23 children with sepsis and DIC (range 6-38 mg/dl), therefore it is possible he had a primary deficiency. The investigation of FN levels in all newborns with severe infections or other disturbs is recommended, since these patients could be benefit from purified FN or cryoprecipitate therapy.
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PMID:[Absence of fibronectin in a 40-day-old child who died as a result of septicemia with disseminated intravascular coagulation]. 271 Dec 87

Using an enzyme-linked immunosorbent assay, we measured the concentration of fibronectin containing an extra type III domain (ED1) in the circulation of humans. Plasma levels of ED1 + fibronectin averaged 2.8 +/- 1.0 micrograms/ml in healthy individuals and did not differ substantially according to age or sex. In comparison with those from normal subjects, plasma samples obtained from patients with collagen vascular disorders contained increased average levels of ED1 + fibronectin. Among this group, levels of ED1 + fibronectin were significantly greater in samples taken from individuals with clinical evidence of vasculitis. Although levels of total (ED1 + plus ED1 -) fibronectin were also elevated in plasma samples from patients with vasculitis, only the concentration of the ED1 + variant correlated with severity of disease in two patients examined serially. Elevations in plasma content of ED1 + fibronectin, but not total fibronectin, were also noted in patients with acute vascular tissue injury associated with major trauma or sepsis syndrome. Western blot examination revealed the presence of intact dimeric ED1 + fibronectin in the circulation of all patients studied, although fragments bearing the ED1 were also detected. Human plasma normally contains small quantities of soluble ED1 + ("cellular") fibronectin, and these levels are increased in disorders involving vascular injury.
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PMID:Elevated plasma levels of ED1+ ("cellular") fibronectin in patients with vascular injury. 271 81

Antithrombin (AT), prekallikrein (PK), and fibronectin (FN) were measured in the plasma of 400 patients with a variety of disease states seen at Detroit Receiving Hospital from October 1983 through June 1987. The average lowest AT measured in these 400 patients was 69 +/- 19 per cent (SD) (Normal = 75-120%). The average lowest AT level in 152 septic patients (50 +/- 17%) was significantly lower than in the 248 patients without sepsis (79 +/- 22%) (P less than 0.001). The average lowest PK levels measured in 132 patients was 52 +/- 19 (Normal = 80-120%). The average PK level in 64 septic patients (34 +/- 17%) was significantly lower than in 68 who were not septic (69 +/- 21%) (P less than 0.001). The average lowest FN levels measured in 109 patients was 230 +/- 118 mcg/ml (Normal = 200-350 mcg/ml). The average FN level in 47 septic patients (162 +/- 88 mcg/ml) was significantly lower than in the 62 nonseptic patients (285 +/- 138) mcg/ml. AT or PK levels less than 50 per cent or FN levels less than 150 mcg/ml during the first 24 to 48 hours after severe trauma or burns were associated with a development of later sepsis in 90 per cent, 77 per cent, and 70 per cent, respectively. Thus, low or falling levels of AT, PK, and FN may be of great help in predicting sepsis or providing an early diagnosis in critically ill or injured patients.
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PMID:Sepsis and antithrombin III, prekallikrein, and fibronectin levels in surgical patients. 274 28

To study the role of lysosomal protease released from polymorphonuclear leukocytes during MOF, plasma PMNE levels were measured serially in 38 patients. The patients were divided into two groups, 14 patients of MOF from sepsis (group 1), and 24 injured patients without MOF (group 2). The normal value of PMNE was from 21 to 165 micrograms/l. The PMNE levels of the group 1 elevated (831 +/- 241 micrograms/l) at the time of diagnosis of sepsis and remained high during MOF. On the contrary, those of the group 2 were high on admission (574 +/- 131 micrograms/l), but returned to normal within seven days. There was no relationship between the levels of PMNE and the number of neutrophils. However, the PMNE/neutrophils ratio was significantly higher in group 1. Correlations were demonstrated between the amount of PMNE and the decrease in the levels of platelet counts, fibronectin and coagulation factor XIII. It is suggested that PMNE might play a major role in the pathobiochemical changes and tissue injury during MOF.
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PMID:[Polymorphonuclear leukocyte elastase (PMNE) levels in sepsis; the effect of PMNE on multiple organ failure (MOF)]. 278 1

Fibronectin is found in plasma as well as in association with connective tissue and cell surfaces. Depletion of plasma fibronectin is often observed in septic trauma and burned patients, while experimental rats often manifest hyperfibronectinemia with sepsis. Since Factor XIII may influence the rate of clearance and deposition of plasma fibronectin into tissues, we evaluated the temporal changes in plasma fibronectin and plasma Factor XIII following bacteremia and RE blockade in rats in an attempt to understand the mechanism leading to elevation of fibronectin levels in bacteremic rats, which is distinct from that observed with RE blockade. Clearance of exogenously administered fibronectin after bacteremia was also determined. Rats received either saline, Pseudomonas aeruginosa (1 X 10(9) organisms), gelatinized RE test lipid emulsion (50 mg/100 gm B.W.), or emulsion followed by Pseudomonas. Plasma fibronectin and Factor XIII were determined at 0, 2, 24, and 48 hours post-blockade or bacteremia. At 24 and 48 hr following bacteremia alone or bacteremia after RE blockade, there was a significant elevation (p less than 0.05) of plasma fibronectin and a concomitant decrease (p less than 0.05) of plasma factor XIII activity. Extractable tissue fibronectin from liver and spleen was also increased at 24 and 48 hours following R.E. blockade plus bacteremia. In addition, the plasma clearance of human fibronectin was significantly prolonged (p less than 0.05) following bacterial challenge. Infusion of activated Factor XIII (20 units/rat) during a period of hyperfibronectinemia (908.0 +/- 55.1 micrograms/ml) resulted in a significant (p less than 0.05) decrease in plasma fibronectin (548.5 +/- 49.9 micrograms/ml) within 30 min. Thus Factor XIII deficiency in rats with bacteremia may contribute to the elevation in plasma fibronectin by altering kinetics associated with the clearance of fibronectin from the blood.
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PMID:Factor XIII as a modulator of plasma fibronectin alterations during experimental bacteremia. 287 87

Serum angiotensin converting enzyme (serum ACE) levels and plasma fibronectin levels were measured daily in 46 septic patients during a ten day period. Thirty-eight patients developed ARDS; 28 survived (group 1), ten died (group 2), eight patients had no features of ARDS and survived (group 3). Sequential measurements of ACE and fibronectin levels were compared and plotted against indexes of respiratory impairment: PaO2 max Qs/Qt, static compliance and VD/VA ratio. These indexes were taken as criteria of weaning from controlled ventilation. During ARDS (groups 1 and 2), serum ACE levels decreased and were closely correlated with the severity of lung injury. Persistently decreased levels after eight days were consistent with continuing injury or lack of endothelial repair. On the other hand, plasma fibronectin levels increased throughout the study in survivors (group 1 and 3) and decreased in the group with fatal ARDS only (group 2). These results indicate that serum ACE levels might be a good index of endothelial injury and repair during ARDS and fibronectin a better index for evolution of sepsis and vital prognosis.
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PMID:Compared evolution of plasma fibronectin and angiotensin-converting enzyme levels in septic ARDS. 298 57


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