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)

Between October 1985 and March 1988, 16 patients received the Jarvik-7 total artificial heart as an interim device before transplantation. Ten patients were afflicted with cardiomyopathy, and 6 had end-stage ischemic disease. All but 1 were men; the mean age was 47 years (range, 27 to 59 years). Thirteen patients developed cardiogenic shock despite the use of intravenous inotropic agents (mean, 23 days; range, two to 83 days) and the intraaortic balloon pump (mean, 13 days; range, two to 65 days). Three other patients became candidates because of failed transplantation. The 100-mL Jarvik-7 device was used in the first 3 patients; all subsequent recipients were treated with the 70-mL Jarvik-7. Postoperative anticoagulation was designed to keep the partial thromboplastin time between 2 and 2.5 times control. The control values were obtained during administration of heparin and dipyridamole. In all cases the function of the total artificial heart was adequate to support the needs of the recipient, and there were no mechanical difficulties with the device or the drive system. The average time of implantation was 9 days (range, one to 35 days). Two patients died before transplantation, 1 with sepsis from fungus and the other with hemorrhage from a torn pulmonary arterial anastomosis. Fourteen patients received cardiac allografts, and 7 continue to survive without restrictions. Infection within the mediastinum caused the death of 4 patients after transplantation; in 3 of these mediastinitis was not recognized before transplantation but occurred within the first 2 weeks after transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interim use of the Jarvik-7 artificial heart: lessons learned at Presbyterian-University Hospital of Pittsburgh. 264 3

Gram-negative septicemia/endotoxemia remains a serious clinical disorder that is often complicated by disseminated intravascular coagulation (DIC). Plasma antithrombin-III (AT-III) levels usually decrease during gram-negative septicemia/endotoxemia, and even moderate decreases in this major inhibitor of the coagulation system are associated with serious DIC. We demonstrated in an earlier study that prophylactic treatment of rats with 250 U/kg of AT-III followed by endotoxin challenge markedly attenuates DIC, indices of organ damage, and metabolic dysfunction. The present study was to determine whether treatment with 250 U/kg AT-III 1 hr after endotoxin challenge would be similarly efficacious. Rats treated with 250 U/kg of AT-III inactivated by human sputum elastase (ATX) served as protein controls. Blood samples for analysis were obtained 4 hr after AT-III or ATX treatment (5 hr after endotoxin challenge). Rats in the ATX treatment group exhibited abnormalities characteristic of endotoxemia, i.e., decreased fibrinogen levels and platelet counts, increases in prothrombin time and activated partial thromboplastin time, elevated serum glutamic oxaloacetic transaminase (SGOT) and alkaline phosphatase (AKP), and hypoglycemia. Treatment with AT-III markedly and significantly (P less than .05) attenuated all of these abnormalities, although survival was not increased. This study strongly suggests that supplementation of plasma AT-III is efficacious after the development of sepsis, although not as efficacious as prophylactic treatment.
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PMID:Antithrombin-III treatment limits disseminated intravascular coagulation in endotoxemia. 273 21

The levels of protein C (PC) and other coagulation factors were monitored during endotoxin-induced disseminated intravascular coagulation (DIC) in the dog. Initial evaluation of the effectiveness of intradermal administration of bolus endotoxin quantities into the dog, demonstrated induction of DIC in the canine, without the severe side effects associated with bacterial sepsis. Quantitative determination of canine plasma protein C levels were performed using a multiple step amidolytic assay, that included a specific precipitation of the vitamin K-dependent proteins from citrated plasma, followed by thrombin activation (and neutralization) and subsequent measurement of the activated protein C (APC) by chromogen hydrolysis. This investigation demonstrated, that over a twenty-four hour interval, intradermal administration of endotoxin produces a gradual decrease in the PC activity levels, concomitant with a significant reduction in the Factor V, Factor VIII and fibrinogen levels and platelet count, and a prolongation of the Prothrombin Time and Partial Thromboplastin Time. During the first 6 hours, protein C levels fell below the pre-levels and remained significantly lower in the surviving dogs. Thus, this endotoxin-induced DIC animal model permits evaluation of various hemostatic parameters, yet diminishes the severe clinical findings associated with DIC.
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PMID:Protein C activity levels in endotoxin-induced disseminated intravascular coagulation in a dog model. 278 30

A patient with T-polyagglutinable red cells and a severe coagulopathy provided an opportunity to observe the results of plasma transfusion in the face of T-activation. The patient was a 52-year-old Navajo Indian with a perforated gall bladder and related sepsis due to Clostridium perfringens. The gall bladder was removed surgically. Postoperatively, he had severe thrombocytopenia, and prolonged partial thromboplastin and prothrombin times. The patient's red cells were agglutinated by Arachis hypogaea and Glycine soja lectins but were unagglutinated by extracts of Salvia horminum, Salvia sclarea, and Bandeiraea simplicifolia. No untoward reactions or any evidence of hemolysis were observed when the patient was given platelet concentrates and 4 units of single-donor plasma. Serial plasma hemoglobin and haptoglobin levels documented that there was no hemolysis. His coagulopathy responded, and he had a successful surgical re-exploration and recovery. This case documents that serious adverse consequences do not necessarily follow transfusion of plasma in a recipient with T-activated red cells. T-activation is a relative but not absolute contraindication to plasma transfusion.
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PMID:Uneventful administration of plasma products in a recipient with T-activated red cells. 286

Adult respiratory distress syndrome (ARDS) is a complex pulmonary clinicopathologic condition associated with pulmonary endothelial injury and blood coagulation activation. In patients with ARDS from all causes, factor VII levels were significantly reduced. Patients with ARDS caused by sepsis had more evidence of intravascular coagulation and fibrinolysis than did patients with trauma-related ARDS by having significantly (p less than or equal to 0.05) increased prothrombin times, activated partial thromboplastin times, and fibrin degradation products, and decreased antithrombin III concentration. We sought to determine whether the proteins of the contact system of plasma proteolysis (factor XII, prekallikrein, high molecular weight kininogen, and C1 inhibitor) were also activated after acute lung injury. Patients with ARDS caused by either trauma or sepsis had significantly (p less than or equal to 0.01) reduced factor XII levels, high molecular weight kininogen functional activity, prekallikrein activity, and prekallikrein antigen levels compared with controls. In both the sepsis-related and trauma-related ARDS groups, C1 inhibitor activity was significantly reduced but C1 inhibitor antigen levels were significantly elevated from control. These findings showed that the proteins of the contact system were more extensively activated in ARDS than were the proteins that contribute to later reactions in intravascular coagulation and fibrinolysis. Activation of the contact system proteins could be the result of endothelial injury occurring as part of ARDS. Intravascular coagulation and fibrinolysis in patients with ARDS also arise from components independent from contact system activation.
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PMID:Activation of the contact system of plasma proteolysis in the adult respiratory distress syndrome. 339 29

The author analyses the reported data and his own findings concerned with the involvement of mononuclear phagocytes in the regulation of hemostasis and in the pathogenesis of a number of frequently occurring forms of the hemostatic system pathology. The content of monocytic thromboplastin was measured in 56 patients with the intravascular blood coagulation syndrome of varying etiology. Production of monocytic thromboplastin reached the highest degree in patients with purulent conditions whereas in patients presenting with the terminal stage of sepsis, it did not exceed normal or even dropped down, which may be connected with depletion of monocytes because of their preliminary hyperactivation.
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PMID:[Mononuclear phagocytes, the hemostasis system and the intravascular coagulation syndrome]. 353 69

Gram-negative septic shock remains a major clinical problem. One frequently encountered complication of sepsis is disseminated intravascular coagulation (DIC). The present study was to determine in an Escherichia coli endotoxemia awake rat model the efficacy of antithrombin-III (AT-III) prophylaxis and to explore the role of DIC in the pathogenesis of endotoxemia. We demonstrated that DIC occurs very early, before the appearance of detectable serious abnormalities in cardiovascular, metabolic, and biochemical variables indicative of organ damage or dysfunction; AT-III prophylaxis significantly ameliorates DIC, as evidenced by completely preventing the fall in plasma fibrinogen concentration and significantly limiting the increases in prothrombin time and activated partial thromboplastin time after 4 hours of endotoxemia; and AT-III prophylaxis dramatically increases permanent survival. Results of this study suggest that AT-III prophylaxis is very protective above a threshold dosage in an endotoxemic rat model and that protection is in part due to ameliorating DIC. Our data also suggest that DIC occurs very early during endotoxemia and may in part be responsible for the pathogenesis of endotoxemia in the rat. We conclude that AT-III prophylaxis may be efficacious in conditions of impending DIC, such as gram-negative septicemia/endotoxemia.
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PMID:Protection against disseminated intravascular coagulation and death by antithrombin-III in the Escherichia coli endotoxemic rat. 354 29

The relationship between mononuclear phagocyte thromboplastin activity, microorganisms and levels of endotoxin in peritoneal fluid and splanchnic and systemic circulation was evaluated during experimental endogenous gram-negative peritonitis in the rat. Significant rise in thromboplastin activity of mononuclear phagocytes was demonstrated in all three compartments. This newly synthesized thromboplastin is a trigger for important biologic systems such as the coagulation cascade, and thus may play a major role in the development of disseminated intravascular coagulation so often occurring in gram-negative sepsis. It probably also participates in the formation of fibrous intraabdominal adhesions. Aerobic and anaerobic microorganisms together with endotoxin were detected already 1 1/2 hours after induction of peritonitis, and subsequently were found to increase in parallel fashion. Determination of endotoxin is a rapid and seemingly reliable method for early detection of gram-negative infection and thus may be of clinical value.
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PMID:Mononuclear phagocyte thromboplastin, bacterial counts and endotoxin levels in experimental endogenous gram-negative sepsis. 373 43

Factors associated with prolongation of the prothrombin time were analyzed in 94 patients with intra-abdominal sepsis. Patients were randomized prospectively to receive either the combination of tobramycin and clindamycin (TM/C) or moxalactam (MOX). This paper presents a retrospective review designed to compare the frequency of prolonged clotting times and to analyze predisposing factors. Prothrombin time (PT) prolongation occurred more frequently in patients given moxalactam (19 of 47 patients) than in patients given the combination of tobramycin and clindamycin (9 of 47 patients) (p less than 0.05). Prolongation of the partial thromboplastin time (PTT) occurred in all patients with a prolonged PT. Liver disease, upper gastrointestinal surgery, and use of cimetidine were more frequent in those patients with abnormal PT/PTT values (p less than 0.05). Two moxalactam-treated patients with subsequent PT/PTT prolongation had individual clotting factors assayed before moxalactam treatment and at the time of detection of the abnormal PT. The activity of clotting factors II, VII, VIII, IX, X, and XII was reduced during MOX therapy. Treatment with vitamin K reversed the abnormality. In view of underlying abnormalities and rapid response to parenteral vitamin K, the mechanism is probably an acute vitamin K deficiency superimposed upon chronic vitamin K deficiency. In patients with intra-abdominal infection, those treated with MOX are more likely to develop abnormal PT than those treated with TM/C. Since abnormal PT/PTT was common even in TM/C patients, supplemental vitamin K should be considered for all seriously ill, older patients with abdominal infections.
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PMID:Clinical risk factors for prolonged PT/PTT in abdominal sepsis patients treated with moxalactam or tobramycin plus clindamycin. 396 31

Central venous plasma concentrations of thromboxane B2 (TXB2) the stable metabolite of the vasoconstrictor platelet aggregator thromboxane A2, were measured in 12 patients with septic shock. In 8 patients dying with septic shock the concentration of plasma TXB2 (912 +/- 250 pg/ml) was ten times higher than that in 4 survivors of septic shock (92 +/- 25 pg/ml) and 6 controls (91 +/- 18 pg/ml). Prothrombin time and partial thromboplastin time were significantly prolonged in nonsurvivors compared with survivors. Similarly, the alveolar-arterial oxygen gradient was significantly raised in nonsurvivors (233 +/- 39 mm Hg) compared with survivors (112 +/- 47 mm Hg). This study demonstrates that the metabolism of arachidonic acid to thromboxanes is increased in patients dying of septic shock and this raises the possibility that thromboxanes may be involved in the disseminated intravascular coagulation and respiratory distress syndrome associated with severe sepsis.
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PMID:Plasma thromboxane concentrations are raised in patients dying with septic shock. 612 85


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