Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old, full-term pregnant woman with progressive systemic sclerosis (PSS) came to the hospital with marked proteinuria and edema. Two days later, she gave birth to a normal baby. After delivery and during the next 48 hours, renal failure developed. A renal biopsy specimen disclosed findings characteristic of PSS, and immunofluorescence studies displayed nonspecific deposits of fibrinogen and complement. The patient's general condition deteriorated, with development of pericarditis and pulmonary failure; after several peritoneal dialysis treatments, a peritoneal infection developed, and the patient died of Gram-negative sepsis. The association of PSS and nephrotic syndrome is unusual.
 ...
PMID:Progressive systemic sclerosis and nephrotic syndrome. An unusual association resulting in postpartum acute renal failure. 721 97

After splenectomy the immunologic impairment and the susceptibility to infection is increased, but the most important impetus for splenic preservation has been the observation of the overwhelming postsplenectomy sepsis. Successful results with surgical repair of traumatized spleen and several different techniques have been reported. Instead of suture of splenorrhaphy we used in our experiences a new biological adhesive-system, consisting in thrombin, highly concentrated native human fibrinogen and clotting factor XIII. The highly adhesive properties, the excellent tissue compatibility and the haemostyptic effects recommend this system for using in preservation of the injured spleen as well as possible.
 ...
PMID:[The tissue adhesion of the ruptured spleen with highly concentrated human fibrinogen (author's transl)]. 728 72

The serum concentration of fibrinogen degradation product D (Fg D) is elevated after injury and sepsis. Purified human Fg D infused into awake rabbits causes progressive thrombocytopenia, complement depletion, hypoxia, vascular permeability to albumin and neutrophil congestion. In previous work experimentally induced thrombocytopenia protected lungs of rabbits against the effects of Fg D. The present study was designed to determine the role of the neutrophil in the development of Fg D-induced respiratory distress by rendering rabbits neutropenic with antiserum. Neutrophil depletion offered some, but not total, protection of the lungs against the toxic effects of Fg D infusion. Only one neutropenic rabbit became hypoxic. Vascular leak to albumin and water was diminished. Platelet and white blood cell counts decreased. However, complement activity was unaffected. The results suggest that neutrophils, like platelets, also contribute to the onset of respiratory failure in this model.
 ...
PMID:Cellular mediation of respiratory distress syndrome induced by fragment D. 733 1

Acute respiratory failure is a common complication in patients with disseminated intravascular coagulation associated with sepsis. To elucidate the role of coagulation abnormalities in acute lung injury in sepsis, we investigated the effect of anticoagulants on the pulmonary vascular injury in rat induced by lipopolysaccharide (LPS). When administered intravenously, LPS (5 mg/kg body weight) significantly increased the accumulation of 111indium-labeled neutrophils in lung 30 min after administration. Subsequently, the pulmonary vascular permeability and the serum level of fibrin and fibrinogen degradation products (E) [FDP (E)] increased and remained elevated for several hours. Neither heparin alone, heparin plus antithrombin III, or dansyl-Glu-Gly-Arg-chloromethyl ketone-treated factor Xa, a selective inhibitor of thrombin generation, prevented LPS-induced vascular injury 6 hours after LPS administration, whereas these substances significantly inhibited the increase in serum FDP (E) at that time. LPS-induced pulmonary vascular injury was significantly attenuated in rats with methotrexate-induced leukocytopenia or treated with ONO-5046, a potent granulocyte elastase inhibitor, although ONO-5046 did not inhibit the LPS-induced increase in serum FDP (E). Thus, activated leukocytes play a more important role than coagulation abnormalities in the pathogenesis of LPS-induced pulmonary vascular injury in an experimental rat model of endotoxemia.
 ...
PMID:Endotoxin-induced pulmonary vascular injury is mainly mediated by activated neutrophils in rats. 748 29

To obtain quantitative information on the in vivo activation of the protein C system during the acute phase of sepsis, several components of the protein C pathway were studied in 18 patients. Blood samples were obtained one day after diagnosis (day 1) and, in 11 patients, also on the fourth and tenth days after diagnosis (days 4 and 10). On day 1, patients showed laboratory signs of haemostatic alterations such as positive fibrinogen/fibrin degradation products, and increased thrombin:antithrombin-III (TAT) complex levels. Compared with the control group, patients on day 1 had significantly decreased (p < 0.001) antigenic protein C (69 +/- 28%) and protein C inhibitor (PCI) (33 +/- 22%) whereas a significant increase in the levels of activated protein C (APC) complexed with alpha 1-antitrypsin (alpha 1AT) (APC:alpha 1AT, 26 +/- 15 ng/mL) and APC:PCI complex (3.0 +/- 2.0 ng/mL), and in the level of plasma kallikrein (KK) complexes with PCI (KK:PCI) (31 +/- 22 ng/mL) was observed. There was a positive correlation between APC:alpha 1AT and TAT complex levels (r = 0.597, p = 0.009). In the follow-up a trend toward normal values in antigenic protein C and PCI, and in APC:PCI and KK:PCI complex levels was found. However, PCI remained significantly decreased compared to normal values. C4b-binding protein, alpha 1AT, and TAT and APC:alpha 1AT complexes did not show any significant variations during the course of the disease, suggesting the contribution of the inflammatory and haemostatic responses, in spite of the good recovery of the patients. This study shows that in the course of sepsis, patients experience a generalized activation of the protein C pathway which was more prominent on day 1, resulting in the consumption of protein C and PCI and in the increase of APC:inhibitor complexes. Moreover, these data provide further evidence that KK:PCI circulating complexes occur in vivo.
 ...
PMID:Activation of the protein C pathway in acute sepsis. 749 7

In septic patients capable of normal white cell responses, high plasma levels of PAI-I, t-PA antigen and t-PA-PAI-I complex were observed. The ratios of t-PA and PAI-I were such that free PA activity was almost never observed. In patients severely leucopenic prior to becoming septic the changes were significantly less marked, so presence of leucocytes enhances the fibrinolytic inhibition occurring in sepsis. The non-leucopenic septic group showed greater evidence of thrombin generation in that FPA levels were higher but fibrinogen levels were only slightly less and antithrombin levels not different from those in the leucopenic group. A greater tendency to fibrin deposition and the striking fibrinolytic inhibition noted in patients with normal white cell responses may contribute to the development of some of the complications of sepsis in which fibrin deposition participates and may explain their relative rarity in leucopenic patients. When shock supervened, levels of PAI-I were high in both leucopenic and non-leucopenic groups, indicating that a source of PAI-I outwith the leucocytes themselves contributes to the phenomena observed.
 ...
PMID:Influence of white blood cells on the fibrinolytic response to sepsis: studies of septic patients with or without severe leucopenia. 764 91

Radiolabeled antithrombin III (ATIII) was incubated at 37 degrees C with purified vitronectin (VN) or fibrinogen-deficient plasma before thrombin was added to initiate complex formation. Incorporation of radiolabeled ATIII was detected using polyacrylamide gel electrophoresis (PAGE) and autoradiography. The PAGE conditions appeared to be crucial for the detection of VN.TAT complexes. In the absence of SDS, ternary complexes formed instantaneously, whereas in the presence of SDS, only 50% of the TAT was associated with VN after a 60-min incubation. Formation of ternary complexes could be confirmed by gel filtration of the plasma to which thrombin was added. Furthermore, TAT in patient plasmas (disseminated intravascular coagulation and sepsis) was found to bind to heparin-Sepharose, indicating that this endogenously formed TAT was also associated with VN. The amino-terminal region of VN and the thrombin moiety of the TAT complex were found to be responsible for their interaction, which was stabilized by disulfide bridges. These results indicate that in normal plasma all TAT is complexed with VN. This association alters the conformational state of plasma VN, which appears to be responsible for the clearance of thrombin complexes from the circulation.
 ...
PMID:Ternary vitronectin-thrombin-antithrombin III complexes in human plasma. Detection and mode of association. 767 52

PMN (polymorphonuclear neutrophil) elastase is a proteolytic enzyme which is a biochemical marker for abnormal granulocyte stimulation. In inflammation and sepsis, excessive neutrophil stimulation results in significant amounts of PMN elastase being released into the plasma which indicates the severity of the disease and its prognosis. In 62 patients with osteomyelitis or suppurative arthritis, PMN elastase had a diagnostic sensitivity of 81%, which is comparable to the nonspecific erythrocyte sedimentation rate. Sensitivity of C-reactive protein (CRP) was 71%, fibrinogen 54% and leucocyte count 26%. PMN elastase was also useful in the follow up of patients with bone and joint infections; in the early post-operative period it became normal more quickly than the other findings unless the patients developed complications. Ten days after operation, PMN elastase was normal in 75% of the patients compared to the CRP which became normal in only 25%. Later both results were similar: on discharge from hospital, PMN elastase was normal in 77% and CRP in 71%.
 ...
PMID:PMN elastase in bone and joint infections. 769 65

Multiple hemostatic changes occur in sepsis and multiple organ failure (MOF). To evaluate the role of platelets in patients with sepsis and MOF, we examined changes in surface glycoproteins on circulating platelets of 14 patients with suspected sepsis and MOF. The severity of sepsis and MOF was assessed by the Elebute and APACHE II scoring systems, respectively. Using flow cytometric techniques and platelet specific monoclonal antibodies, platelet surface expression of fibrinogen receptor on GPIIb-IIIa, of von Willebrand Factor receptor GPIb, and of granule glycoproteins (thrombospondin (TSP), GMP-140, GP53) was measured. Plasma membrane expression of GPIIb-IIIa and GPIb on circulating platelets was not affected by sepsis of MOF. Septic patients, however, showed a significantly elevated fibrinogen receptor activity (LIBS1 expression) (p < 0.05) that correlated with severity of disease (r = 0.597, p = 0.043). No significant change in surface expression of granule glycoproteins (TSP, GMP-140, GP53) was noted in septic patients. In contrast, degranulation of granule glycoproteins was significantly elevated in MOF (p < 0.05) which well with severity of MOF (GMP-140, r = 0.611, p = 0.013; TSP, r = 0.643, p = 0.026). We speculate that platelets in sepsis circulate in a hyperaggregable but still reversible state that results in increased risk of microthrombotic events. In the course of the disease, irreversible platelet degranulation of adhesion molecules occurs that may play an important role in the development of MOF.
 ...
PMID:Severity of multiple organ failure (MOF) but not of sepsis correlates with irreversible platelet degranulation. 774 87

The organic symptoms and results of coagulation tests of disseminated intravascular coagulopathy (DIC) in 17 patients with infection were compared with those in 12 patients with malignancy. The infectious diseases were mainly sepsis and pneumonia, and the malignancy was mainly lung cancer. The mean antithrombin III (AT III) before treatment was 54% in infection and 68% in malignancy, and the AT III values improved after administration of 1500 U of AT III concentrates per day. The mean thrombin-antithrombin complex level decreased from 22 ng/ml to 9 ng/ml after the treatment in infection, but it increased in malignancy. There were no differences in DIC scores between infection and malignancy before treatment; however, the scores were significantly more improved in infection than in malignancy after treatment (p < 0.05). The fibrin/fibrinogen degradation product level, platelet count, and fibronectin level were also significantly more improved in infection than in malignancy. This better response to treatment in infection than in malignancy is probably due to eradication of the causative organisms by antibiotics in infection. These data suggest that therapy against both DIC and the underlying disease is crucial for successful treatment.
 ...
PMID:Disseminated intravascular coagulopathy in infection compared with that in malignant neoplasia. 774 1


<< Previous 1 2 3 4 5 6 7 8 9 10