Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrinogen degradation products (FDP) D and E are typically present in blood of patients with disseminated intravascular coagulation and related conditions in which granulocyte (PMN) defense against bacterial infection may be compromised. This study was intended to determine whether FDP modify PMN functions critical to their bactericidal activity. Incubation of human PMN and Escherichia coli with 50-100 micrograms/ml FDP did not affect phagocytosis, but reduced by greater than 90% the cells' ability to inhibit bacterial colony growth compared with control PMN incubated with albumin or fibrinogen. FDP (10-100 micrograms/ml) inhibited PMN O2- release and chemotaxis stimulated by FMLP by 17-50% (P less than 0.005) and 41% (P less than 0.01), respectively. Fragment E3, and not fragment D1, was primarily responsible for inhibition of FMLP-induced PMN O2- release. Phorbol myristate acetate (10 ng/ml), 1-oleoyl-2-acetylglycerol (10(-6) M), AA (4.2 x 10(-5) M), and zymosan-activated serum-stimulated PMN O2- release were also decreased 37-63% by FDP compared with control protein. There are at least two mechanisms by which FDP may impair PMN responses. With respect to FMLP, FDP (16-100 micrograms/ml) inhibited specific binding to the cell surface over a ligand concentration range of 1.4-85 nM [3H]FMLP. In contrast, FDP did not effect the extent of phorbol ester binding to PMN but blocked activation of protein kinase C. These data suggest that elevated plasma FDP inhibit several PMN functions critical to the bactericidal role of these inflammatory cells.
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PMID:Modulation of polymorphonuclear leukocyte microbicidal activity and oxidative metabolism by fibrinogen degradation products D and E. 254 77

The Shwartzman reaction is a classic biologic response in which the coagulation system is activated in vivo. Cellular initiation of the extrinsic coagulation protease cascade can be mediated by one or more limbs of the lymphoid response to diverse biological stimuli. The T cell-instructed monocyte and macrophage responses that have been implicated are mediated by a number of different cellular pathways and are elicited not only by antigens and allogeneic cells but also by other stimuli such as immune complexes and the lipid A moiety of bacterial lipopolysaccharide (LPS). The latter response has been implicated in the pathogenesis of the disseminated intravascular coagulation associated with bacterial infection. In the rapid collaborative cellular pathway response to LPS, we have described a relatively rigorous requirement for T helper cells in induction of the biosynthesis of tissue factor and Factor VII by monocytes. To elucidate potential regulatory aspects of this cellular procoagulant response, we provide the first evidence for the existence of T suppressor cells for the cellular procoagulant response to LPS by the rapid T cell-instructed pathway. Human peripheral blood lymphocytes were separated by cytoaffinity into Fc gamma-positive and Fc mu-positive cells and were characterized for their functional properties in the procoagulant response. T mu cells mediated the monocyte response, consistent with their identity with instructor cells. T gamma cells suppressed the response of monocytes to LPS in the presence of T mu cells, suggesting that they possess suppressor function for this response. The T gamma suppressor cells required stimulation by LPS to express their suppressor function and they exerted their suppressive effect directly on the monocyte. The existence and participation of LPS-responsive T suppressor cells on the cellular procoagulant response in vitro add a new dimension to the complexity of the rapid pathway of the collaborative cellular procoagulant response and may be important in the pathogenesis of disseminated intravascular coagulation.
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PMID:Regulatory roles of T mu and T gamma cells in the collaborative cellular initiation of the extrinsic coagulation pathway by bacterial lipopolysaccharide. 316 8

This case illustrates a unique clinical presentation of primary systemic amyloidosis, namely, overwhelming pneumococcal sepsis. Although there exists a well-established association between hyposplenism and overwhelming bacterial infection, amyloid replacement of the spleen as a primary cause of the hyposplenism has not been reported. Functional hyposplenism in regard to the effect of the spleen on erythrocytes has been reported in cases of diffuse splenic amyloid infiltration. The patient described had a fulminant course and associated disseminated intravascular coagulation, two clinical features more commonly seen in pneumococcemia occurring in asplenic patients as opposed to patients with normal splenic function. He had no predisposing factors, other than amyloid replacement of the spleen, to account for the development of overwhelming pneumococcemia. The immunologic function of the spleen in protection against overwhelming bacterial infection is briefly discussed.
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PMID:Primary amyloidosis with diffuse splenic infiltration presenting as fulminant pneumococcal sepsis. 382 9

Bacterial infection is associated with disseminated intravascular coagulation and fibrin deposition in the microcirculation; the mechanism of these effects in humans is still unclear. We have studied the generation of procoagulant activity (PCA) by cultured human endothelial cells (EC) in response to endotoxin. Cells from umbilical cord veins were grown in Eagle's minimum essential medium with 20% fetal calf serum till confluence. Absence of fibroblasts and macrophages was carefully checked. Endotoxin (Salmonella enteritidis lipopolysaccharide (LPS) W or Escherichia coli 0111:B4 LPS W, 0.01-1.0 micrograms/ml) was added to culture dishes for 4-6 h. PCA of EC was measured by a one-stage clotting assay and/or a two-stage amidolytic assay with the chromogenic substrate S-2222. In the absence of endotoxin, EC generated little, if any PCA (2-5 units/10(5) cells). In contrast, the addition of endotoxin resulted in generation of strong PCA that reached a maximum within 4-6 h (185-241 units/10(5) cells) and was dose-dependent between 1 and 0.01 microgram endotoxin/ml of culture medium. The generation of PCA required RNA and protein synthesis but did not require the presence of serum. No activity was found in the culture medium. The activity was of tissue thromboplastin type, as indicated by biological and immunological criteria. These endotoxin effects were observed in the absence of endothelial damage, as shown by phase-contrast microscopy and lack of 51Cr release. These data could contribute to elucidate the pathogenesis of vascular complications associated with endotoxemia in man.
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PMID:Cultured human endothelial cells generate tissue factor in response to endotoxin. 634 90

We describe two adults with fulminant pneumococcemia and disseminated intravascular coagulation aftertraumatic splenectomy. One died in a few days, and the other survived with amputation of gangrenous toes and fingers. Although the relationship between the serious blood-borne bacterial infection with disseminated intravascular coagulation and lack of adequate splenic tissue has been well established, the mechanism is poorly understood and there are no specific therapeutic measures available. We review the literature in regard to the possible prophylactic measures and discuss the benefits of various measures.
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PMID:Postsplenectomy pneumococcemia in adults. 689 58

Association of a circulating factor XI anticoagulant and disseminated intravascular coagulation (DIC) is described in a 33-year-old woman. Although the patient had rheumatoid arthritis and a bacterial infection treated with antibiotics, the anticoagulant was thought to be secondary to systemic lupus erythematosus. Curiously, the low levels of factor XI did not prevent the DIC from developing.
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PMID:Circulating factor XI antibody and disseminated intravascular coagulation. 721 96

Thrombocytopenia occurs in 20% to 40% of infants admitted to a neonatal intensive care unit. Approximately 30% of the newborns with severe thrombocytopenia below 50.10(9)/l platelets receive platelet transfusions. The etiology may be: bacterial infection, DIC and immune mediated thrombocytopenia. The consequences of thrombocytopenia are significant risks of severe intracranial hemorrhage and neurologic morbidity. Therapeutic platelet transfusions are given to actively bleeding neonates with less than 50.10(9)/l platelets. Prophylactic platelet concentrates are usually given to infants with platelets counts below 20.10(9)/l. The standard platelet concentrate (CMV-negative donor) is the product of choice for newborns. Fetal intracranial hemorrhage is possible as soon as 20 weeks of gestation in allo-immune thrombocytopenia. Actually percutaneous umbilical blood sampling is very useful to measure fetal platelets count in order to decide in utero maternal platelet transfusion. Maternal irradiated plateletpheresis concentrates are preferentially infused in this indication. At the end of pregnancy, cesarean section is preferred to normal vaginal delivery if fetal thrombocytopenia below 100.10(9)/l is observed. In pregnant women with auto-immune thrombocytopenia, the decision to carry out percutaneous umbilical blood samples should be weigh relatively to the 3-5% estimated risk of serious consequences. Platelets transfusions are particularly successful in immune thrombocytopenia but less effective in other clinical circumstances.
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PMID:[Platelet transfusions in neonatology]. 772 65

Idiopathic purpura fulminans usually occurs in young children and is frequently preceded by a preparatory viral or bacterial infection. Following a severe streptococcal pharyngitis, an 8-year-old boy developed purpura fulminans with disseminated intravascular coagulation and severe protein S deficiency (total antigen < 0.05 u/ml). Despite generous plasma infusions, skin necrosis progressed rapidly into compartment syndrome which required fasciotomy and skin grafting and resulted in the loss of three digits of the right foot. Total protein S remained low for over a month despite plasma supplementation and complete normalization of protein C levels. A polyclonal anti-protein S IgG was demonstrated in the patient's plasma, which decreased to 25% of baseline titre after 1 month and was undetectable 6 months after purpura fulminans, when plasma protein S had returned to normal. Transient, isolated and severe deficiencies of protein S have been reported in patients with idiopathic purpura fulminans and a previous preparatory infection. Autoimmune protein S deficiency may play a key role in the aetiopathogenesis of idiopathic purpura fulminans.
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PMID:Severe autoimmune protein S deficiency in a boy with idiopathic purpura fulminans. 773 61

Bone marrow necrosis (BMN), defined morphologically by destruction of hematopoietic tissue, including the stroma, with preservation of the bone, is a rare syndrome. The conditions in which it is seen include sickle cell disease, acute leukemia, metastatic neoplasia, and bacterial infection, particularly when hypovolemia and septic shock are present. BMN is also associated with disseminated intravascular coagulation (DIC) following irradiation and antineoplastic therapy. The antiphospolipid syndrome (APS) is characterized by antibodies directed against the antiphospolipid substrate. Because this substrate is prominently involved in the coagulation cascade and widely distributed on cell walls, patients present with venous or arterial thromboses, recurrent abortion, thrombocytopenia, and Coombs' positive hemolytic anemia, typically with raised anticardiolipin antibodies or a diagnostic lupus anticoagulant test. BMN does not appear to have been previously recognized in this context. We report what we believe to be the first such case and suggest that the high titers of antibodies present may have played a central role in its pathogenesis.
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PMID:Extensive bone marrow necrosis associated with antiphospholipid antibodies. 777 73

A 10-year-old boy was injured in a traffic accident, and computed tomography revealed cavitary pulmonary lesions in the left lower lobe. Although there was no evidence of bacterial infection, thrombocytopenia due to disseminated intravascular coagulation progressed. We performed a left lower lobectomy, and the patient improved rapidly.
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PMID:Lobectomy for traumatic pulmonary pseudocysts with disseminated intravascular coagulation: case report. 789 16


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