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)

Sepsis and its complications are severe clinical syndrome that is caused by systemic inflammatory response of the host to infection. Despite the use of common and numerous new therapeutic protocols, mortality from this severe disease is still very high. In the study are presented 155 patients (111 males, 44 females) of average age 49.6 years with mean septic score 12.9 (2-40). Mortality in our patients was 20.6%, septic shock developed in 31.6%, ARF in 20.0%, DIC in 12.9%, and MODS in 25.8% of patients. Positive correlation existed between initial sepsis score and mortality. Older age and the presence of primary diseases (34.2% of patients) were associated with significantly higher septic score and were good prognostic factor for the poor outcome of sepsis. Between mean arterial pressure in the first 24 h after the admission and mortality existed negative correlation (p < 0.05). Positive hemocultures were found in 69.7%, and bacterial infection in 78.7% of patients. GP bacteremia was found in 55.6% of patients and GN in 45.4% of all positive hemocultures. Confirmed bacteremia and bacteremia caused by GPB were associated with the higher mortality rate compared to the patients with negative hemocultures and GN bacteremia (p < 0.05). Concentrations of fibrinogen and urea in the blood at the admission in the patients with sepsis were very good prognostic factors of the disease outcome, and leukopenia, leukocytosis and neutropenia were associated with the increased mortality. Negative correlation existed between fibrinogen concentration and mortality (p < 0.001), while positive correlation (p < 0.001) existed between urea concentration and mortality. In the absence of more efficacious therapeutic protocols, fast recognition of the sepsis, evaluation of its severity, knowledge of the risk factors for its poor outcome and aggressive use of antibiotic and existing supportive therapy can significantly decrease high mortality of this too severe clinical syndrome.
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PMID:[Significance of determination of certain clinical and laboratory parameters in the evaluation of severity and outcome in sepsis]. 1070 10

Carboxypeptidase R (EC 3.4.17.20; CPR) and carboxypeptidase N (EC 3. 4.17.3; CPN) cleave carboxyl-terminal arginine and lysine residues from biologically active peptides such as kinins and anaphylatoxins, resulting in regulation of their biological activity. Human proCPR, also known as thrombin-activatable fibrinolysis inhibitor, plasma pro-carboxypeptidase B, and pro-carboxypeptidase U, is a plasma zymogen activated during coagulation. CPN, however, previously termed kininase I and anaphylatoxin inactivator, is present in a stable active form in plasma. We report here the isolation of mouse proCPR and CPN cDNA clones that can induce their respective enzymatic activities in culture supernatants of transiently transfected cells. Potato carboxypeptidase inhibitor can inhibit carboxypeptidase activity in culture medium of mouse proCPR-transfected cells. The expression of proCPR mRNA in murine liver is greatly enhanced following LPS injection, whereas CPN mRNA expression remains unaffected. Furthermore, the CPR activity in plasma increased 2-fold at 24 h after LPS treatment. Therefore, proCPR can be considered a type of acute phase protein, whereas CPN is not. An increase in CPR activity may facilitate rapid inactivation of inflammatory mediators generated at the site of Gram-negative bacterial infection and may consequently prevent septic shock. In view of the ability of proCPR to also inhibit fibrinolysis, an excess of proCPR induced by LPS may contribute to hypofibrinolysis in patients suffering from disseminated intravascular coagulation caused by sepsis.
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PMID:Pro-carboxypeptidase R is an acute phase protein in the mouse, whereas carboxypeptidase N is not. 1087 83

A 24-year-old, nulliparous woman in her 30th week of pregnancy was admitted due to threatened premature delivery. Ritodrin chloride relieved the premature contraction of the uterus but jaundice and drowsiness appeared 7 weeks later. Laboratory data revealed disseminated intravascular coagulation (DIC) with intrahepatic cholestasis, and ultrasound examination showed fatty liver. The patient was diagnosed with acute fatty liver of pregnancy (AFLP). Emergency delivery by Caesarean section was performed at 37 weeks of pregnancy and the liver function and DIC improved immediately. Liver biopsy 13 days after delivery showed nuclear swelling and cytoplasmic ballooning with mild fatty deposition. These findings were relatively compatible with acute AFLP. Higher magnification and electron microscopy revealed intracytoplasmic bacteria and fungus in the residual stage. The bacterial infection could be considered related to AFLP.
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PMID:Acute fatty liver of pregnancy showing microbial infection in the liver. 1119 91

Carboxypeptidase R (CPR) exists in precursor form (proCPR) in plasma in contrast to carboxypeptidase N (CPN), which is present in the active state. CPR plays two important roles, one of which appears to be the control of the inflammatory response by inactivation of anaphylatoxins such as complement-derived C3a and C5a. Therefore, an increase in CPR activity may facilitate rapid inactivation of these inflammatory mediators generated at the site of bacterial infection. Upregulation of proCPR expression during the inflammatory response initiated for instance by endotoxin (lipopolysaccharide) should play a role in suppressing hyper-reactivity as seen in septic shock. CPR also functions as an inhibitor of fibrinolysis, where its ability to prevent binding of plasminogen to lysine residues on fibrin clots significantly lengthens tissue plasminogen activator (tPA)-induced fibrinolysis time. Therefore, upregulation of proCPR production during the inflammatory response may exacerbate thrombosis contributing to the development of disseminated intravascular coagulation as well as other conditions involving thrombosis. Co-administration of tPA and a specific inhibitor of CPR, such as potato carboxypeptidase inhibitor, which does not affect CPN, may be useful in thrombolytic therapy.
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PMID:Carboxypeptidase R is an inactivator of complement-derived inflammatory peptides and an inhibitor of fibrinolysis. 1141 58

We measured Thrombopoietin (Tpo) levels in thrombocytopenic term and preterm babies with infection to investigate the relationship between thrombopietin levels and platelet counts. Sixteen preterm (27-34 weeks' gestational age) and 5 term neonates (38-41 weeks' gestational age) with the diagnosis of neonatal infection and thrombocytopenia (platelets <150 x 10(9)/L) but, without the evidence of disseminated intravascular coagulation, were prospectively enrolled in the study. Fifteen preterm (27-34 weeks' gestational age) and 9 term (38-40 weeks' gestational age) age-matched healthy neonates were enrolled in the study as control. Blood samples were obtained from each subject at the time when infection and thrombocytopenia were detected and stored until assay. Bacterial infection was confirmed by blood cultures in five patients and by tracheal cultures in five. Median Tpo levels of term controls were lower than those of preterm controls (62 pg/mL vs. 87 pg/mL) (p <0.05). Median Tpo levels of thrombocyopenic preterm patients were higher than the levels of healthy preterms (258 pg/mL vs. 87 pg/mL) (p <0.05). Similarly, median Tpo levels of sick terms were significantly higher than those of healthy term controls (209 pg/mL vs. 62 pg/mL) (p <0.001). There was not significant difference between the median Tpo levels of term and preterm babies with infection (258 pg/mL vs. 209 pg/mL) (p >0.05). There was no correlation between platelet counts and Tpo levels in both term and preterm groups. The results of our study show that healthy term and preterm babies have detectable levels of Tpo and preterm babies have higher Tpo levels than term infants. Although thrombocytopenic babies with infection have increased levels of Tpo, these levels are still lower than the levels of thrombocytopenic children/adult patients and there seems to be no correlation between platelet counts and thrombopoietin levels. So our observation of increased Tpo levels may still be inadequate for normal platelet production in this period. and this group of babies may also be candidates for the administration of recombinant human Tpo.
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PMID:Thrombopoietin levels of thrombocytopenic term and preterm newborns with infection. 1155 80

Several cases of granulomatous phlebitis of small hepatic veins are reported in the literature, though the etiology remains unclear. We experienced a similar case of granulomatous phlebitis involving terminal hepatic venules and this case will be reported in comparison with two previous cases presenting in our laboratory. A 39-year-old-female had a long course of medical treatment for epilepsy. She suffered from acute liver injury after prolonged fever for more than 1 week. Leukocytosis (11,100/ micro L) without eosinophilia, and inflammatory reactions such as C-reactive protein (21.0 mg/dL) were pointed out. She suffered from transient disseminated intravascular coagulation, but these abnormalities recovered with antibiotic and steroid therapy. Liver biopsy revealed granulomatous lesions mainly involving terminal hepatic venules. The possibility of tuberculosis was excluded by a negative Thiel-Nielsen stain and a negative molecular study for bacterial deoxyribonucleic acid of Mycobacteria species. Extrahepatic involvements were not clear clinically. This case and the previous two cases shared granulomatous phlebitis of the intrahepatic small hepatic veins, as well as clinical features suggestive of bacterial infection. Clinicians should be aware of such a rare clinicopathological entity.
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PMID:Granulomatous phlebitis of small hepatic vein. 1242 83

Autoimmune hemolytic anemia is rare in children. It is generally diagnosed in relation to a viral or bacterial infection but has also been described in association with drugs, autoimmune disease, malignancy, and immunodeficiency. The authors describe a 5-month-old infant who presented with severe autoimmune hemolytic anemia and disseminated intravascular coagulation as his initial manifestation of HIV infection.
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PMID:HIV infection presenting as severe autoimmune hemolytic anemia with disseminated intravascular coagulation in an infant. 1470 3

We describe a case of cord blood harvest for autologous transfusion in a neonate weighing 3,992 g with a giant sacrococcygeal teratoma. The umbilical vein was pierced with an 18-gauge needle, and placental blood was withdrawn into two 50-ml syringes filled with 4 ml of citrate-phosphate-dextrose solution. Resection of the sacrococcygeal teratoma was performed on day one. During the operation the infant lost 46 ml of whole blood, more than 15% of the estimated total blood volume, and thus underwent autologous transfusion with 27.8 ml of packed red cells obtained from autologous cord blood. Consequently, she could avoid homologous blood transfusion during the hospital stay. This case highlights the safety of this procedure, with no evidence of consumption coagulopathy, hemolysis or bacterial infection.
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PMID:Autologous cord blood transfusion in an infant with a huge sacrococcygeal teratoma. 1508 99

Disseminated intravascular coagulation (DIC) can develop infrequently in patients with tuberculosis and has a very high mortality rate. We conducted a retrospective study to evaluate the incidence of tuberculosis-induced DIC and to investigate the clinical manifestation, outcome, and prognostic factors of such patients. From January 2002 to December 2003, all culture-proven tuberculosis patients who developed DIC before starting anti-tuberculosis treatments were selected for this study. Patients who had other clinical conditions or were infected by other pathogens that may have been responsible for their DIC were excluded. Survival analysis was performed for each variable with possible prognostic significance. Our results showed that 27 (3.2%) out of the 833 patients with culture-proven tuberculosis had tuberculosis-induced DIC with a mortality rate of 63.0%. The most common clinical manifestations were fever (63.0%) and multiple patches of pulmonary consolidation (59.3%). Seven (25.9%) patients had disseminated tuberculosis. Twelve (44.4%) developed acute respiratory distress syndrome and three (11.1%) were associated with hemophagocytosis. Twenty-four (88.9%) patients had findings that were unusual for an acute bacterial infection, such as positive acid-fast smear, miliary pulmonary lesions, lymphocytotic exudative pleural effusion, and mediastinal lymphadenopathy. Early anti-tuberculosis treatment significantly improved survival. In conclusion, tuberculosis can cause DIC. Patients with non-miliary, non-disseminated tuberculosis could also develop the rare clinical manifestation. Since the prognosis was very poor in patients not treated at an early stage, a high index of suspicion is required, especially in those with clinical findings suggestive of tuberculosis.
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PMID:Mycobacterium tuberculosis inducing disseminated intravascular coagulation. 1584 21

The immune response to infection includes activation of the blood clotting system, leading to extravascular fibrin deposition to limit the spread of invasive microorganisms. Some bacteria have evolved mechanisms to counteract this host response. Pla, a member of the omptin family of Gram-negative bacterial proteases, promotes the invasiveness of the plague bacterium, Yersinia pestis, by activating plasminogen to plasmin to digest fibrin. We now show that the endogenous anticoagulant tissue factor pathway inhibitor (TFPI) is also highly sensitive to proteolysis by Pla and its orthologs OmpT in Escherichia coli and PgtE in Salmonella enterica serovar Typhimurium. Using gene deletions, we demonstrate that bacterial inactivation of TFPI requires omptin expression. TFPI inactivation is mediated by proteolysis since Western blot analysis showed that TFPI cleavage correlated with loss of anticoagulant function in clotting assays. Rates of TFPI inactivation were much higher than rates of plasminogen activation, indicating that TFPI is a better substrate for omptins. We hypothesize that TFPI has evolved sensitivity to proteolytic inactivation by bacterial omptins to potentiate procoagulant responses to bacterial infection. This may contribute to the hemostatic imbalance in disseminated intravascular coagulation and other coagulopathies accompanying severe sepsis.
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PMID:Proteolytic inactivation of tissue factor pathway inhibitor by bacterial omptins. 1898 66


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