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)

Tissue plasminogen activator (t-PA) in plasma obtained from patients with acute hepatitis, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, drug-induced intrahepatic cholestasis, obstructive jaundice, fulminant hepatitis or disseminated intravascular coagulation (DIC), was analysed chromatographically. Liver disease cases showed a new peak (peak C) on HPLC fractionation. The protein of peak C had a lower molecular weight than ovalbumin. Lysine- and zinc- chelating affinity chromatography revealed that the peak C consist with the light chain (L-chain) of t-PA. The L-chain was also found in patients with DIC, but disappeared after improvement of DIC. Therefore, it was suggested that appearance of the L-chain would be related to acceleration of secondary fibrinolysis in plasma. The L-chain was especially high in plasma obtained from patients with decompensated liver cirrhosis. These results indicated that high increase of the L-chain in cases of severe liver disease may be due to either impaired clearance of t-PA in the liver or secondary hyperfibrinolysis accompanied by DIC. We concluded that determination of the L-chain of t-PA may contribute to clarify the mechanism of hyperfibrinolysis in liver diseases.
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PMID:[Qualitative analysis of tissue plasminogen activator in plasma obtained from various liver diseases by gel filtration and affinity chromatography]. 210 95

Mean serum zinc and copper levels were depressed in 94 children aged 1 month to 9 years who presented with meningococcal disease. The mean serum zinc level was 44 micrograms/dl (reference value 78 micrograms/dl, SD 18) and the mean serum copper level 157 micrograms/dl (reference value 159 micrograms/dl, SD 27). Nineteen patients had serum zinc levels less than 25 micrograms/dl and ten patients had serum copper levels less than 101 micrograms/dl. Serum zinc levels were significantly lower in patients who were septicaemic or in whom manifestations of severe disease such as shock, more than 20 petechiae, ecchymoses and evidence of disseminated intravascular coagulation occurred compared to those without these features. Serum copper concentrations were higher than reference levels in patients with meningitis and in less severely ill patients. Copper levels were significantly lower in patients with septicaemia, severe disease, shock, more than 20 petechiae, ecchymoses, disseminated intravascular coagulation, leucopenia and patients who died compared with patients without these features.
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PMID:Serum zinc and copper levels in children with meningococcal disease. 404 25

Acute zinc poisoning has been observed in dogs following the ingestion of metallic zinc objects. A 1 1/2-y-old female miniature bull terrier exhibiting anorexia, vomiting, depression, fever (39.9 C), icterus and intravascular hemolysis was diagnosed with acute zinc poisoning. Anemia, Heinz body production, azotemia and bilirubinemia were also evident. Abnormal pancreatic, hepatic and renal functions were also apparent. A radio opaque object was observed in the stomach. Based upon an elevated plasma zinc level of 28.6 ppm, a tentative diagnosis of zinc poisoning was made. Following surgical removal of the metallic zinc object, a blood transfusion and fluid therapy were given to restore the normal blood volume. Heparin, Cephazolin and Raniditine were also given, although chelation therapy was not provided. Zinc levels in the plasma declined in a steady fashion (half-life = 7.6 d). Complications, such as disseminated intravascular coagulation, chronic pancreatitis, renal or hepatic failure, were not observed. By 20 d post surgery, only mild elevation of liver enzymes was evident. Measurements of the half-life of zinc may provide a useful indication of prognosis and the success of treatment.
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PMID:Diagnosis and treatment of zinc poisoning in a dog. 1548 53

This review describes the role of oxidative stress caused by endotoxin challenge in sepsis or septic shock symptoms. We observed that endotoxin injection resulted in lipid peroxide formation and membrane damage (near 60-150 kDa) in the livers of experimental animals, causing decreased levels of scavengers or quenchers of free radicals. The administration of alpha-tocopherol completely prevented injury to the liver plasma membrane caused by endotoxin, and suggested that lipid peroxidation by free radicals might occur in a tissue ischemic state, probably by disseminated intravascular coagulation (DIC), in endotoxemia. In mice, depression of Ca(2+)-ATPase activity in the liver plasma membrane may contribute to the membrane damage caused by endotoxin, and the increase of [Ca(2+)](i) in the liver cytoplasm may partially explain the oxidative stress that occurs in endotoxemia. It seems that endotoxin-induced free radical formation is regulated by Ca(2+) mobilization. Moreover, we have suggested that the oxidative stress caused by endotoxin may be due, at least in part, to the changes in endogenous zinc or selenium regulation during endotoxemia. Interestingly, the extent of TNF-alpha-induced oxidative stress may be the result of a synergism between TNF-alpha and gut-derived endotoxin. It is likely that bacterial or endotoxin translocation plays a significant role in TNF-alpha-induced septic shock. On the other hand, although nitric oxide (NO) has been implicated in the pathogenesis of vascular hyporesponsiveness and hypotension in septic shock in our experimental model, it is unlikely that NO plays a significant role in liver injury caused by free radical generation in endotoxemia.
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PMID:Oxidative stress and septic shock: metabolic aspects of oxygen-derived free radicals generated in the liver during endotoxemia. 1683 Dec 3

Neisseria meningitidis (Nm) is a leading cause of septicemia in childhood. Nm septicemia is unique with respect to very quick disease progression, high in vivo bacterial replication rate and its considerable mortality. Nm circumvents major mechanisms of innate immunity such as complement system and phagocytosis. Neutrophil extracellular traps (NETs) are formed from neutrophils during systemic infection and are suggested to contain invading microorganisms. Here, we investigated the interaction of Nm with NETs. Both, meningococci and spontaneously released outer membrane vesicles (SOMVs) were potent NET inducers. NETs were unable to kill NET bound meningococci, but slowed down their proliferation rate. Using Nm as model organism we identified three novel mechanisms how bacteria can evade NET-mediated killing: (i) modification of lipid A of meningococcal LPS with phosphoethanolamine protected Nm from NET-bound cathepsin G; (ii) expression of the high-affinity zinc uptake receptor ZnuD allowed Nm to escape NET-mediated nutritional immunity; (iii) binding of SOMVs to NETs saved Nm from NET binding and the consequent bacteriostatic effect. Escape from NETs may contribute to the most rapid progression of meningococcal disease. The induction of NET formation by Nm in vivo might aggravate thrombosis in vessels ultimately directing to disseminated intravascular coagulation (DIC).
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PMID:In vitro resistance mechanisms of Neisseria meningitidis against neutrophil extracellular traps. 2375 Aug 48

Amniotic fluid embolism (AFE) is a disorder with a high mortarity rate, because it often causes sudden respiratory failure, circulatory collapse and disseminated intravascular coagulation (DIC). We present a case of AFE in which an obstetric anesthesiologist promptly initiated resuscitation of a parturient and saved her without any sequelae. Her fetus was diagnosed as intrauterine fetal demise on 25th gestational week and vaginal delivery under epidural analgesia was planned. One hundred and five minutes after induction of labor with prostaglandine E1, sudden tetanic convulsion occurred with a loss of consciousness. An obstetric anesthesiologist immediately started to resuscitate her and her consciousness was restored. However, noncoagulable vaginal bleeding followed. As the hemorrhage persisted, AFE was suspected. Anesthesiologists gave effective massive transfusion therapy, and she recovered from coagulopathy. Total blood loss was 5,524 g. This case was diagnosed as AFE with high serum sialyl-Tn antigen and zinc-coproporphyrin. The obstetric anesthesiologists are one of the best groups of physicans for resuscitation because they have skills in managing obstetric emergencies such as AFE. In this case, the crucial points for successful resuscitation were prompt obstetric anesthesiologist involvement and good communications with obstetricians and midwives.
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PMID:[Prompt resuscitation by obstetric anesthesiologists saved a parturient with amniotic fluid embolism: a case report]. 2449 77

The registry program of amniotic fluid embolism (AFE) in Japan started in 2003. More than 400 hundred clinical diagnosed amniotic fluid embolism has been accumulated. Those data showed that there were two etiologies of AFE: the fetal materials create physical obstructions in the maternal microvessels in various organs, such as the lung; and (ii) the liquids cause an anaphylactoid reaction that leads to pulmonary vasospasm and activation of platelets, white blood cells and/or complements. The clinical findings showed that AFE was characterized mainly by cardiopulmonary collapse, the other involves the presence of disseminated intravascular coagulation (DIC) and atonic bleeding. Zinc coproporphyrin-1, sialyl Tn antigen (STN), complement C3, C4 and interleukin-8 have been used as serum markers of AFE. The levels of zinc coproporphyrin-1 and STN were increased in cardiopulmonary collapse type AFE, and a marked reduction of C3 and C4 was observed in DIC type AFE. At the primary medical institution, initial treatments for shock airway management, vascular management, fluid replacement, administration of anti-DIC therapy such as antithrombin, and administration of fresh frozen plasma should be provided. C1 esterase inhibitor activity in AFE cases was significantly lower than those of normal pregnant women. C1 esterase inhibitor may be a promising candidate of treatment of AFE.
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PMID:Amniotic fluid embolism: pathophysiology and new strategies for management. 2488 9

Acinetobacter baumannii is an important nosocomial pathogen that displays high antibiotic resistance. It causes a variety of infections including pneumonias and sepsis which may result in disseminated intravascular coagulation. In this work, we identify and characterize a novel secreted, zinc-dependent, metallo-endopeptidase CpaA (coagulation targeting metallo-endopeptidase of Acinetobacter baumannii) which deregulates human blood coagulation in vitro and thus is likely to contribute to A. baumannii virulence. Three quarters of the clinical isolates tested (n = 16) had the cpaA gene; however, it was absent from two type strains, A. baumannii ATCC 17978 and A. baumannii ATCC 19606. The CpaA protein was purified from one clinical isolate and was able to cleave purified factor (F) V and fibrinogen and reduce the coagulation activity of FV in human plasma. CpaA-treated plasma showed reduced clotting activity in contact pathway-activated partial thromboplastin time (aPTT) assays, but increased clotting activity in tissue factor pathway prothrombin time (PT) assays. A significant portion of clinically relevant A. baumannii isolates secrete a protease which targets and deregulates the coagulation system.
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PMID:CpaA a novel protease from Acinetobacter baumannii clinical isolates deregulates blood coagulation. 2491 20

Amniotic fluid embolism (AFE) is a rare, high-risk obstetric complication primarily found in the lungs and potentially related to anaphylaxis. Tryptase release from the mast cell reflects anaphylaxis. Case report and findings: A female, aged over 40 years, presented with uterine atony and lethal hemorrhage after induced vaginal labor. Cervical laceration was accompanied by severe hemorrhage. Stromal edema and myometrial swelling were consistent with uterine atony. Alcian blue staining and zinc coproporphyrin immunostaining disclosed AFE, which was more prominent in the uterus than in the lungs. Tryptase immunostaining was diffuse and prominent around the activated mast cells (halos) in the uterus, including the cervix. Similar distribution of findings on the AFE markers, tryptase halos, complement receptor C5aR, and atony in the uterus suggested the causality of AFE to anaphylaxis, complement activation and atony. It is probable that disseminated intravascular coagulation (DIC), induced by AFE, uterine atony and cervical laceration, caused the lethal hemorrhage. It is likely that AFE, in association with cervical laceration, induces uterine anaphylaxis, complement activation, atony, DIC and lethal hemorrhage.
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PMID:Amniotic fluid embolism induces uterine anaphylaxis and atony following cervical laceration. 2492 37

Zinc is necessary for successful gametogenesis in mammals; however the role of zinc in the gonad function of non-mammalian species has not been investigated. The genetic tractability, short generation time, and hermaphroditic reproduction of the nematode C. elegans offer distinct advantages for the study of impaired gametogenesis as a result of zinc deficiency. However the phenotypic reproductive effects arising from zinc restriction have not been established in this model. We therefore examined the effect of zinc deficiency on C. elegans reproduction by exposing worms to the zinc chelator N,N,N',N'-tetrakis (2-pyridylmethyl)ethane-1,2-diamine (TPEN). Treatment began at the early larval stage and continued until reproductive senescence. TPEN treatment reduced the total number of progeny produced by C. elegans hermaphrodites compared with control subjects, with the largest difference in output observed 48h after larval stage 4. At this time-point, zinc deficient worms displayed fewer embryos in the uterus and disorganized oocyte development when observed under DIC microscopy. DAPI staining revealed impaired oogenesis and chromosome dynamics with an expanded region of pachytene stage oocytes extending into the proximal arm of the gonad. This phenotype was not seen in control or zinc-rescue subjects. This study demonstrates that reproduction in C. elegans is sensitive to environmental perturbations in zinc, indicating that this is a good model for future studies in zinc-mediated subfertility. Aberrant oocyte development and disruption of the pachytene-diplotene transition indicate that oogenesis in particular is affected by zinc deficiency in this model.
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PMID:Zinc deficiency reduces fertility in C. elegans hermaphrodites and disrupts oogenesis and meiotic progression. 2766 71


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