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)

Anticoagulants in the form of heparin, dipyridimole, steroids, prostaglandin E1, Macrodex, and antithrombin III were administered in separate experiments prior to endotoxin infusion in the dog. The pattern of disseminated intravascular coagulation (DIC) developed consistently when endotoxin alone was administered. Heparin dosages from 1 to 10 mg/kg did not influence the appearance of thrombocytopenia but effectively eliminated the decrease in fibrinogen levels ordinarily found. Antithrombin III (AT III), obtained from the National Red Cross, administered in a dose designed to provide a doubling of the circulating AT III, reduced the fibrinogen utilization to a similar degree as heparin without affecting the platelet loss. Dipyridimole, as administered, was ineffective in this model, and did not alter the development of thrombocytopenia or the hypofibrinogenemia. Steroids, Macrodex, and prostaglandin E1 had minimal effect on the coagulopathy. Our finding would suggest that the endotoxin effect on dog platelets id direct, and not mediated by thrombin, and that the role of heparin in the clinical management of DIC should be considered only in instances in which renal complications exist.
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PMID:Endotoxin-induced intravascular coagulation (DIC) and its therapy. 40 May 81

After successful animal studies since 1986, a single left lung transplantation was performed on a 35-year-old male patient with end-stage silicosis in July 1991. The surgical technique was similar to that used by the Toronto Transplant Group, except for some modification in bronchial anastomosis. The donor lung was preserved by simple surface cooling after the administration of heparin, methylprednisolone and PGE1. The ischemic time for the donor lung was 3.5 hours. A cardiopulmonary bypass through the femoral vessels was applied for a duration of 90 minutes. Immediate postoperative complications included massive bleeding, disseminated intravascular coagulation, adult respiratory distress syndrome and acute graft rejection. Fortunately, we overcame these complications through intensive care. Immunosuppression included antilymphocytic globulin, cyclosporine, azathioprine and corticosteroids. The results of this single lung transplantation were satisfactory. The patient was doing well and was able to satisfactorily breathe room air six weeks after the transplantation. Unfortunately, the patient died of opportunistic systemic aspergillosis six months after the transplantation. In conclusion, lung transplantation is an effective treatment for patients with end-stage lung diseases, and the results of this first single lung transplantation in Taiwan are encouraging and promising.
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PMID:Single lung transplantation for end-stage silicosis: report of a case. Lung Transplant Group. 136 97

A woman underwent cesarean delivery for premature labor, breech presentation, and ruptured membranes. Placenta accreta associated with uterine atony and severe hemorrhage was diagnosed. Prostaglandin E1 instead of prostaglandin F2 alpha was inadvertently administered in an effort to control the hemorrhage. The resulting complications included profound hypotension, disseminated intravascular coagulation, and ventricular tachycardia.
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PMID:Inadvertent administration of prostaglandin E1 instead of prostaglandin F2 alpha in a patient with uterine atony and hemorrhage. 156

Increased pulmonary vascular resistance (PVR) and microvascular hyperpermeability resulting in lung edema and arterial hypoxemia are mainstays in the development of adult respiratory distress syndrome (ARDS). The proposed pathophysiologic mechanisms include activation of complement and polymorphonuclear leukocytes secreting lysosomal enzymes, toxic oxygen metabolites (TOM) and eicosanoids. Platelets and coagulation factors are also involved, and in the most severe cases even monocytes are activated as reflected in release of thromboplastin. The latter may elicit disseminated intravascular coagulation (DIC). Under physiologic conditions lung blood flow is diverted from poorly to better oxygenated areas by way of hypoxic pulmonary vasoconstriction (HPV), thereby counteracting a decrease in arterial oxygenation. Many vasoactive substances have been proposed and again refuted as possible mediators of HPV. In this study we have focused on the following: histamine, catecholamines, arachidonates, calcium, phosphoinositides and TOM as well as endothelium-derived relaxing and constricting factors. Whether HPV is present in ARDS and whether it is advantageous or not seems to depend on the stage and extent of disease. We discuss possible interactions between HPV and ARDS mediators and between HPV and various vasoactive agents tested for therapeutic effects. Out of the abundance of mediators released, prostacyclin, prostaglandin E1, activated complement and platelet activating factor have been shown explicitly to inhibit HPV whereas others are suspected of doing so. In therapeutical use, prostacyclin has proved to reduce PVR and at the same time enhance cardiac output and oxygen delivery. In mild to moderate ARDS, improvement of arterial oxygenation has also been obtained employing almitrine bismesylate, a potentiator of HPV. Experimentally, adenosine effectively reduces increments in PVR and microvascular permeability with modest effects on systemic circulation. However, further investigations are warranted to decide whether adenosine or more specific blockers as, for instance, monoclonal antibodies against tumor necrosis factor should be integrated in ARDS therapy in the future.
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PMID:Hypoxic pulmonary vasoconstriction in the adult respiratory distress syndrome. 192 27

Prostaglandin E1 (PGE1) has a direct vasodilating effect to smooth muscles of resistant vessel much more than that of capacitance one. In afterload mismatch, vasodilator which acts on resistant vessel mainly should be selected. We used PGE1 for vasodilator therapy to two patients with low cardiac output syndrome (LOS) in intensive care unit. One patient undergoing coronary artery bypass grafting developed LOS and disseminated intravascular coagulation which derived from post-transfusional anaphylactoid reaction. Another patient undergoing mitral valve replacement, tricuspid valve annuloplasty and coronary artery bypass grafting also developed LOS with massive thrombosis caused by cold agglutinin during cardio-pulmonary bypass. In both patients, PGE1 decreased systemic vascular resistance index and pulmonary arterial resistance index, and increased cardiac output. PGE1 inhibits release of lysosomal enzymes from polymorphonuclear leukocytes and increases splanchnic blood flow. These effects lead to inhibit production of myocardial depressant factor and might relate to the improvement of LOS partially. We suggest that PGE1 was effective for LOS after cardiac surgery, especially in afterload mismatch.
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PMID:[Prostaglandin E1, as a vasodilator therapy, for low output syndrome after cardiac surgery]. 261 23

Twenty-six patients underwent resection and graft replacement of an aortic arch aneurysm (proximal arch,5; transverse arch:2, distal arch,8; and type A dissecting aneurysm. Retrograde cerebral perfusion with pharmacological cerebral protection was carried out during aortic arch aneurysm surgery. Prostaglandin E1, thiopental methylpredonisolone were administered for cerebral protection during core cooling. D-Mannitol and deferoxamine mesylate (radical scavengers) were administered for prevention of reperfusion injury. retrograde cerebral perfusion time was 48 +/- 16 minutes (range 20-80 minutes). Perfusion flow was 288 +/- 93 mL/min (range 150-500 mL/min). Since retrograde cerebral perfusion requires no arterial cannulation or aortic cross clamp, the operative field is simplified, and the risks of air and debris emboli to the brain were minimized. Reconstruction was designed to minimize the circulatory arrest time. Eleven cases underwent emergency surgery due to rupture and acute dissection. Five patients (19.2%) died (three from bleeding from the distal anastomosis, one from postoperative DIC and, one from intraoperative dissection). The remaining 21 patients survived neurologically intact. Retrograde cerebral perfusion with pharmacological cerebral protection is a very simple method to prevent air embolism or thromboembolism in aortic arch aneurysm surgery and allows aortic arch replacement in a bloodless field. In spite of the extended circulatory arrest time, recovery of consciousness was complete.
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PMID:Retrograde cerebral perfusion with pharmacological cerebral protection in the repair of aortic arch aneurysm. 923 55

A twenty-year-old woman with anorexia nervosa (body mass index=11) suffered from severe liver dysfunction (aspartate aminotransferase 5,000 IU/l, alanine aminotransferase 3,980 IU/l, prothrombin time 32%), hypoglycemia (serum glucose 27 mg/dl), and pancreatic dysfunction (amylase 820 IU/l, lipase 558 IU/l). She fell into a depressive state with irritability, which was not improved by intravenous glucose. Despite treatment with plasmapheresis for the liver dysfunction, she subsequently developed pulmonary edema, acute renal failure, gastrointestinal bleeding, and disseminated intravascular coagulation. Hemodialysis, mechanical ventilation and drug therapy including prednisolone, prostaglandin E1, and branched-chain amino acid, improved her critical condition. In this case, malnutrition may have been the cause for the liver dysfunction and subsequent complications.
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PMID:Anorexia nervosa with severe liver dysfunction and subsequent critical complications. 1043 64

The developments and trends of hemostatic and antithrombotic drugs in Japan were investigated chronologically for the last 50 years after the 2nd World War. 1. Hemostatic drugs are classified into three groups ; capillary stabilizers, blood coagulants and antifibrinolytics. l) As to capillary stabilizers, flavonoid (rutin, 1949), adrenochrome derivative (carbazochrome, 1954) and conjugated estrogen (Premarin, 1964) were introduced therapeutically. Especially, the soluble types of adrenochrome compounds (Adona 1956, S-Adchnon, 1962) were devised and used widely in Japan. 2) Drugs concerning blood coagulation, thrombin, introduced in 1953, and hemocoagulase, a snake venom introduced in 1966, were used clinically. V.K. groups producing various coagulation factors were introduced as V.K1 (Phytonadione, 1962) and V.K2 (rnenatetrenone,1972), and they were admitted in "The Japanese Pharmacopoeia"editions 8 and 14, respectively). 3) Regarding antifibrinolytic drugs, Japanese researchers have made remarkable contributions. e-Aminocapronic acid (Ipsilon, 1962) and tranexamic acid (Transamin, 1965) were developed and used for various abnormal bleedings or hemorrhage associated with plasmin over-activation. tranexamic acid also proved to suppress inflammations of the throat such as tonsillitis, pharyngitis or laryngitis. 2. Antithrombotic drugs are also divided into three groups; anticoagulants, antiplatelet drugs and fibrinolytics.1) The anticoagulants used therapeutically by injection are heparins (Na-salt, 1951; Ca-salt, 1962) and low-molecular-weight heparins such as dalteparin (1992), parnaparin (1994) and reviparin (1999). The low molecule compounds are superior to the original heparins in reducing the risk of bleeding. As oral anticoagulants, coumarin derivatives, dicumarol (1950), ethylbiscoumacetate (1954), phenylindandione (1956) and warfarin (1962) are known. Warfarin potassium is the main drug for oral therapy of thromboembolism lately. Gabexate mesilate (1989) and nafamostat mesilate (1989) were developed in Japan and used for DIC and acute pancreatitis to inhibit protease enzymes. Argatroban is a unique antithrombin product developed by Japanese researchers in 1990, and is used for vascular or cerebral thrombosis. After noticing in 1968 that aspirin inhibits platelet aggregation and prevents myocardial infraction, projects for developing antiplatelet drugs were initiated worldwide. Ticlopidine, originally developed in France, was introduced in 1981 and prevailed widely in Japan for reducing the risk of thrombotic stroke. Aspirin itself was recognized by the FDA (USA) as an antithrombotic drug in 1988, and was also approved by Japanese authorities in 2000. PGE1 clathrate compounds have also been developed as antiplatelet drugs; alprostadil alfadex for injection (1979), and limaprost alfadex for oral use (1988). The PGI2 product, beraprost sodium, for oral use followed them in 1992. Other antiplatelet drugs with unique mechanisms explored in Japan: Ozagrel (1988), which inhibits TXA2 synthetase, cilostazol (1988), which inhibits cAMP phosphodiesterase, and sarpogrelate (1993), which blocks 5HT in platelets, are the notable drugs in this field. Ethyl icosapentate, from fish oil, is available for antiplatelet therapy. Concerning the fibrinolytic system, plasminogen activators are useful for thromboembolism. The streptokinase from bacterial origin developed in the USA and Europe was not introduced, and urokinase (1965) was the first plasminogen activator developed in Japan. Then tissue plasminogen activators (t-PA) tisokinase (cell culture, 1991), alteplase (genetical recombination, 1991), nateplase (genetical recombination, 1996), monteplase (1998) and pamiteplase (1998) were developed and approved for acute myocardial infarction. Nasaruplase (prourokinase, cell culture,1991) was also approved for the same indication. While the development of the hemostatic drugs ceased in the 1960s, avid project studies for antithrombotic drugs including fibrinolytics began in the 1980s and are progressing now towards new molecular targets. This may be due to the increasing tendency of cardiovascular thromboembolic diathesis in Japan. (The figures in parentheses are the years approved by the Japanese Ministry of Health, Labor and Welfare.)
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PMID:[A 50-year history of new drugs in Japan-the development and trends of hemostatics and antithrombotic drugs]. 1457 69

A study was conducted on the changes in platelet function and platelet count in the Sprague-Dawley rat induced by a bends-producing N2-O2 compression-decompression cycle. In those instances where mild to moderate cases of decompression sickness were produced, a decrease in platelet reactivity to ADP-induced aggregation occurred immediately postdive along with an increase in inhibition of aggregation by prostaglandin E1. Both effects returned to control levels 24 hours postdive. In moderately affected animals, platelet counts were lower than normal 24 hours postdive but were similar to control values 72 hours postdive. These results tend to support current hypotheses regarding the etiological relationship between disseminated intravascular coagulation and decompression sickness as a function of bubble nucleation.
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PMID:Supportive evidence for altered platelet function in the dived rat. 1562 36

Although in Japan, transplant organs obtained from brain-dead donors (BDD) has been allowed since October 1997, to date only 27 liver grafts from BDD have been obtained. The severe shortage of transplantable organs is a big problem, not only in liver transplantation but also other organ transplants. Liver transplantation is a fundamental treatment for end-stage liver disease. In order to perform living-donor liver transplantation (LDLT) in a safer manner, apheresis (plasmapheresis) plays a major role in Japan because of the prevalence of LDLT wherein later re-transplantation is difficult. Therefore, because of a limited donor supply and because the need of patients with end-stage liver disease is critical, use of grafts from ABO-incompatible donors may be the only available option. From June 1990 to November 2004, 1010 patients underwent 1060 LDLT cases at Kyoto University Hospital. Of these, 139 LDLT cases (13.1%) received ABO-incompatible living-donor liver grafts. The role of apheresis in ABO-incompatible LDLT is the reduction of antibody titers such as anti-A or anti-B antibody. We perform preoperative apheresis as a general rule for incompatible cases, and the recipient's antibody level against the donor's blood type is decreased to one eighth of the baseline value before LDLT. Up to the present, baseline antirejection regimens included steroids, tacrolimus and cyclophosphamide. At first, splenectomy was performed during operation to suppress antibody production, and intraportal infusion therapy was performed to control local disseminated intravascular coagulation (DIC) occurring in ABO-incompatible grafts. At that time, three agents--methylprednisolone, prostaglandin E1, and gabexate mesilate--were infused continuously for 3 weeks after LDLT. At present, instead of intraportal infusion therapy, hepatic artery infusion therapy without splenectomy is adopted because of portal thrombosis, and two agents--methylprednisolone and prostaglandin E1--are infused continuously for 3 weeks after LDLT. Recently, we introduced an anti-CD20 monoclonal antibody (Rituximab) instead of splenectomy for B cell deletion before ABO-incompatible LDLT. In this article, we describe our therapeutic strategy and the role of apheresis around ABO-incompatible LDLT.
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PMID:Therapeutic strategy and the role of apheresis therapy for ABO incompatible living donor liver transplantation. 1607 68


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