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)

The Malignant Neuroleptic Syndrome (MNS) is characterised by the acute appearance of hyperthermia, muscular rigidity, loss of motor control, and alterations in the level of consciousness, which could prove fatal if not rapidly diagnosed and treated. It is held to be a serious idiosyncratic reaction which appears in patients being treated with neuroleptics, independently of the dosage and the length of time the drug has been prescribed. Relapses do not usually occur when the drug is re-prescribed, once the acute phase has been passed, which suggests the existence of predisposing factors. There are frequent complications (acute respiration difficulties, acute kidney failure, disseminated intravascular coagulation and multiorganic failure) which condition the prognosis. The treatment consists of the suppression of the neuroleptic, rehydration, and specific drugs (bromocryptine, sodium dantroline). We have analysed two new cases which reacted badly, one of them with a multiorganic failure and the other, who had a good initial therapeutical response but who went on to develop a peripheral neuropathy, an infrequent complication in international medical casebooks.
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PMID:[Neuroleptic malignant syndrome, multiorgan failure and peripheral polyneuropathy]. 854 8

We report a 53-year-old woman who developed a cerebral infarction in the left middle cerebral artery area. Although she did not have a hemorrhagic tendency, the results of her examination showed a chronic disseminated intravascular coagulation (DIC) and a left ovarian carcinoma. Gabexate mesilate (FOY) and nafamostat mesilate (FUT) were not effective for her DIC. One month after admission, she had another cerebral infarction in the right posterior cerebral artery area. She was treated by heparin sodium and her chronic DIC improved. Then, she was operated on for ovarian carcinoma; the histologic finding was clear cell adenocarcinoma. No recurrence of DIC nor cerebral infarction was observed postoperatively. Patients with cerebral infarctions caused by chronic DIC due to ovarian carcinoma have been reported in the literature, but few patients had a favorable prognosis such as the present case. Heparin therapy appears to be the treatment of choice for chronic DIC rather than FOY or FUT, if there is no hemorrhagic tendency. When a patient with DIC develops cerebral infarction, one should always investigate for possible malignant tumors.
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PMID:[Favorable prognosis in a case of recurrent cerebral infarctions caused by chronic disseminated intravascular coagulation due to ovarian carcinoma]. 870 62

1. Nafamostat mesilate (NM) is a novel serine-protease inhibitor used for the treatment of acute pancreatitis and disseminated intravascular coagulation. Recently, NM has been reported to cause hyperkalemia due to reduced urinary excretion of potassium (K). 2. This review briefly summarizes the roles of the cortical collecting duct (CCD) in the renal K excretion. 3. In vitro microperfusion technique was applied to examine whether NM, and its two metabolites, p-guanidinobenzoic acid (PGBA) and 6-amidino-2-naphthol, directly act on the CCD. 4. It was demonstrated that these compounds act mainly on the apical membrane of the collecting duct cell in the CCD and inhibit the amiloride-sensitive sodium (Na) conductance, resulting in an inhibition of K secretion. PGBA had the most potent action. 5. This direct action of these two metabolites, rather than NM, could contribute to the NM-induced hyperkalemia.
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PMID:Mechanisms of hyperkalemia caused by nafamostat mesilate. 874 49

After clinical assessment, pertinent history, and family history, the clinician often has a good idea concerning the cause of a patient's bleeding. The most appropriate laboratory tests can then be ordered. Routine screening tests include a complete blood cell count, platelet count, and evaluation of a peripheral blood sample, a prothrombin time, and an activated partial thromboplastin time. Thrombocytopenia may result from idiopathic thrombocytopenic purpura, disseminated intravascular coagulation, or, less commonly, acute leukemia, aplastic anemia, thrombotic thrombocytopenic purpura, or a particular drug that a patient is taking. Again, the patient's history, physical findings, and evaluation of a well-prepared peripheral blood smear will be helpful in determining the cause of the patient's thrombocytopenia. An isolated prolongation of the activated partial thromboplastin time may result from low levels of factors VIII, IX, or XI. A slightly prolonged activated partial thromboplastin time and a moderate decrease in factor VIII may reflect von Willebrand disease or the "carrier" state for hemophilia A. In women a greatly prolonged activated partial thromboplastin time and very low levels of factor VIII (< 3%) most often result from an acquired factor VIII inhibitor (autoantibody against factor VIII) or from severe (type III) von Willebrand disease. If von Willebrand disease is suspected (because of menorrhagia with or without other mucous membrane bleeding, a positive family history, and a prolonged activated partial thromboplastin time), more specific laboratory tests for this disease should be done. These include assays of factor VIII, von Willebrand factor antigen, von Willebrand factor activity (measured by the ristocetin cofactor assay), and template bleeding time. In von Willebrand disease the defect is in von Willebrand factor. The affected individual may have subnormal levels of structurally and functionally normal von Willebrand factor (this is called "classic" or type I von Willebrand disease) or may produce von Willebrand factor that is structurally and functionally abnormal (von Willebrand disease type 2). Individuals who inherit a gene for von Willebrand disease from both parents have severe (type 3) von Willebrand disease and will have extremely low levels (< 3%) of von Willebrand factor and factor VIII and will have a very prolonged bleeding time. In most populations type I disease is the most common form, whereas type 3 is the least commonly encountered form. It should be noted that levels of von Willebrand factor can be influenced by the patient's blood type (persons who have blood type AB have 60% to 70% higher levels than do persons who have blood type O) and can be elevated during pregnancy, stress, and hyperthyroidism. The two major functions of von Willebrand factor are to serve as a "bridge" between platelets and injury sites in blood vessel walls and to protect circulating factor VIII from rapid proteolytic degradation. Thus, if a patient has either too little or functionally abnormal von Willebrand factor, the bleeding time will be prolonged and factor VIII will be decreased (because it is not being protected by von Willebrand factor). It should be determined which type of von Willebrand disease a particular patient has because treatment depends on type. Multimeric analysis of von Willebrand factor can be done with use of sodium dodecyl sulfate gels, radiolabeled antibody to von Willebrand's factor, and autoradiography. This will allow visualization of the multimeric structure of von Willebrand factor. In type I disease all bands are present, whereas in the type 2 variants 2A and 2B no high-molecular-weight multimers are seen. Desmopressin acetate (which is available in parenteral form for intravenous use and in a highly concentrated intranasal spray formulation) is the treatment of choice for classic type I disease. The drug effects a rapid release of von Willebrand factor from endothelial cell stor
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PMID:Screening and diagnosis of coagulation disorders. 882 61

Infrared differential interference contrast (IR DIC) videomicroscopy was used to measure and characterize cell swelling induced by activation of glutamate receptors (GluR) in a neostriatal brain slice preparation. This swelling is, in many cases, a prelude to necrotic cell death. Activation of N-methyl-D-aspartate (NMDA) and non-NMDA ionotropic GluRs caused cell swelling. The concentration-response relationships and the time courses of the onset of agonist-induced swelling were very similar for NMDA and kainate (KA). However, cells were able to recover from KA but not NMDA-induced swelling. Results from ion substitution experiments suggest that sodium, chloride and to a lesser extent calcium ions play critical roles in this swelling. Heterogeneity in the response to NMDA occurred within cells of the neostriatum. Approximately 15% of the cells did not swell when exposed to NMDA. The magnitude of the NMDA-induced swelling also varied depending on the region of the nervous system. Swelling was greater in the neostriatum and neocortex than in the hippocampus and it did not occur in the suprachiasmatic nucleus. In conclusion, IR DIC videomicroscopy can be used to follow quantitatively the dynamics of GluR-evoked responses in single cells and should be instrumental in determining the factors capable of modifying excitotoxicity.
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PMID:Glutamate receptor-induced toxicity in neostriatal cells. 882 70

Experimental infection of three indigenous breeds of sheep in Nigeria, namely the West African Dwarf (WAD), Yankasa and Ouda resulted in fatal disease with the Zinga Rift Valley Fever virus. Infected sheep of the three breeds responded by pyrexia within 24 h of infection, that lasted 6 to 7 days, but peaked between day 2 and 4 post-infection. Viraemia coincided with pyrexia and peaked (10(9) PFU/ml) 3 days p.i. in Yankasa and WAD sheep, but with highest titre (10(7.5) PFU/ml) in Ouda sheep. Zinga Rift Valley Fever virus infection of sheep was characterised by hyperactivity, watery and mucoid nasal discharges, projectiles and bloody diarrhoea, external haemorrhage and clinical manifestations of nervous disorders. Viraemia was followed by low level of antibody development in all the infected sheep. Haemotological changes included a sharp fall in the PCV, Hb concentration and total RBC count during the course of the disease. These changes were most severe in the Yankasa, followed by WAD and Ouda breeds. There were thrombocytopaenia, prolongation of prothrombin and clotting times in all the infected sheep. There was also progressive leucopaenia associated with lymphopaenia. The total protein and albumin levels were depressed, but the globulin level rose from day 5 p.i. The changes in the serum biochemical constituents included sharp and progressive increase in the level of alanine aminotransferase and aspartate aminotransferase. The sodium level decreased gradually while that of potassium was initially stable but later increased until the infected animals died. There was a significant increase in the level of blood urea nitrogen from day 3 p.i. that continued until the infected animals died. Gross and microscopic examinations of the carcasses of the infected sheep showed significant lesions in many organs, including disseminated intravascular coagulation.
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PMID:Experimental infection of three Nigerian breeds of sheep with the Zinga strain of the Rift Valley Fever virus. 888 13

A 34-year-old man was admitted to our hospital for a headache in March, 1995. The patient's hemoglobin was 7.5 g/dl, platelet count was 1.8 x 10(4)/microliter and white blood cell (WBC) count was 12,400/microliters with 99% myeloblasts. Myeloblasts were agranular or hypogranular but electron microscopy revealed microgranules in cytoplasm, and a few faggots were observed. The bone marrow was hyperplastic due to myeloblasts and chromosomal abnormality was recognized: 46, XY, t(15; 17) (q22; q12). PML-RAR alpha with intron 3 breakpoint of the PML locus, and rearrangements of the T-cell receptor beta and gamma genes were detected. These cells were positive for CD2 (63%), CD8 (47%), CD13 (87%) and CD33 (99%). Microgranular variant type of acute promyelocytic leukemia (APL) was diagnosed. Disseminated intravascular coagulation (DIC) was also present. The patient was treated with enocitabine, daunorubicin, 6-mercaptopurine, dalteparin sodium, anti-thrombin III concentrates and gabexate mesilate with prophylactic frozen transfusions of fresh plasma and platelet transfusions for 5 days, but WBC count did not decrease and DIC did not improve. The patient died of cerebral hemorrhage 7 days after diagnosis of APL. APL with CD8 expression has never been reported. We suggest that therapy should be modified in this type of APL and conclusions concerning the most appropriate therapeutic strategy will depend on the results of treatment of similar cases in the future.
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PMID:[CD2 and CD8 expression in acute promyelocytic leukemia]. 899 25

Both trauma and infection cause a rise in body temperature, white blood cell count, acute phase proteins, fluid and sodium retention and negative nitrogen balance. This phenomenon is often described as "acute phase response" or "systemic inflammatory response syndrome" to denote a coordinated systemic response to significant tissue injury and/or microbial invasion. It is generally agreed that the acute phase response is mediated through the interaction of cytokine and neuroendocrine pathways. Tumor Necrosis Factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are two of the major key cytokines involved in the generation of acute phase response. Interleukin-6 are consistently found in septic, trauma and post-operative patients and correlated well with the severity of sepsis or injury. IL-6 is responsible for the fever and metabolic changes in the acute phase. In addition to IL-6, TNF-alpha was proved to be the mediator that orchestrates the hemodynamic and tissue injury in septic shock. TNF-alpha destroys endothelial cells and induces disseminated intravascular coagulation, fluid shift, shock, multiple organ system failure and death. On many clinical occasions, both infection and trauma may happen simultaneously on the same patient. Our study demonstrated that operation on the infected patients would cause a synergistic effect on both TNF-alpha and IL-6 levels. The pulse increase in TNF-alpha and the persistent elevation of IL-6 were responsible for the post-operative unstable clinical condition in the infected patients. Should we block the cytokine signal and inflammatory response that appear to be harmful? Animal studies have shown that the septic shock to endotoxin challenge can be prevented by pretreatment with monoclonal antibody against TNF-alpha. The transcription of TNF-alpha can be blocked with corticosteroid in vivo. The post-operative increase in IL-6 and its related inflammation can be attenuated with corticosteroid, epidural anesthesia and narcotics. However, although blocking the inflammatory response has a beneficial effect of stress free it also eliminates our ability to fight with bacterial infection by lowering our immune response. How to manipulate these cytokines is a question of art more than science.
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PMID:[Similarity and synergy of trauma and sepsis: role of tumor necrosis factor-alpha and interleukin-6]. 908 32

Five of fourteen patients with multiple system atrophy (MSA) experienced a total of eight episodes of malignant syndrome, three episodes in 1, two episodes in 1 patient, and a single episode in each of the other patients. Four patients had extrapyramidal symptoms and required antiparkinson therapy, including dopaminergic agonists. Five episodes occurred in the summer season. Two were caused by decreased or irregular doses of antiparkinson drugs, one by administration of an antidepressant drug, three by complications, and two by elevation of body temperature of environmental origin. A patient without parkinsonism became febrile after administration of droxidopa, which may be a central pyrogenic substance that acts via the noradrenergic system. Administration of dopaminergic drugs and dantrolene sodium was followed by recovery in four episodes in three patients. One patient manifested dysautonomia after recovery from the malignant syndrome. Another patient with high serum creatine kinase levels and myoglobinuria developed renal failure requiring hemodialysis. Another patient died of DIC. Besides withdrawal of dopaminergic agents, which alter monoaminergic neuron activity, stress to the body and heating by a variety of factors tend to trigger the malignant syndrome in MSA.
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PMID:[Malignant syndrome in multiple system atrophy]. 919 91

We investigated fibrin(ogen)-related antigens in liver tissues of rabbits infected with rabbit haemorrhagic disease (RHD) virus. Fibrin(ogen)-related antigens were detected in the sinusoids of liver at six hours post infection (pi). At 18 hours pi, the antigens were clearly detected in the hepatocytes infiltrated with heterophils rather than in the sinusoid. In the rabbits that spontaneously died (30 hours pi), fibrin(ogen)-related antigens were detected in both degenerating and some intact hepatocytes. They were also expressed in the necrotic foci of hepatocytes infiltrated by heterophils. By immunoprecipitation fibrin(ogen)-related antigens were extracted from the infected liver homogenates and analysed by sodium dodecyl sulphate polyacrylamide gel electrophoresis and Western blot analysis. There was an increase in fibrinogen and A alpha polypeptide chains in the liver homogenates from rabbits sacrificed at 18 and 24 hours pi, including those that died. Disseminated intravascular coagulation developed after progress of degeneration and necrosis of hepatocytes in RHD. It is assumed that the resultant consumption of fibrinogen triggers replenishment of fibrinogen by hepatocytes.
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PMID:Fibrin(ogen)-related antigens in rabbits experimentally infected with rabbit haemorrhagic disease virus. 942 44


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