Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections due to Streptococcus pneumoniae and products from the organism have been associated with alterations in blood clotting and function of platelets. Pneumococci and pneumococcal polysaccharide shortened the clotting times of whole blood, platelet-rich plasma (PRP), and platelet-poor plasma (PPP) in vitro. Clotting times of PPP and PRP from C6-deficient animals were likewise decreased. The bacteria had no effect on the one-stage prothrombin time or the partial thromboplastin time when the organisms were used as activating agents. Platelets aggregated in the presence of pneumococci, but aggregation was prevented by the addition of cyclic adenosine 3', 5'-monophosphate (cAMP). Furthermore, cAMP corrected the shortened clotting time of PRP in the presence of pneumococci. The clumping and release of polymorphonuclear coagulant that was induced by pneumococci was not prevented by cAMP. Thus, pneumococci exert several dose-dependent thromboplastic effects: (i) release of platelet thromboplastic substances; (ii) a direct thromboplastic effect; and (iii) release of polymorphonuclear coagulant.
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PMID:Effect of pneumococci on blood clotting, platelets, and polymorphonuclear leukocytes. 0 Mar 31

The effect of flomoxef, a newly developed oxacephem antibiotic with an N-hydroxyethyltetrazolethiol (HTT) side chain, on blood coagulation and alcohol metabolism was compared with that of a series of cephalosporin antibiotics with N-methyltetrazolethiol (NMTT), thiadiazolethiol (TDT) or methylthiadiazolethiol (MTDT) side chains in position 3' of the cephalosporin nucleus known to cause hypoprothrombinemia and bleeding in patients who are malnourished, debilitated and/or of high age. A disulfiram-like effect caused by inhibition of aldehyde dehydrogenase was observed for NMTT-containing antibiotics. Studies were carried out on healthy volunteers and on rats. Eight-day treatment with 2 g flomoxef i.v. once or twice daily in five and six healthy male volunteers, respectively, did not cause any significant changes in prothrombin time (PT), coagulation factors II, VII, IX or X, in hepaplastin values or fibrinogen levels, activated partial thromboplastin time (APTT), platelet counts, bleeding time, or collagen- and ADP-induced platelet aggregation. Inhibition of vitamin K epoxide reductase was observed in rats treated with flomoxef, yet to a much lesser extent than observed for cephalosporins with NMTT, TDT or MTDT side chains. This defect was quickly normalized by vitamin K injection. There were no differences between oxacephem (1-O) and cephem (1-S) compounds with respect to effects on blood clotting and platelet aggregation. Flomoxef and its side chain HTT showed no influence on alcohol metbolism.
Infection 1991
PMID:Effect of flomoxef on blood coagulation and alcohol metabolism. 178 45

Between October 1985 and March 1988, 16 patients received the Jarvik-7 total artificial heart as an interim device before transplantation. Ten patients were afflicted with cardiomyopathy, and 6 had end-stage ischemic disease. All but 1 were men; the mean age was 47 years (range, 27 to 59 years). Thirteen patients developed cardiogenic shock despite the use of intravenous inotropic agents (mean, 23 days; range, two to 83 days) and the intraaortic balloon pump (mean, 13 days; range, two to 65 days). Three other patients became candidates because of failed transplantation. The 100-mL Jarvik-7 device was used in the first 3 patients; all subsequent recipients were treated with the 70-mL Jarvik-7. Postoperative anticoagulation was designed to keep the partial thromboplastin time between 2 and 2.5 times control. The control values were obtained during administration of heparin and dipyridamole. In all cases the function of the total artificial heart was adequate to support the needs of the recipient, and there were no mechanical difficulties with the device or the drive system. The average time of implantation was 9 days (range, one to 35 days). Two patients died before transplantation, 1 with sepsis from fungus and the other with hemorrhage from a torn pulmonary arterial anastomosis. Fourteen patients received cardiac allografts, and 7 continue to survive without restrictions. Infection within the mediastinum caused the death of 4 patients after transplantation; in 3 of these mediastinitis was not recognized before transplantation but occurred within the first 2 weeks after transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interim use of the Jarvik-7 artificial heart: lessons learned at Presbyterian-University Hospital of Pittsburgh. 264 3

Eleven patients with terminal renal insufficiency requiring dialysis were treated with 3 X 2 g cefotaxime in an open study lasting five days when the clinical findings strongly indicated a serious bacterial infection. The effect of the administration of the high-dose antibiotic on the coagulation system (Quick test, partial thromboplastin time, thrombin time, antithrombin III and platelets) and on brain function (EEG) was investigated. The serum levels showed that the serum concentrations were not abnormally high in cases of terminal renal insufficiency requiring dialysis. In contrast to previous investigations in other beta-lactam antibiotics, no changes in the coagulation system or EEG occurred. On the basis of these findings, no reduction in the dose appears necessary for cefotaxime, if therapy does not exceed five days.
Infection 1985
PMID:Tolerance in patients with terminal renal insufficiency of high doses of cefotaxime. 405 48

Pigs were infected with highly virulent (Tengani '62), with moderately virulent (DR '79) African swine fever (ASF) virus, or with virulent hog cholera (HC) virus. Changes in platelet counts, selected coagulation assays and concentrations of factor VIII-related antigen (VIIIR:Ag) were monitored. Permeability of aortic endothelium was studied after the injection of Evan's blue dye on various days after infection with DR '79 ASF virus. Virulent ASF virus caused prolongation of the activated partial thromboplastin time (APTT), 1-stage prothrombin time, and thrombin clotting time as early as postinoculation day (PID) 4. These changes became progressively more severe until death. Both virulent HC and DR'79 viruses induced an increase APPT and thrombin clotting time at PID 3 to 4, only occasionally did the prothrombin time increased significantly (P less than 0.01). The APPT began to decrease on PID 7 and 8, but only DR'79-infected pigs lived long enough to regain a normal APTT. Infection by ASF viruses caused acute thrombocytopenia after PID 6 and platelet counts of HC virus-infected pigs decreased progressively from the onset of fever to levels of 1 to 2 X 10(5)/mm3 at PID 6 to 7. All ASF virus-infected pigs had an increase in VIIIR:Ag beginning at PID 3, with maximum increases at PID 6 to 7. Hog cholera virus infection did not cause consistent changes in levels of VIIIR:Ag. Pigs infected with DR'79 virus did not have increased vascular permeability to Evan's blue dye during infection; however, there was markedly decreased staining of the aorta after pigs became thrombocytopenic.
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PMID:Coagulation changes in African swine fever virus infection. 644 89

Bacterial adherence as a result of specific surface properties may be a contributory factor in the pathogenesis of bacterial endocarditis giving certain types of bacteria a selective advantage to cause this disease. Adherence could interact with other pathogenetic mechanisms, and this interaction could promote or hamper the development of endocarditis. Dextran production by streptococci, the activation of the clotting system by monocyte tissue thromboplastin, and phagocytic removal of bacteria from the vegetational surface by granulocytes and monocytes are examples of interacting mechanisms that could contribute to the pathogenesis of bacterial endocarditis.
Infection 1982
PMID:The role of bacterial adherence in the pathogenesis of infective endocarditis. 710 16

Theileria lawrencei tick-derived stabilate infection of 8 cattle resulted in the development of panleukopenia and hypoproteinemia. In addition to these changes, T. parva infection caused mild normocytic, normochromic, non-responsive anemia at either of two dose rates. Disseminated intravascular coagulation, as indicate by positive protamine paracoagulation tests, prolonged prothrombin and partial thromboplastin times, and thrombocytopenia, developed in cattle infected with either of the Theileria spp., and was probably an important intermediary mechanism leading to death. Infection of calves with a high dose of T. parva stabilate resulted in more rapid onset of clinico-pathologic changes than did the low dose infection. Theileria lawrencei infection produced a severe, acute syndrome, the clinico-pathologic alterations of which varied in time of onset and severity between those of the T. parva high dose and low dose groups.
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PMID:A comparative study of the disease in cattle caused by Theileria parva or T. lawrencei: II. Hematology, clinical chemistry, coagulation studies and complement. 720 9

Infection of naive North American horses with 10(4) cell culture infectious doses (CCID50) of virulence variants of African horsesickness virus (AHSV), designated AHSV/4SP, AHSV/9PI, and AHSV/4PI, reproduced three classical forms of African horsesickness: acute (pulmonary), subacute (cardiac), and febrile, respectively. Distinct clinicopathologic and hemostatic abnormalities were associated with each form of disease. Hemostatic abnormalities included increased concentration of fibrin degradation products and prolongation of prothrombin, activated partial thromboplastin, and thrombin clotting times. Hemostatic findings indicated activation of the coagulation and fibrinolytic systems with clotting factor consumption in acute and subacute cases of African horsesickness. Hematologic abnormalities in acute and subacute cases of African horsesickness included leukopenia, decreased platelet counts, elevated hematocrit, and increased erythrocyte counts and hemoglobin concentration. Leukopenia was characterized by lymphopenia, neutropenia, and a left shift. Increased levels of serum creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and alkaline phosphatase, hypocalcemia, hypoalbuminemia, hypoproteinemia, and elevated creatinine, phosphorus, and total bilirubin levels were present in some but not all horses. Metabolic acidosis, indicated by decreased total bicarbonate and increased lactate and anion gap, was present in horses with the acute form of disease. Mild thrombocytopenia and leukopenia were occasionally associated with the febrile form of disease. These results suggest a role for intravascular coagulation in the pathogenesis of African horsesickness.
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PMID:Clinical pathology and hemostatic abnormalities in experimental African horsesickness. 777 Oct 50

Disseminated intravascular coagulation (DIC) is uncommon in acquired immunodeficiency syndrome (AIDS), despite the high incidence of infectious diseases. We describe an HIV-infected patient presenting with disseminated cryptococcosis, who had clear-cut laboratory evidence of progressively worsening DIC (thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, hypofibrinogenemia, increased fibrin(ogen) degradation products and D-Dimer, reduced antithrombin III), although the clinical signs of the disease were rather scarce. The patient died despite intense treatment, which included heparin and fresh frozen plasma, and DIC was confirmed histologically. It is suggested that, in a patient with AIDS presenting with an opportunistic infection, laboratory signs of DIC should be carefully checked to early recognize this complication and promptly initiate the required therapy.
Infection
PMID:Disseminated intravascular coagulation associated with disseminated cryptococcosis in a patient with acquired immunodeficiency syndrome. 836 14

Fulminant hepatic failure as a result of hepatitis A is a rarely diagnosed complication entity in developed countries. With the advent of specific serologic markers for acute hepatitis A virus infection, the incidence and pathology of fulminant hepatitis A can be more clearly defined. We describe four patients (one adult, three children; two males and two females, ages 2 1/2-58 years) referred to our institution for orthotopic liver transplantation subsequent to fulminant hepatic failure following hepatitis A infection. All of these patients had a history of residence in or travel to hepatitis A endemic areas. Hepatitis A infection was documented by the presence of serum IgM against hepatitis A virus prior to transplantation. Infection with hepatitis B virus, cytomegalovirus, Epstein-Barr virus, and herpes simplex virus was excluded by clinical and specific serologic examinations. All patients presented with varying degrees of encephalopathy, progressing to coma. Coagulopathy in the form of prolonged prothrombin time and partial thromboplastin time was present in all patients. Peak liver parenchymal enzymes increased to greater than ten times the upper limit of the normal range. Total and direct bilirubin levels increased to > 20 and 10 mg/dl, respectively. Histologic evaluation of the explanted livers showed a spectrum of changes ranging from periportal hepatocellular necrosis with focal parenchymal collapse and prominent bile duct proliferation to massive necrosis with complete loss of hepatic architecture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fulminant hepatic failure with massive necrosis as a result of hepatitis A infection. 840 20


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