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)

Homozygous protein C (PC) deficiency is a rare genetic defect that usually results in fatal thrombotic complications (purpura fulminans and DIC), but it can be successfully managed with oral anticoagulants or PC replacement. The successful use of PC replacement for two individuals is described. The activity and antigen levels of PC in fresh frozen plasma (FFP) and prothrombin complex concentrate (PCC) are also reported. The concentration of PC in FFP is 87 +/- 15 units/dl. PC is present in all PCC analyzed; however, a ten-fold difference between the various brands and/or lots is noted. The PC activity and antigen correlates well with no significant levels of APC. Upon infusion of FFP into two homozygous PC-deficient children, the PC levels obtained were less than or equal to 30 units/dl post-infusion and undetectable after 12-18 hr. With infusions of PCC, plasma levels of PC obtained were 100-145 units/dl and less than 10 units/dl after 48 hr. The percent recovery and half-lives of PC from FFP and PCC were 49.8% and 7.8 hr, and 84% and 7.4 hr, respectively. One infant was treated every 48 hr for 2 years without significant purpura fulminans or DIC complications. The levels of the other PC system components did not change during the infusion of the PC-rich material. Based on this information, a specific replacement protocol has been developed using a PC-rich concentrate. However, several problems may arise with the "less pure" PC-rich concentrates: catheter-tip thrombosis, related large vessel thrombosis and blood-transmitted diseases. With a specific PC concentrate, replacement therapy is a viable alternative for the long-term management/treatment of homozygous PC deficiency.
Am J Hematol 1992 Sep
PMID:Protein C survival during replacement therapy in homozygous protein C deficiency. 150 96

The aim of the present study was to determine the diagnostic accuracy of ultrasonically guided fine-needle aspiration for liver lesions detected by ultrasound scan. A total of 142 aspirations were carried out in 129 patients with unifocal or multifocal liver lesions suspected of malignancy. The aspiration was made with a 22-gauge needle, guided by ultrasound. Based on histological, cytological, and clinical findings, final diagnoses were reached in 123 patients, 96 of whom had malignant liver disease and 27 benign liver disease. Among the 96 patients with malignant liver disease, the cytological findings revealed malignancy in 78 patients (81.3%) and suspected malignancy in five patients (5.1%), but failed to demonstrate malignancy in 13 patients (13.3%). Among 27 patients with benign liver disease, all the cytological findings indicated benignancy. The overall sensitivity, specificity, and positive and negative predictive values for cytological findings were 86.5%, 100%, 100%, and 76.9%, respectively. The diagnostic accuracy of ultrasonically guided fine-needle aspiration was 89.4%. In one patient with incipient chronic disseminated intravascular coagulation, a fatal intraperitoneal bleeding complicated the procedure. We conclude that ultrasonically guided FNA for cytologic diagnosis of liver lesions is highly accurate and is only rarely associated with fatal complication.
Am J Gastroenterol 1992 Sep
PMID:Ultrasonically guided fine-needle aspiration of liver lesions. 832 53

We report a retrospective, clinicopathologic study of 139 patients who died during treatment of a severe burn. Fifty-three percent of the patients had central nervous system (CNS) complications-infections, cerebral infarcts and hemorrhages, metabolic encephalopathies, central pontine myelinolysis, and cerebral trauma. Children and adults were equally affected. Sixteen percent of the patients had a CNS infection. Candida species, Staphylococcus aureus and Pseudomonas aeruginosa caused almost 80% of them. S. aureus and candida caused cerebral microabscesses and septic infarcts. P. aeruginosa caused meningitis and infarcts due to meningitis. CNS infections arose as a result of spread from a systemic source. The major risk factors for CNS infection were an extensive burn, S. aureus endocarditis, and a burn wound infection due to candida or P. aeruginosa. Patients with burns of less than 30% of the surface area of their body, those without a systemic infection, and those in the first week after their burn were at low risk. Eighteen percent of the patients had cerebral infarcts. In almost half the patients, the infarcts were caused by septic arterial occlusions or other complications of the burn, viz, disseminated intravascular coagulation (DIC) and septic shock. In only one-third of the patients were infarcts due to atherosclerosis, atrial fibrillation, or other causes prevalent in the general population. Intracranial hemorrhages were only one-fifth as frequent as infarcts and were due to DIC and thrombocytopenia, caused by bacteremia. Diagnosis during life was difficult, because the neurologic picture of focal cerebral lesions and meningitis was indistinguishable from that of metabolic encephalopathies, and because many patients had more than 1 neurologic complication. However, our results suggest that a clinical approach that includes analysis of risk factors for CNS infection, cerebral imaging, examination of cerebrospinal fluid, and tests for DIC can lead to a neurologic and microbiologic diagnosis in most patients.
Medicine (Baltimore) 1992 Sep
PMID:Central nervous system complications of thermal burns. A postmortem study of 139 patients. 152 3

Thrombomodulin (TM) is an endothelial cell membrane glycoprotein which neutralizes thrombin clotting activity and accelerates thrombin-catalyzed activation of plasma protein C. Its role is considered to be very important to prevent thrombosis. Recently, TM has been found in circulating blood and the roles and the functions have been investigated. In this study, we evaluated the reliance and the clinical usefulness of a TM-measuring-kit by enzyme immunoassay (MGC-01-001: Mitsubishi Gas chemical company). Intraassay reproducibility test, dilution linearity test and in vitro recovery test was obtained satisfactory results. A correlation between plasma and serum on TM levels of healthy individuals was very good and the difference between them was not significant. Normal value of plasma TM levels was instituted 15.73 +/- 6.98 ng/ml by measuring 52 healthy adults. The difference between male and female was not significant. Plasma TM levels did not change significantly after venous occlusion test and on circadian fluctuation. Plasma TM levels in patients with occlusion test and on circadian fluctuation. Plasma TM levels in patients with disseminated intravascular coagulation (DIC) was 40.15 +/- 22.68 ng/ml (mean +/- SD, n = 14). It is significantly higher than the levels in healthy adults. However, the levels in patients with angina pectoris, acute myocardial infarction and aortic aneurysm were not significantly different from those of healthy adults. These findings suggest that the precision of this TM-measuring-kit is satisfactory and the measurement of plasma TM can be useful to diagnose of DIC.
Rinsho Byori 1991 Sep
PMID:[Evaluation of an enzyme immunoassay for plasma thrombomodulin]. 165 17

Five antiplatelet agents have been isolated from Chinese herbs. Apigenin and magnolol are inhibitors of thromboxane synthesis, while osthole, protopine and norathyriol are inhibitiors of phosphoinositide breakdown. Thirty min after intraperitoneal (i.p.) administration of these drugs, tail bleeding time of mice was prolonged markedly in a dose-dependent manner by norathyriol, protopine, osthole and magnolol, but not by apigenin. However, the antiplatelet agents (up to 200 mg kg-1, i.p.) could not prevent acute thromboembolic death in mice. In endotoxin-induced experimental disseminated intravascular coagulation in rats, norathyriol (50-100 mg kg-1, i.p.) prevented the decrease in platelet counts and fibrinogen, and the prolongation of plasma prothrombin time. Norathyriol (100 mg kg-1, i.p.) also suppressed ex-vivo platelet aggregation induced by collagen and ADP in rat plasma.
J Pharm Pharmacol 1991 Sep
PMID:Antihaemostatic and antithrombotic effect of some antiplatelet agents isolated from Chinese herbs. 168 29

In Japan, we experienced the first case of Hafnia alvei septicemia with shock and disseminated intravascular coagulation (DIC) in an adult with postoperative lung cancer. A 63 year-old male, who had been followed up in our department since 1987, was admitted to our hospital with the complaints of fever, hemoptysis and dyspnea on June 25, 1989. After admission, he was treated with sulbactam/cefoperazone 4 g/day intravenously for suspicion of respiratory-tract infection. After antibiotic administration, the fever subsided and the general condition became almost good. The patient experienced fever again after the antibiotic was stopped. For this reason subsequent Clavulanic acid/Amoxicillin, Flomoxef, and Ceftazidime was administered, but was not effective. Therefore septicemia was suspected and blood culture was done. The bacteria isolated from blood culture was identified as Hafnia alvei. Hafnia alvei is a gram-negative organism belonging to the Enterobacteriaceae family and quite rare pathogen in human.
Kansenshogaku Zasshi 1991 Sep
PMID:[Hafnia alvei septicemia with shock and DIC in an adult with postoperative lung cancer]. 176 1

Thirty-nine patients with untreated acute promyelocytic leukemia (APL) were randomly allocated to receive rubidazone (zorubicin) 200 mg/m2/d, days 1 to 4 plus cytarabine (Ara C) 200 mg/m2/d, days 1 to 7 (arm A, 21 patients), or amsacrine (Amsa) 150 mg/m2/d, days 1 to 4 plus Ara C 200 mg/m2/d, days 1 to 7 (arm B, 18 patients). Prophylaxis of disseminated intravascular coagulation was made by platelet transfusions and heparin. In case of leukemic resistance, patients received a second course with 2 days of rubidazone (arm A) or Amsa (arm B) and 3 days of Ara C. Patients who achieved complete remission (CR) received three consolidation courses with the two drugs used for induction and maintenance therapy for 3 years. Two patients in arm A and one in arm B were allografted in first CR. Initial characteristics were similar in both arms. In arm A, 18 patients (86%) reached CR, two had hypoplastic death, and one had leukemic resistance after two courses. In arm B, 12 patients (66%) achieved CR, two had early death (CNS bleeding, one case; ventricular fibrillation, one case), and four had resistant leukemia after two courses. The difference in CR rate between the two arms was not significant. In arm A, disease-free survival (DFS) showed a plateau at 54.3% after 34 months (95% confidence interval [CI], 32.1% to 74.9%), with eight CRs longer than 34 months. In arm B, DFS was significantly shorter (P less than .03), showing a plateau at 16.7% after 38 months (95% confidence interval, 4.7% to 44.6%), and only two prolonged CRs were seen. The difference in DFS remained significant after censoring allografted patients and patients who died in CR (one in arm A, two in arm B). Our results suggest that Amsa-Ara C combinations may be inferior to anthracycline-Ara C combinations in the treatment of APL, because they seem to provide shorter DFS and, possibly, a higher incidence of initial leukemic resistance. However, studies with larger numbers of patients are required.
J Clin Oncol 1991 Sep
PMID:A randomized trial of amsacrine and rubidazone in 39 patients with acute promyelocytic leukemia. 172 18

Lysosomal protease was determined in the serum of patients with disseminated intravascular coagulation (DIC) to clarify whether the platelet count is an appropriate diagnostic index which allows the early initiation of treatment. The platelet count and the serum level of cathepsin D, a lysosomal protease, were determined in 60 patients diagnosed to have DIC. The cathepsin D activity could not be detected in the sera of healthy individuals with a platelet count of 100,000 or above, but was detectable in the serum of DIC patients with a platelet count of 100,000, and this activity increased as the platelet count decreased to 70,000 and 50,000, and was about 5 times higher at a platelet count of 30,000 than at 70,000. In DIC patients, the decrease in the platelet count was correlated with the increase in the serum lysosomal protease activity. The appearance of cathepsin D activity in the serum of DIC patients is considered to reflect the release of lysosomal enzyme activities from damaged organs, and the treatment for DIC must be initiated before the platelet count decrease below 100,000, and cathepsin D activity then appears in the serum. At a platelet count of 30,000 or less, DIC becomes established, and no therapeutic effects can be expected because of the associated multiple organ failure.
Jpn J Surg 1991 Sep
PMID:Change in the acid protease activity in plasma of patients with disseminated intravascular coagulation. 181 88

We measured FPB beta 15-42, and alpha 2 plasmin inhibitor-plasmin-complex (PAC), which are direct indexes of plasmin activity, as well as D-dimer in 204 samples from patients with subarachnoid hemorrhage, trauma, and the patients during cardiopulmonary bypass. In all patients, these molecular markers increased due to secondary fibrinolysis; these increases were significantly higher in DIC patients. There were positive correlations among the molecular markers. The correlation coefficient for FPB beta 15-42 and D-dimer was significantly higher than that for PAC and D-dimer in the DIC patients. In conclusion, it might be better to measure both FPB beta 15-42 and PAC as indexes of plasmin activity in DIC patients, because of the significant difference between the correlation coefficient for PAC and D-dimer, and that for FPB beta 15-42 and D-dimer.
Rinsho Byori 1991 Sep
PMID:[Correlations among FPB beta 15-42, PAC and D-dimer]. 183 76

Eight pts with acute myeloid leukemia were studied to assess coagulation and fibrinolysis disturbances as a cause of hemorrhages associated to thrombopenia. Fibrinogen, products of fibrinogen to fibrin degradation, D-dimer, antithrombin III, protein C, plasminogen and alpha-2 antiplasmin determinations were performed at admission, during and after chemotherapy. All pts were on heparin during induction chemotherapy. Coagulation activation, which increased with the onset of chemotherapy (increases in D-dimer) and a decreasing trend at the end of the antileukemic therapy (normalization of fibrinogen levels) was observed. During the whole observation period alpha-2 antiplasmin levels remained very low. No significant changes were observed in antithrombin III or protein C levels. In conclusion, disseminated intravascular coagulation with associated thrombopenia is an important event in acute leukemia and an increased fibrinolytic activity due to low alpha-2 antiplasmin levels may take part in the genesis of hemorrhage. These data suggest that both heparin administration and the use of antifibrinolytic drugs may have a therapeutic effect.
Rev Med Chil 1991 Sep
PMID:[Intravascular coagulation in acute promyelocytic leukemia: analysis of coagulation and fibrinolysis parameters]. 184 6


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