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 risks and adverse reactions of fresh frozen plasma (FFP) and coagulation components have changed considerably in the last few years because of the spread of HIV on the one hand, and the advances in preparation and sterilisation of the coagulation components on the other hand. Therefore, the indication for FFP and the various coagulation components deserves permanent consideration. FFP is still the therapeutical means of choice for the treatment of acquired (complex) plasmatic coagulation disorders, even though the (still) small risk of virus transmission in Middle Europe has to be taken into account. Coagulation components are primarily indicated in congenital (isolated) plasmatic coagulation disorders. Only in gross or very acute acquired coagulation disorders are coagulation components needed in addition to FFP. The same regimen is recommended for the use of antithrombin III (AT III) concentrates. In cases of acquired antithrombin deficiency, antithrombin III substitution is indicated only when the anticoagulation by heparin alone or in combination with FFP is insufficient or when the heparin dose required might cause an unacceptable bleeding risk, e.g. in simultaneous thrombocytopenia. Then AT III becomes an important therapeutic agent, especially in DIC. In addition, information regarding a rational and economic substitution of FFP and coagulation components is given, and other substitutes are mentioned which could possibly be used with less risk. Finally, the necessity of accurate diagnosing is emphasized. Close cooperation between the physicians in the clinics and in the department of transfusion medicine/hemostaseology reduces unnecessary and inadequate application of coagulation components. This also means an improvement in the patient's therapy.
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PMID:[Perioperative blood coagulation therapy and diagnosis]. 219 26

The plasma concentration of the thrombin-antithrombin III-complex (TAT) was investigated during uncomplicated pregnancy in 15 women in the first, 22 in the second and 46 in the third trimester, and in 19 women with hypertensive disorders between 25 and 40 weeks gestation. Eight women at term after a normal pregnancy were studied before the onset of labour and within 60 min and 24 h after delivery. A comparison group of 16 healthy, non-pregnant women was investigated. The mean TAT concentration in normal pregnancies increased significantly in the second and third trimester compared with values in the first trimester and in non-pregnant women. In the group with hypertensive disorders during pregnancy TAT levels were significantly higher than in uncomplicated pregnancies. Within 60 min after delivery a distinct increase of TAT concentrations occurred compared to levels before the onset of labour but the levels had returned to normal by 24 h after delivery. Our findings suggest that an activation of the coagulation system occurs in normal pregnancy. A further activation takes place immediately after delivery. The significantly increased TAT levels in pregnancies with hypertensive disorders suggest a state of chronic disseminated intravascular coagulation leading to an enhanced consumption of and a decreased plasma concentration of antithrombin III.
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PMID:Thrombin-antithrombin III complex levels in normal pregnancy with hypertensive disorders and after delivery. 219 19

Hemostatic abnormalities are present in a majority of patients with metastatic cancer. These abnormalities can be categorized as 1) increased platelet aggregation and activation, 2) abnormal activation of coagulation cascade, 3) release of plasminogen activator, and 4) decreased hepatic synthesis of anticoagulant proteins like Protein C and antithrombin III. The abnormal activation of coagulation cascade is mediated through release of Tissue Factor, Factor X activators, and other miscellaneous procoagulants from the plasma membrane vesicles of tumor cells. Macrophages of a tumor-bearing host also produce increased amounts of Tissue Factor. Production of Factor X activators and macrophage Tissue Factor is decreased by warfarin. The ability of the tumor cells to produce platelet-aggregating activity and plasminogen activator parallels their metastatic potential in animal and experimental systems. These studies also show that antiplatelet agents and antibodies against plasminogen activator can suppress the metastatic process. One or more laboratory abnormalities of hemostasis can be shown in up to 95% of patients with metastatic cancer. These abnormalities, however, are unable to predict subsequent development of thromboembolic or hemorrhagic complications. Clinical complications occur in 9-15% of the patients in the form of thrombotic or hemorrhagic disorders. The therapy of tumor-related coagulopathy should be guided by its clinical expression. Subclinical DIC should not be treated. Coumadin is generally ineffective for therapy of thrombosis in cancer patients. There is no consensus regarding the use of heparin in acute promyelocytic leukemia (APL). The defibrination in APL may be from disseminated intravascular coagulation as well as systemic fibrinolysis, as shown by decreased alpha 2 antiplasmin levels. In such cases, epsilon aminocaproic acid plus heparin therapy may be of benefit.
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PMID:Hemostasis in malignancy. 174 46

Patients received 2,000 ml of dialysate intraperitoneally with five exchanges per day during continuous peritoneal dialysis (CAPD) for the treatment of terminal renal insufficiency. During a dwell time of 4 h the dialysate reached a total protein concentration up to 100 mg/dl by mass transfer of intravascular proteins. The composition is dependent on the molecular weight of the proteins. This results in an intraperitoneal hemostatic system of low concentration and different composition. We found an intraperitoneal fibrinogen cleavage and thrombin-antithrombin III-complex formation leading to increased levels of fibrinopeptide A (FPA: 33.3 +/- 7.0 ng/ml) and thrombin-antithrombin III-complex (TAT: 4.7 +/- 0.4 ng/ml) in plasma by mass transfer from dialysate to plasma. t-PA (tissue plasminogen activator) and PAI-1 (plasminogen activator inhibitor type 1) concentrations in plasma were within the normal range. The dialysate concentrations indicated a low local secretion. The fibrinolytic fibrin fragment D-dimer and the fibrinogen degradation product concentrations in plasma were greater than in dialysate. But the relations of the proteins between plasma and dialysate refer to a local intraperitoneal production as well. The results show that intraperitoneal coagulation predominates over fibrinolysis which is accompanied by an intravascular fibrinolysis in patients undergoing CAPD. Neoantigens produced in dialysate and diffused to plasma are comparable to changes seen in disseminated intravascular coagulation.
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PMID:Relation of intraperitoneal and intravascular coagulation and fibrinolysis related antigens in peritoneal dialysis. 220 48

Consumption coagulopathy with clinical symptoms reveals aortic arterial aneurysm in less than 5%. Aneurysmal repair with graft is able to remove hemostasis abnormalities for a long time. The physiopathology of these abnormalities is described here through the study of an operated case. It is questionable to use heparinotherapy as exclusive treatment for non operated patients. Heparinotherapy during perioperative period is also a matter of debate. Surgical implications of the consumption coagulopathy are listed: preoperative plasma and platelets transfusions, fibrinogen and antithrombin III perfusions, meticulous hemostasis, minor dissection, use of a women graft. Coagulation disorders disappear before the first postoperative week. Persistent or recurrent consumption coagulopathy invite us to look for a pathological association which often turns out to be a neoplasm.
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PMID:[Abdominal aortic aneurysm detected by a consumption coagulopathy]. 221 90

Patients with acute myeloid leukemia have multiple hemostatic and thrombotic complications, which may or may not result from disseminated intravascular coagulation. Previous studies incorporating routine coagulation analyses failed to detect any clinically useful information in most of these patients. In this study, the first comprehensive evaluation of the various aspects of the hemostatic system in a population of patients with acute myeloid leukemia was performed. Eighteen patients (23-71 years of age) were studied at either diagnosis or relapse. Hemostatic studies were performed at onset and on days 3, 7, and 30 after initiation of therapy. The bone marrow blast counts ranged from 8% to 98%; prothrombin time and activated partial thromboplastin time showed only minor prolongations in a few of these patients. However, in all patients measurement of platelet-associated markers revealed elevated platelet factor 4 and thromboxane B2 and normal 6-keto-prostaglandin F1 alpha levels. Fibrinolytic markers showed an increase in D-dimer and tissue plasminogen activator and a decrease in alpha 2-antiplasmin levels. Plasminogen, plasminogen activator inhibitor, and fibrinogen levels were normal. Coagulation markers demonstrated a decrease in protein C and antithrombin III levels and an elevation of the thrombin-antithrombin complex. The pretreatment values for all hemostatic markers studied were similar to the values obtained on days 3, 7, and 30 during treatment. This investigation demonstrated a subclinical activation of the components of the hemostatic system possibly leading to a hypercoagulable state. Although only six patients (33%) experienced hemorrhagic complications, the risk of bleeding and/or thrombosis was strongly evident in all patients. The significance of finding abnormal levels of specific molecular markers of hemostasis will be established in the future application of such markers in clinical evaluations of leukemic patients known to be at risk for coagulation disorders.
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PMID:Global and molecular hemostatic markers in acute myeloid leukemia. 222 Jun 67

The necessity of modifying the scheme of blood coagulation employed in the practice of clinicians is determined by the fact that the schemes offered before were short of the following important moments: 1) the whole totality of the mechanisms of factor VII activation (by factors III, XIIa, IXa, Xa, IIa, phospholipids and lipoproteins) and importance of its activation and increase of the level to reveal the risk of the development of the DIC syndrome, thromboses, sudden cardiac death; 2) formation during transformation of fibrinogen to fibrin of high molecular weight complexes of fibrin monomers (stabilized and not stabilized by factor XIIIa), whose presence in the blood plasma and serum provides important evidence for intravascular coagulation; 3) peptide splitting from prothrombin (fragments 1, 2) and fibrinogen (peptides A and B, 1-42, 15-42) the determination of which is also used for revealing activation of the blood and fibrinolytic system. Those and a number of other characteristic features are taken into account in the scheme of blood coagulation offered by the authors. A scheme of the functioning of the main anticoagulant mechanisms (antithrombin III and heparinoids; thrombomodulin, the system of proteins C and S) is also provided.
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PMID:[The advisability of modifying the current outline of blood coagulation]. 225 71

Blood coagulation, fibrinolytic and unspecific proteolytic parameters were investigated in 34 patients with acute myeloid leukemia. An increased activity of the coagulation system, documented by elevated thrombin-antithrombin III-complex (TAT) plasma levels, was found in 91% of the patients; 50% had increased elastase plasma levels. Hyperfibrinolysis, as shown by elevated fibrin split-product D-Dimer plasma levels, was detected in 91% of AML patients. Activation of these enzyme systems was not associated with relevant defects in blood coagulation or fibrinolysis in the majority of the patients investigated. In selected cases of promyelocytic M3 and monoblastic M5 leukemia, however, hypofibrinogenemia and alpha 2-plasmininhibitor deficiency was found, most likely due to depletion of these proteins in the course of disseminated intravascular coagulation and secondary hyperfibrinolysis. Significant correlations were calculated between TAT and fibrinogen (r = -0.57, P less than 0.005), TAT and D-Dimer (r = 0.89, P less than 0.0005), and D-Dimer and alpha 2-plasmininhibitor (r = -0.77, P less than 0.0005) levels. Indications of a pathogenetic importance of primary hyperfibrinolysis or unspecific proteolysis for hypofibrinogenemia and alpha 2-PI deficiency were not found.
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PMID:Hemostatic and fibrinolytic parameters in patients with acute myeloid leukemia: activation of blood coagulation, fibrinolysis and unspecific proteolysis. 227 76

The hemostasis system has been assessed in 42 patients in the age range of 18 to 60 years with secondary urosepsis. All patients had been operated for upper urinary tract obstruction or suppurative destructive renal and retroperitoneal lesions. Hemostasis was examined before and after the operation using coagulation screen. Middle-molecular peptides were assayed in the patients before and after plasmapheresis. Revealed hemostatic disorders were treated with heparin, antibacterial agents and infusion of fresh frozen plasma. Plasmapheresis is indicated in patients who are unresponsive to antibacterial therapy and surgical drainage of suppurative lesions. Postoperative hemostatic disorders presented as both hypo- and hypercoagulation, with thrombinemia in most cases. The patients with urosepsis showed latent hypercoagulation phase of DIC. By removing acute phase proteins, plasmapheresis prevented fibrinolytic failure. Exfusion of small volumes of plasma did not affect antithrombin III levels and produced a coagulation-anticoagulation balance. Declining levels of middle-molecular peptides after plasmapheresis were indicative of detoxication, presenting as better clinical status and improvement of laboratory findings.
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PMID:[The treatment of the disseminated intravascular coagulation syndrome in urosepsis patients]. 227 53

Protein C and antithrombin III represent main inhibitors of the plasmatic coagulation system. Due to the lack of practicable assays the clinical importance of protein C was only established during the last six years. In familial protein C deficiency 77% of patients present with recurrent venous thromboses, half of them below the age of 30. In addition to recurrent superficial thrombophlebitis more serious manifestations like deep vein thrombosis and pulmonary embolism have been described. Mesenteric vein thrombosis has been reported in only 5 cases all of which could be controlled by conservative treatment. In our patient protein C deficiency was discovered 10 years after the angiographic diagnosis of portal and mesenteric vein thrombosis. Thereafter, the patient complained of recurrent abdominal discomfort. Intestinal ischaemia due to mesenteric vein thrombosis required segmental resection twice. Postoperatively the patient was heparinized. After excluding a secondary protein C deficiency due to a lack in vitamin K, hepatic disease, or disseminated intravascular coagulation, long-term anticoagulation by dicumarol was implemented as therapy of first choice.
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PMID:[Protein C deficiency with recurrent infarct of the small intestine]. 231 54


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