Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation and fibrinolysis studies were performed on 64 newborns; 16 premature infants with hyaline membrane disease (HMD), 17 newborns with other forms of respiratory distress syndrome (RDS) (8 of them were premature), 31 healthy newborns (11 of them were premature). All the babies were studied once in the first 48 hours of life. There was no significant difference between sick and healthy babies for 5 parameters; platelet count, factor VIII, fibrinogen, fibrin(ogen) degradation products, euglobulin lysis time. Factor II, VII and X were low in all infants, and premature infants had significantly lower levels compared to full term newborns. Factor V, plasminogen, alpha 2 macroglobulin (alpha 2M) and antithrombin III (AT III) levels were significantly lower in sick infants. Except for AT III, these deficiencies were not related to prematurity. No significant difference was found between HMD and other RDS. Of the 33 sick infants, 5 developed laboratory findings consistent with disseminated intravascular coagulation (DIC). The results indicate that the coagulation and fibrinolytic abnormalities reported are not specific to HMD.
Intensive Care Med 1977 Dec
PMID:Haemostatic disorders and respiratory distress in the newborn. 7 54

Complement component C3, component C4, and total hemolytic complement CH50 were measured in blood from ten patients with acute disseminated intravascular coagulation (aDIC) syndromes. The study group was selected on the basis of history to exclude antecedent immunologic, infectious, or hepatic disease. The mortality rate was high (90%), the average duration of illness short (8.5 days), and the utilization of blood products extensive. The behaviors of C3 and C4 were found to be analogous to fibrinogen, plasminogen, antiplasmin, and platelets. CH50 activity paralled C3 and C4, as well as results of the soluble coagulation factor screening tests. It is concluded that serum complement is consumed as part of the multisystem dysfunction, aDIC, and that in conjunction with traditional indicators it may be utilized to gauge the severity of this syndrome.
Am J Clin Pathol 1976 Dec
PMID:Complement consumption in acute disseminated intravascular coagulation without antecedent immunopathology. 13 95

Both deep venous thrombosis and DIC are intermediate mechanisms of disease--both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.
Thromb Haemost 1977 Dec 15
PMID:The intravascular generation of fibrinogen derivatives and the blood vessel wall in venous thrombosis and disseminated intravascular coagulation. 14 74

Hematological studied were carried out serially in the rats transplanted subcutaneously with Yoshida ascites hepatoma AH-109A. Significant changes were observed in fibrinogen level, fibrinogen degradation products, recalcification time, platelet count, and fragmentation of red blood cells. Formation of thrombi was revealed in the vessels of tumor tissue morphologically from early stage when the tumor grew to a palpable size. Thrombi were formed also in the arterioles of the lungs in the terminal stage. Bleeding tendency was noted in some cases at death. These findings suggested the experimental induction of a type of disseminated intravascular coagulation. The systemic changes of the blood occurring in the terminal stage were preceded by localized intravascular coagulation and fibrinolysis in the tumor in early stage of tumor growth.
Gan 1977 Dec
PMID:Hematological alterations in tumor-bearing rats, with reference to pathogenesis of chronic type of disseminated intravascular coagulation syndrome. 20 34

In November 1976, a 52 year old woman presented with a Moschowitz syndrome with clinical manifestations of continuous fever at 39 degrees and a transient Wernicke type aphasia. Laboratory findings included schizocytosis, a peripheral thrombocytopaenia and functional renal insufficiency. The ethanol tests was positive but there was no frank defibrination syndrome. After corticosteroid therapy failed, the patient was treated with Dipyridamole 400 mg/24 hours IV and acetylsalicylic acid 4 g/24 hours IV. Fever disappeared on the same day and the thrombocytopaenia was corrected in 48 hours. The patient was considered to be cured 15 days later. No precise aetiology to explain the Moschowitz syndrome was discovered apart from the recent ingestion of oestrogens. The authors emphasise the considerable progress which this use of a combination of Dipyridamole and aspirin represents, resulting in the cure of Moschowitz syndrome, a condition considered to be fatal up until a few years ago.
Nouv Presse Med 1977 Dec 10
PMID:[Moschowitz's disease: efficacy of anti-platelet aggregation agents]. 20 23

The effectiveness of heparin in acute leukaemia complicated by disseminated intravascular coagulation (DIC) is still controversial. In this regard low-dose heparin was found to be therapeutically effective in three patients suffering from acute myelocytic leukaemia and DIC. With respect to the contraindication of high-dose heparin in these conditions the low dose regimen appears to be a valuable alternative.
Blut 1978 Dec 15
PMID:Low-dose heparin in the management of acute myelocytic leukaemia. 28 71

The clinical and laboratory features of nine patients with chronic myelomonocytic leukemia are described. Hepatic or splenic enlargement accompanied by an absolute monocytosis in an older patient with an elevated serum or urine lysozyme and serum vitamin B12 levels were characteristic of the majority of patients in this series. No single clinical or laboratory finding was diagnostic for the disease. Most importantly, seven of nine patients had abnormal coagulation values; in two cases the abnormalities were consistent with disseminated intravascular coagulation and correlated with a hemorrhagic diathesis. It is concluded that patients with chronic myelomonocytic leukemia who have thrombocytopenia or a bleeding tendency should be evaluated for evidence of disseminated intravascular coagulation.
Cancer 1979 Dec
PMID:Disseminated coagulopathy in chronic myelomonocytic leukemia. 29 10

The fibrinogen and fibrin degradation products (FDP) in serum samples taken from nine patients with suspected disseminated intravascular coagulation have been characterized using a method of immunoprecipitation followed by sodium dodecyl sulphate polyacrylamide gel electrophoresis. Aall of the serum samples contained a fragment with the same electrophoretic mobility as fibrinogen fragment X, while the majority also had evidence of fragments with similar mobility to fibrinogen fragments Y and D. In eight of the nine serum samples there was strong evidence of the D-dimer fragment that is released by plasmin lysis of crosslinked fibrin. Also present in all but one of the samples were fragments of higher molecular weight than fibrinogen which were probably soluble, non-clottable, factor XIIIa induced crosslinked derivatives of fibrinogen. These results suggest that during disseminated intravascular coagulation thrombin and activated factor XIII act upon fibrin(ogen) to form complexes that are subsequently lysed by plasmin to produce soluble crosslinked derivatives of fibrin.
Br J Haematol 1978 Dec
PMID:Characterization of serum fibrinogen and fibrin fragments produced during disseminated intravascular coagulation. 36 18

Disseminated intravascular coagulation is a clinicopathologic process of man and animals which occurs secondary to many diseases. The process may manifest in a variety of clinical syndromes including medical shock, haemorrhage, haemolysis and organ failure. A diagnosis can be confirmed by detecting a deficiency of several haemostatic components and the presence of raised levels of circulating fibrinogen (fibrin) degradation products. Therapy of the disorder includes the removal of the initiating factors which have provoked the clotting process together with the use of anticoagulants. The disease processes in which disseminated intravascular coagulation is implicated in the dog are enumerated.
J S Afr Vet Assoc 1979 Dec
PMID:Disseminated intravascular coagulation: a review of its pathogenesis, manifestations and treatment. 39 75

A technique has been developed to identify and quantitate unique plasmic degradation products of crosslinked fibrin in plasma. In this method, fibrin derivatives are extracted by heat precipitation and dissolved with disulfide bond reduction, after which the crosslinked gamma-gamma chain remnants are identified by SDS-polyacrylamide gradient gel electrophoresis and quantitated by densitometric analysis. A heterogenous group of gamma-gamma chains with molecular weights between 100,000 and 76,000 daltons was identified in lysates of crosslinked fibrin during plasmic degradation in vitro. Three stages of crosslinked fibrin degradation have been arbitrarily defined based primarily on the extent of degradation of these gamma-gamma polypeptide chains. As little as 20 microgram of crosslinked fibrin digests added to 1 ml of normal plasma could be detected by the heat-extraction--gel-electrophoresis technique, identifying the gamma-gamma derivatives with molecular weights of 96,000, 86,000, 82,000, and 76,000 daltons. Plasmic derivatives of gamma-gamma chains were not found in normal plasma, but they were identified in the plasma of patients with disseminated intravascular coagulation and deep-vein thrombosis, both before and in increased quantity during successful thrombolytic therapy.
Blood 1979 Dec
PMID:Detection of circulating crosslinked fibrin derivatives by a heat extraction-SDS gradient gel electrophoretic technique. 50 38


1 2 3 4 5 6 7 8 9 10 Next >>