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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Am J Hematol 1990 Sep
PMID:Hemostasis in malignancy. 174 46

To assess immune responses to malaria-induced thrombocytopenia, an haematologic and immunologic study was performed on 25 patients with imported malaria upon admission and 8 days after treatment. Thrombocytopenia (150 x 10(9)/litre) was detected in 19 cases (P. falciparum: 11 cases, P. ovale: 6 cases, P. vivax: 2 cases). No laboratory evidence of disseminated intravascular coagulation impairment was found in any of the patients. Bone marrow examination performed in 9 cases showed no abnormality in the megakaryocyte series. Platelet count was independent of circulating parasite levels (r = 0.27) and inversely related to the number of antibody binding sites (ABS) on platelets (r = -0.6, p. less than 0.01). The indirect Coombs test (r = -0.54; p less than 0.01) and IgG and IgE levels (p less than 0.02) gave similar findings. A statistical correlation was observed between the level of circulating immune complex and the number of ABS (r = 0.525, p less than 0.01). Thus malaria-induced thrombocytopenia seems to mainly involve IgG type antiplatelet antibody activity. Although they may be implicated in the binding of antibodies to platelets, circulating immune complexes do not appear to mediate thrombocytopenia.
Pathol Biol (Paris) 1990 Sep
PMID:[Platelet antibody activity in malaria thrombocytopenia]. 223 82

Blood was obtained from four patients envenomated by the Australian common brown snake, Pseudonaja textilis textilis. This elapid snake has one of the most toxic venoms in the world, containing extremely potent neurotoxic and coagulant components. The latter is a potent complete prothrombinase, converting prothrombin to alpha-thrombin, and comprises more than 30% of the total venom protein. The four envenomated patients developed a typical consumption coagulopathy. Serial serum and plasma samples from patients were studied by immunoaffinity adsorption, 2-alanine precipitation of fibrinogen and fibrinogen-related products and 2-dimensional immunoelectrophoresis, and assayed for crosslinked fibrin degradation products as D dimer, using the monoclonal antibody, DD-3B6/22. These procedures showed the virtually complete disappearance of fibrinogen, accompanied by the appearance of large quantities of fibrinogen and fibrin degradation products consisting of both crosslinked and noncrosslinked species. With recovery, a homogeneous high molecular weight fibrinogen was observed. The data suggest that the prothrombin activator of this venom causes the generation of thrombin which subsequently converts fibrinogen to fibrin and stimulates partial crosslinking of both alpha and gamma-chains. The resultant disseminated intravascular coagulation is accompanied by very active secondary fibrinolysis which apparently limits the extent of any microvascular thrombosis but which may contribute to a bleeding tendency.
Thromb Res 1990 Sep 01
PMID:Fibrinolysis as a feature of disseminated intravascular coagulation (DIC) after Pseudonaja textilis textilis envenomation. 223 40

Disseminated intravascular coagulation (DIC) occurred after closed Ender's pinning of a pathologic fracture of the humerus in a 58-year-old man with metastatic prostatic carcinoma. A review of the oncologic and urologic literature revealed that coagulopathy can be associated with prostatic carcinoma. This association seems not to have been previously reported in the orthopedic literature.
Clin Orthop Relat Res 1990 Sep
PMID:Disseminated intravascular coagulation complicating Ender's nailing of a pathologic fracture in prostatic carcinoma. A case report. 239 52

Patients with sickle cell disease are predisposed to infection caused by Streptococcus pneumoniae. However, there has been only one published case of bacteremic pneumococcal meningitis in an adult with sickle cell anemia. We report here the cases of six adults with sickle cell disease, pneumococcal sepsis, and meningitis. Five patients were male and one was female. Their ages ranged from 18 to 34 years (mean, 25.7 years). Five patients had the SS and one had the SC hemoglobin phenotype. Only one patient had received pneumococcal vaccine (14 valent). This vaccine did not protect against the pneumococcal serotype causing his infection. All patients had high fever (mean, 39.8 degrees C [103.7 degrees F]) on admission; five had generalized weakness and four had neck stiffness. Leukocyte counts were greater than 30,000/mm3 in all patients. Streptococcus pneumoniae was isolated from the blood and the cerebrospinal fluid in all patients. The cerebrospinal fluid showed pleocytosis in six patients, an elevated protein level in five, and hypoglycorrhachia in two. Complications included renal failure in four patients, disseminated intravascular coagulation in one, and seizures in another. Two patients died. Pneumococcal sepsis and meningitis are uncommon in adults with sickle cell disease, but they carry a high morbidity and mortality. Wider use of the new 23-valent polysaccharide vaccine in these patients is recommended.
South Med J 1990 Sep
PMID:Pneumococcal sepsis and meningitis in adults with sickle cell disease. 240 40

Methods for the study of axons involve whole nerve preparations, teased preparations of axons that are excised from their proximal and distal connections, and tissue culture models. As a complement to these, it would be advantageous to study separated, isolated axons in vivo, still in continuity with the end organ distally and the spinal cord central nervous system neuron proximally. This would allow the study of axon function, normal or pathological, in a close relationship to its biological environment. To achieve this, we have passed the surgically isolated sciatic nerve of a rat through a chamber specially designed for enzymatic dissociation. This was based on principles derived from a prior in vitro method for dissociating nerve into axons. The chamber has controlled temperature and flow and is on an inverted microscope stage, allowing observation of the process. We perfused the chamber with a calcium-free solution followed by a series of enzymes: collagenase, trypsin, and hyaluronidase. This dissociates that part of the extracellular matrix external to the Schwann cells, leaving free, myelinated axons with their Schwann cells. In this acute preparation, the axons continue to conduct action potentials for at least 8 hours. Furthermore, an in vitro study of the axon after the in vivo dissociation demonstrated that axonal transport was maintained in over 90% of the axons, directly visualized on an AVEC-DIC type of microscope system. Properties of axonal transport or active spike propagation can thus be studied individually in an in vivo axon preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
Neurosurgery 1985 Sep
PMID:Model for the study of individual mammalian axons in vivo, with anatomical continuity and function maintained. 241 87

Preparations yielding a high percentage of undamaged axons from fresh peripheral nerve or nerve root were made using an enzymatic dissociation regimen. The nerve was placed in a temperature-controlled chamber mounted over an inverted phase-contrast microscope. An oxygenated solution (Brimijoins) or modified Hank's solution was pumped through the chamber, first in a calcium-free form and then containing enzymes. The enzymes for dissociation were collagenase and trypsin, alternated. Enzymatic dissociation of the epineurium, perineurium and extracellular matrix was achieved. We supplemented the gentle agitation of a 10-roller peristaltic pump by periodically raising and lowering the fluid level in the chamber to provide a controlled mechanical agitation that promoted dissociation. A large percentage of the axons can be dissociated from the nerve, varying from approximately one-quarter to occasional complete dissociation. Action potentials were still conducted through dissociated axons, and axon transport was also still present, as documented by direct visualization using an AVEC-DIC type of microscope system. The axons had a better morphological appearance and displayed better transport than comparison preparations prepared by the usual mechanical teasing method, in our hands. The enzymatic method allows study of axons in an adult or developing mammal with regard to their electrical conduction and axon transport mechanisms. It should help to avoid a selection process for more hardy axons which may be imposed by traditional mechanical teasing methods. Mechanical stress was observed to cause widened Schmidt-Lanterman clefts, widened nodes, myelin bubbles, and other abnormal morphology as evidence of damage.
J Neurosci Methods 1985 Sep
PMID:A method for in vitro enzymatic dissociation of nerve roots and peripheral nerves from adult mammals. 241 9

Plasma from 7 septic patients with positive blood cultures were studied. None of them presented either clinical or laboratory evidence of Disseminated Intravascular Coagulation. The white cells count varied between 5 and 45 X 10(9)/l. In plasma functional plasminogen levels varied between 25 and 45%, while those of alpha 2-antiplasmin were normal (80-105%). The levels of elastase ranged between 250 and 750 micrograms/ml. Leukocyte elastase digests plasminogen "in vitro" and is able to produce several fragments; one of them called mini-plasminogen lacking lysine binding sites; therefore it does not bind to lysine-Sepharose 4B. Two different behaviors were observed in the plasmatic plasminogen of these patients with respect to their binding capacity to lysine-Sepharose 4 B. 3 patients had plasminogen which did not bind to lysine-Sepharose 4 B; the other 4 had two different components, one of which bound to lysine-Sepharose 4 B and another one which did not bind. Previous studies "in vitro" have shown that leukocyte elastase modifies alpha 2-antiplasmin, initially producing a non-plasminogen binding form. A free alpha 2-antiplasmin (non-plasminogen binding form) was detected in the plasma of these patients with sepsis by crossed immunoelectrophoresis with plasminogen in the first dimension. It seems tenable that high levels of leukocyte elastase could be responsible for these findings although, the possible relationships to leukocyte elastase still remain to be proven but could possibly explain this effect.
Thromb Res 1987 Sep 01
PMID:Mini-plasminogen like molecule in septic patients. 244 46

Decreases in platelet count, fibrinogen concentration, factor VIII, antithrombin III and alpha 2-antiplasmin activities, increase in FDP-D fraction, and pleural effusion were observed transiently at early fever stage of DHF at grade II, indicating DHF patients had manifestations of the acute type of DIC with increased permeability of vascular wall.
Southeast Asian J Trop Med Public Health 1987 Sep
PMID:DHF characterized by acute type DIC with increased vascular permeability. 244 85

A defibrination syndrome developed in two men (aged 51, and 29 years old) within two hours of having been bitten by vipers Echis carinatus and Agkistrodon halys, respectively. In both the syndrome was characterized by afibrinogenemia with prolongation of the thrombin time, presence of fibrin monomers and split products of fibrinogen. Haemorrhagic signs included oral mucosa bleeding and macrohematuria. Specific serum was administered 9 and 16 hours, respectively, after the bite and achieved normalization of all clotting values within 48 hours.
Dtsch Med Wochenschr 1989 Sep 29
PMID:[Defibrination syndrome after snake bites]. 247 8


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