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)

Two cases of fatal heat stroke, concerning a 20 year-old soldier and a 44 year-old psychiatric patient, treated with neuroleptics, are reported. The clinical picture, starting suddenly with coma and hyperthermia, was quite identical for both. Secondarily, while hyperthermia decreases and the conscience improved partially, an hemorrhagic syndrome similar to a consumption coagulopathy, acute renal insufficiency and acute hepatic failure appear. Death occurred after aggravated neurological disorders and respiratory distress. The anatomical lesions spread on all the viscera include tubular nephritis, and hepatic centro-lobular necrosis and an interstitial and alveolar oedema with hemorrhages and hyaline membranes in the lungs.
 ...
PMID:[Heat stroke and disseminated intravascular coagulation. Apropos of 2 cases]. 21 8

Twenty cases of toxic epidermal necrolysis were studied. 14 male and 6 female. The peak incidence by age was in the first two decades. All of them were related to drugs. Twelve of the cases had received antibiotics and, therefore an infection existed. The remaining 8 cases did not receive antibiotics and had no concomitant infection. We emphasise the clinical observation that in 11 cases the first symptom was an increase in cutaneous sensitivity, and then a rise in temperature, malaise, and extensive cutaneous sloughing resembling extensive burns. As for complications, only in 4 patients could we demonstrate disseminated intravascular coagulation (haematological tests were carried out in only 14 patients). The commonest complication observed was glomerular nephritis. Blood counts, blood chemistry and urine tests were altered more in relation to complications than to TEN. Protein electrophoresis, conversely, showed an increase of gamma globulin in 53.3% of cases, and inverted A/G ratio in 80%. S. aureus was cultured in 12 cases (not all of them children). E.S.R. was increased in 18 cases. Pathological findings with those already described: "in toto" epidermal necrolysis, intra and subepidermal blisters, and occasional inflamatory reaction at the level of the papillae, and the non-uniform presence of melanin in basal cells and Lyell cells. Prognosis was excellent, since we only had one death and one case of blindness due to bilateral ocular perforation. This could be due to the general medical care of the patient, nursing them with D.I.C., which in certain cases substituted by heparin with excellent results. Antibiotics were used in those infected.
 ...
PMID:[Toxic epidermal necrosis. Review of the theme and presentation of 20 cases]. 39 34

Masugi nephritis was induced in dogs in which platelet count, fibrinogen, antithrombin activity, plasma prekallikrein and immediate plasmin inhibitors were coincidentally decreased immediately after the injection of nephrotoxin serum. It was found that the grade of decrease of urinary kallikrein excretion following these immediate reactions were parallel with the grade of renal damages. By the pretreatment with heparin or the defibrination with snake venom, however, the histological findings of Masugi nephritis showed rather severe damage. Based on the consumption of coagulation factors, kallikrein, kinin and their inhibitors in the development of this nephritis, it was postulated that inauguration of coagulation and activation of kallikrein contributed to the development of glomerulonephritis. The treatment or prevention of this coagulation process with heparin or snake venom, however, gave untoward effects on the pathological process in this experiment.
 ...
PMID:Participation of kallikrein, coagulation/fibrinolysis parameters in the development of glomerulonephritis. 49 36

Levels of serum fibrin degradation products (FDP) were determined in patients with acute nephritis, chronic nephritis, lupus nephritis and toxemia of pregnancy by the passive hemagglutination inhibition test. Serum FDP levels were less than 10 mug/ml in normal control adults, averaging 3.2 +/- 1.2 mug/ml. The incidence of serum FDP positive patients (more than 10 mug/ml) in those with acute nephritis, chronic nephritis, lupus nephritis and toxemia of pregnancy was 28%, 73%, 100% and 100%, respectively. Their serum FDP levels averaged 8.4 +/- 5.6 mug/ml, 16.0 +/- 5.9 mug/ml, 21.4 +/- 7.6 mug/ml and 35 mug/ml, respectively. Plasma fibrinogen levels, prothrombin time, partial thromboplastin time, euglobulin lysis time and platelet counts were within normal limits in serum FDP positive patients with renal diseases, indicating that there was no severe disseminated intravascular coagulation. All FDP positive patients with renal diseases of immunological origin demonstrated the deposition of fibrin within glomeruli with complement and immunoglobulin deposits. However, FDP positive patients with toxemia of pregnancy demonstrated fibrin depositions within glomeruli without complement and immunoglobulin deposits. FDP D fragments of urine from lupus nephritis patients showed no changes in immunoelectrophoretic patterns by heat treatment, indicating that urine FDP was derived from secondary fibrinolysis.
 ...
PMID:Fibrin degradation products in renal diseases. 78 95

Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. When further glomerular fibrin deposition was prevented by defibrination, deposited fibrin was rapidly removed, indicating that glomerular fibrin-clearing mechanisms are retained in crescentic nephritis. Defibrination had no effect on the extent of glomerular C3 deposition or on the amount of proteinuria.
 ...
PMID:Defibrination with ancrod in nephrotoxic nephritis in rabbits. 79 57

A radioimmunoassay for fibrinopeptide A (FPA) has been developed. This assay uses rabbit antibodies induced by injection of native FPA-human serum albumin conjugates and 125I introduced into tyrosine-FPA synthesized in out laboratory. Plasma FPA is separated from fibrinogen by TCA extraction. The assay is capable of detecting as little as 50 pg/ml of FPA. In 20 normal donors this assay revealed a mean concentration of 0.9 ng/ml (0.3 SD). In five patients with disseminated intravascular coagulation, FPA concentrations ranged from 13.0 to 346 ng/ml. Two groups of patients with systemic lupus erythematosus (SLE) whose disease had achieved complete remission were studied; one consisted of four patients with no history of lupus nephritis and another with a history of nephritis. Mean FPA concentrations of 1.5 ng/ml (range, 0.7-1.8 ng/ml) and 2.7 ng/ml (range, 1.1-5.6 ng/ml) were found in these two groups, respectively. Another group of nine patients with active SLE, but without evidence of lupus nephritis, had a mean FPA concentration of 4.5 ng/ml (range, 2.4-7.8 ng/ml). Finally, a group of seven patients with active SLE, including active nephritis, had a mean FPA concentration of 10.2 ng/ml (range, 5.3-17.0 ng/ml). A positive correlation was found between the concentration of plasma FPA and serum DNA-binding activity and an inverse correlation was found between plasma FPA and the concentration of serum C3. No correlation existed between plasma FPA and concentration of serum creatinine. Several possibilities for the origin of plasma FPA in patients with SLE were considered; at present it seems most likely that FPA arises through the action of thrombin on fibrinogen.
 ...
PMID:Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus. 93 2

The protective effects of anticoagulants in nephrotoxic nephritis in rabbits have been studied, using various doses of heparin and defibrination with ancrod. Massive doses of heparin (2000 units/kg/day) were required before significant reduction in glomerular fibrin deposition, extracepillary cell proliferation and urea retention occurred. Doses of 300 and 1000 units/kg/day were insufficient to modify fibrin deposition and cell proliferation. Defibrination with ancrod provided protection, judged by histological and functional criteria, comparable to 2000 units of heparin/kg/day; but fibrin could still be demonstrated in the glomeruli of animals treated with 2000 units of heparin/kg/day, contrasting with the virtual absence of fibrin in animals given ancrod.
 ...
PMID:A quantitative evaluation of anticoagulants in experimental nephrotoxic nephritis. 121 1

Quantitative studies of the effects of defibrination (with ancrod) have been undertaken in two forms of allergic glomerular damage, nephrotoxic serum nephritis and acute serum sickness in rabbits. No differences in intrarenal fixation of nephrotoxic antibody, complement activation or host antibody response were detected between defibrinated and untreated rabbits with nephrotoxic serum nephritis. Defibrination prevented intraglomerular fibrin deposition in this disease; but some glomerular damage as shown by a rise in blood urea and endothelial proliferation still occurred in defibrinated animals. No differences in immune elimination of BSA, circulating immune complex formation or intrarenal localization of immune complexes were noted in defibrinated animals with acute serum sickness. No intraglomerular fibrin deposition was detected in treated or untreated animals in this disease model. It is concluded that the protective effects of ancrod are directly related to defibrination, and not to any other modification of allergic events.
 ...
PMID:The effects of defibrination with ancrod in experimental allergic glomerular injury. 121 11

The purpose of the study was to explore hemostasis in children suffering from hemorrhagic vasculitis (HV) by means of the new amidolytic methods using chromogenic substrates. The patient's plasma was studied for the content of thrombin, trypsin, factor Xa, AT-III, kallikrein, plasmin, free heparin, urokinase, factor 3 of platelets, prothrombin and Willebrand's factor. 69 children with HV were entered into the study. All of them were examined during crises. In cutaneous HV, the content of trypsin decreased 3-fold, the content of factor Xa increased 5-fold; there was a negligible increase in the plasmin and AT-III levels; the content of kallikrein rose 2-fold, that of urokinase 60-fold; the release of platelet factor 3 was intensified 1.5-fold, the activity of prothrombin 3-fold. These data indicate that in cutaneous HV, blood coagulation increased. However, the signs of disseminated intravascular coagulation were lacking because of the high blood anticoagulant activity. In mixed HV, the phase of hypercoagulation was not made for by the blood anticoagulant activity, since the latter one was depleted. The capillary toxic nephritis may give rise to disseminated intravascular coagulation associated with the depletion of the anticoagulant component. The gravity of HV and its complications can be predicted according to the characteristics of the anticoagulant component of hemostasis, especially according to the levels of urokinase and AT-III.
 ...
PMID:[State of hemostasis in hemorrhagic vasculitis in children]. 151 26

We have compared the effects of ancrod and recombinant tissue plasminogen activator (rtPA) on nephrotoxic nephritis induced in pre-immunized rabbits by the administration of nephrotoxic globulin (NTG; sheep anti-rabbit glomerular basement membrane). We used three different doses of NTG: in each experiment three groups of six rabbits were preimmunized with normal sheep globulin and given NTG: group A received no further treatment; group B received rtPA, 2 mg/kg 12 hourly; group C received ancrod 2 U/kg 12 hourly. Animals were bled daily for estimation of plasma fibrinogen and serum creatinine, then killed on day 5 and kidneys removed for histology. 1 ml/kg of NTG caused massive glomerular necrosis, all three groups having severe renal failure. With 0.5 ml/kg of NTG, ancrod and rtPA both effectively prevented fibrin deposition in Bowman's space, but all animals had severe proliferative glomerulonephritis and marked renal failure. With 0.25 ml/kg of NTG, control animals developed severe proliferative nephritis and advanced renal failure, ancrod provided almost complete protection, and the rtPA group had renal injury and functional impairment intermediate between the other two groups. We conclude that renal failure in severe nephrotoxic nephritis is fibrin-independent, but in less fulminant nephritis renal function can be protected by defibrination with ancrod. rtPA is capable of reducing glomerular fibrin accumulation as effectively as ancrod, but provides inferior protection of renal function.
 ...
PMID:Effects of ancrod and rtPA on fibrin accumulation, glomerular inflammation and renal function in nephrotoxic nephritis. 176 13


1 2 3 Next >>