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)

Twenty-three cases of delayed hemolytic transfusion reaction (DHTR) occurring at the Mayo Clinic from 1964 through 1973 are reviewed. Nineteen patients had clinical manifestations of hemolysis, of which fever was the most frequent presenting symptom. The degree of hemolysis served as an index of morbidity. In four cases, there was oliguria, two of these patients experiencing renal shutdown. In one case, hemolysis led to a disseminated intravascular coagulation syndrome. Death occurred subsequent of DHTR in three patients. The direct antiglobulin test was positive in all but one case; this finding coincided with elevated unconjugated bilirubin in 14 cases and decreased haptoglobin levels in 15 cases. Anti-Jka antibody accounted for somewhat more than one-third of reactions and, along with anti-E, c, D, Fya, and K antibodies accounted for 91 per cent of cases.
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PMID:Transfusion reaction. An immunologic hazard of blood transfusion. 41 92

Acutely, hemin sensitizes endothelial cells to oxidants but chronically protects the endothelium through the induction of ferritin. By releasing its heme, methemoglobin can sensitize endothelial cells in a fashion similar to free hemin. Furthermore, prolonged incubation with the endothelium allows methemoglobin to induce heme oxygenase and ferritin and concomitantly to modulate oxidant-mediated cytotoxicity. Methemoglobin but not hemoglobin, metmyoglobin or cytochrome c induces heme oxygenase and ferritin. Heme needs to be released from methemoglobin, since sodium cyanide, haptoglobin, and hemopexin inhibit the induction of these proteins. Neutrophils can oxidize hemoglobin to methemoglobin, which can subsequently induce both heme oxygenase and ferritin. We speculate that in shock with disseminated intravascular coagulation, marginated PMNs oxidize hemoglobin to heme-releasing methemoglobin. If critical defenses such as haptoglobin and hemopexin are overwhelmed, heme enters the endothelin cells, sensitizing them to oxidant damage. Endothelial cell adaptation via heme-induced heme oxygenase and ferritin production might limit ultimate progression to pulmonary and other vascular leak syndromes.
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PMID:Endothelial cell heme oxygenase and ferritin induction by heme proteins: a possible mechanism limiting shock damage. 130 86

1. In patients with acute strokes entering a large ongoing randomised double-blind controlled trial of intravenous glycerol therapy, the extent and pathogenesis of any ensuing haemolysis were evaluated using standard clinical investigations and in vitro techniques. 2. Twenty patients received 10% glycerol in saline (500 ml over 4 h on 6 consecutive days) and 15 received corresponding control treatment with saline. 3. Intravascular haemolysis was evident after the first infusion; compared with the controls the glycerol group had i) a greater mean reduction in serum haptoglobin concentration (P less than .05), and ii) a greater proportion exhibiting haemoglobinaemia (P = 0.03). 4. After 6 days of glycerol treatment, the mean reduction in haemoglobin concentration was only 0.8 g more than in controls; this difference being neither clinically nor statistically significant. 5. Glycerol therapy was not associated with haemoglobinuria, renal insufficiency or disseminated intravascular coagulation. 6. Exposure of red blood cells to 1-10% glycerol in vitro did not induce haemolysis per se; on re-exposure to lower concentrations lysis ensued provided a minimum osmotic gradient was present. 7. Whilst taking standard dosage regimes of glycerol, the stroke patients we studied manifested a degree of intravascular haemolysis but its consequences were not clinically significant; lysis probably ensued after venous blood acquiring high glycerol concentrations mixed with blood containing little or no glycerol.
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PMID:Investigation of intravascular haemolysis during treatment of acute stroke with intravenous glycerol. 231 Jun 58

Esophageal varices were injected with 5% sodium morrhuate and a solution containing thrombin, concentrated dextrose, and cephalothin sodium using the flexible gastroscope with balloon cuff modification. Hematologic and coagulating parameters were checked before and after the procedure to look for evidence of disseminated intravascular coagulation. No effect was noted on hematocrit, hemoglobin, platelet count, haptoglobin, prothrombin time, partial thromboplastin time, fibrinogen, fibrin split products, factor V, or factor VIII. Injection sclerotherapy with currently available solutions appears to have no effect on the systemic coagulation system.
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PMID:Absence of disseminated intravascular coagulation with endoscopic sclerosis of esophageal varices. 708 44

Acute necrotizing (hemorrhagic) pancreatitis was induced in 12 dogs by infusing oleic acid into their pancreatic ducts. There were decreases in blood pH, complement, antithrombin III, blood platelets, 24- and 48-hour plasminogen, and 24-hour haptoglobin and modest decreases in serum albumin. There were increases in fibrinogen, 48- to 120-hour haptoglobin, and 96-hour and 120-hour plasminogen and prolongations of prothrombin and activated partial thromboplastin times. The latter 2 changes together with decreases in antithrombin III, platelet numbers, and complement were indicative of consumption coagulopathy. A clinically innocuous but statistically significant decrease in serum total and ionized calcium despite significant acidosis was noted. This indicates that serum total and ionized calcium is helpful in making the diagnosis of acute necrotizing pancreatitis. Methemalbuminemia of 6 mg/dl at 24 hours and 7 mg/dl at 48 hours indicates that methemalbuminemia is a valuable diagnostic and prognostic finding in association with acute necrotizing pancreatitis.
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PMID:Biochemical and coagulation changes in a canine model of acute necrotizing pancreatitis. 725 99

Fifty patients with total joint arthroplasties (28 total hip arthroplasties, 11 total knee arthroplasties, and 11 bilateral total knee arthroplasties) received autotransfusions from their postoperative wound drainage. The blood was collected in a closed sterile drainage system without any additional anticoagulant. Pre- and postoperative measurements were made of the patient's hemoglobin, platelets, fibrinogen, haptoglobin, fibrin degradation products, and D-dimer (a specific type of fibrin degradation product). Red blood cell survival was assessed in 16 of the patients by labeling the shed blood with 51Cr sodium chromate prior to reinfusion. To control for fluid shifts, continued bleeding, and dilution effects of further transfusions in the immediate postoperative period, 10 patients also had their native blood labeled with 111In oxime. In this study, the mean estimated blood loss was 1,062 mL (+/- 1,247) with a mean wound drainage of 836 mL (+/- 338). Of this, a mean of 450 mL (+/- 261) of blood was was given back to the patient in addition to routine, preoperative autologous donated blood. Six (12%) patients experienced transient fevers at the time of retransfusion. Detailed hematologic studies were performed on the shed blood in 19 patients. The collected blood was completely defibrinated, but did contain fibrin degradation products, as indicated by the D-dimer level, and hemolyzed blood as the haptoglobin was reduced. Even though the blood containing the above breakdown products was reinfused to the patients, there were no clinical manifestations of disseminated intravascular coagulation. Both the hemolyzed and defibrinated products were subsequently cleared by the body.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reinfusion of postoperative wound drainage in total joint arthroplasty. Red blood cell survival and coagulopathy risk. 796 65

The HELLP syndrome is a severe and life-threatening complication of preeclampsia with typical laboratory findings. The frequency of the disease is 1 to 150-300 live births in perinatal centers. The median gestational age at presentation is 34 weeks, however, the disease may also develop during the early postpartum period. Right upper quadrant pain is the most striking clinical symptom; in up to 15% of cases neither hypertension nor proteinuria is present on admission. For the detection of hemolysis determination of haptoglobin levels is the most suitable method. Coagulation disorders are more pronounced in patients with the HELLP syndrome as compared to those with preeclampsia without the HELLP constellation, however the full-blown syndrome of disseminated intravascular coagulation (DIC) is not a leading symptom but the consequence of delayed diagnosis and/or therapy of the primary disease. The course of the HELLP syndrome is unpredictable. On the one hand, complete reversal of symptoms under conservative treatment have been reported in individual cases, on the other hand, rapid, therapy-resistant deterioration of the disease had been observed in the majority of patients accompanied by severe complications (e.g. liver rupture). As a consequence the mother and the newborn need intensive care, and these women should be delivered in an obstetric intensive care unit. The maternal mortality reported from the international literature is 3.3%, and the perinatal mortality 22.6%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[HELLP syndrome]. 802 4

We report the case of a 39-year-old para-4 gravida-4 who received polychemotherapy 5-fluorouracil 600 mg/m2, cyclophosphamide 600 mg/m2 and epirubicin 50 mg/m2 for invasive breast cancer (pT2N2Mo) with extensive metastatic involvement of all 23 axillary lymph nodes removed at 29 gestational weeks. Soon after the second course of chemotherapy at 35 weeks, she developed two eclamptic tonic-clonic seizures which were treated by antihypertensive and anticonvulsive drugs and delivery of a healthy infant, 1650 g (< 10th percentile) by cesarean section. That this patient indeed suffered from eclampsia was supported by the findings of transient postpartum severe hypertension (peak 170/110 mmHg), proteinuria (peak 3.2 g/24 h), incomplete features of the HELLP syndrome (thrombocytopenia 81,000/mm3, haptoglobin < 10 mg/dl) and of DIC, and by the results of cerebral CT scanning showing two 1-cm ischemic lesions. Since the detrimental effect of antineoplastic agents on the rapidly proliferating trophoblast is well known and as abnormal placental function, such as in triploidy, trisomy or hydatiform mole, has been associated with an increased risk for preeclampsia/eclampsia, a possible causal relationship between polychemotherapy and the subsequent development of this rare disorder is suggested.
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PMID:Eclampsia after polychemotherapy for nodal-positive breast cancer during pregnancy. 884 12

An increased incidence of TTP has been noted among patients receiving intravascular stents to improve patency in diseased coronary, renal, and peripheral arteries. Placement of transjugular intrahepatic porto-systemic shunt stents is often associated with subsequent development of severe hemolysis. We have prospectively studied the development of microangiopathic hemolysis or TTP in patients undergoing intravascular stent placement for peripheral vascular or renal artery disease. Hemolysis was evaluated both before and after stent placement by measuring complete blood count, total bilirubin, lactate dehydrogenase (LDH), haptoglobin and reticulocyte count, and examining peripheral blood films of all patients. Coagulation parameters, blood urea nitrogen and creatinine were measured to exclude disseminated intravascular coagulation or thrombotic thrombocytopenic purpura as a potential cause of hemolysis. Seventeen patients (median age 69 years) were evaluated. One patient was on ticlopidine. Mean hematocrit fell from 41.8% pre-stenting to 35.5% post-stenting (P = 0.003) but without significant change in reticulocyte count (1.7 vs. 1.6%, P = 0.605), LDH (546 vs. 560 IU/l; P = 0.836), bilirubin (0.62 vs. 0.63 mg/dl; P = 1.0), or haptoglobin (183 vs. 158 mg/dl; P = 0.083). Thus, this drop in hematocrit could not be attributed to hemolysis. Peripheral blood films revealed fewer than 1% schistocytes before and after stent placement in all cases. Absence of significant changes in mean platelet count (240 vs. 210 x 10(9)/L; P = 0.088), fibrinogen (385 vs. 378 mg/dl; P = 0.789), BUN (24.5 vs. 16.8; P = 0.079), and creatinine (1.38 vs. 1.24; P = 0.757) argue against development of TTP or DIC resulting from stent placement. No patient developed new renal impairment, a neurological syndrome, or unexplained fever after stent placement. At a mean of 6 weeks follow-up after stent placement, patients have not developed signs of hemolytic anemia or worsening renal function. Our findings argue against a primary risk of microangiopathic hemolytic anemia or TTP due to intravascular stents in patients not receiving ticlopidine.
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PMID:Intravascular stents do not cause microangiopathic hemolysis or thrombotic microangiopathy. 1054 Mar 68

Release of toxins in the organism trigger a cascade of biological and chemical events. The process involves a large number of molecules produced under genetic control in a perfectly regulated chronological order. Certain molecules (TNFx, IL-1, Il-2.) have inflammatory proprieties, generally producing systemic Inflammatory Response Syndrome (SIRS). Other less numerous molecules (IL-4, IL-10) have antiinflammatory actions. Finally, soluble receptors and these cytokines contribute to the decrease in the quantity of active cytokines at the receptor level. Dozens of other molecules, many of which remain to be fully understood, are also found in the blood stream. They can, for example, facilitate white cell adhesion (ICAM, VCAM, selectins.). Some of them (G-CSF. CM-CSF. IL-5) stimulate production of granulocytes, monocytes, eosinophils. More recently, certain peptides, like macrophage inhibiting factor (MIF) and procalcitonin (PCT) have been added to the list of molecules involved in bacterial infections. Coagulation factors are also very rapidly released in response to toxinic aggression triggering disseminated intravascular coagulation. Later, acute-hase inflammation proteins, such as C-reactive protein (CRP), haptoglobin, serum amyloid A, etc. are found in largely increased quantities. All these molecules are potential markers of inflammation. Only a few have however been retained for routine assay due to their fragility and their short-half life or due to analytical difficulties. CRP and PCT can however be used to differentiate viral infections from bacterial infections and are thus routinely used in clinical applications. In the second part of this review, we briefly discuss therapeutic perspectives for severe infections and septic shock. There have been many attempts to neutralize different cytokines but results have been disappointing to date. There are however many possibilities currently under study, particularly neutralization of endotoxins, immunomodulation, use of recombinant C and S proteins, etc.
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PMID:[Inflammatory cascade response to toxin release: therapeutic perspectives]. 1142 20


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