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)

Heparin cofactor II (HC II) levels were measured by electro-immunoassay in healthy volunteers, and patients with liver disease, DIC, proteinuria or a history of venous thrombosis. Analysis of the data in 107 healthy volunteers revealed that plasma HC II increases with age (at least between 20 and 50 years). HC II was found to be decreased in most patients with liver disease (mean value: 43%) and only in some patients with DIC. Elevated levels were found in patients with proteinuria (mean value 145%). In 277 patients with a history of unexplained venous thrombosis three patients were identified with a HC II below the lower limit of the normal range (60%). Family studies demonstrated hereditary HC II deficiency in two cases. Among the 9 heterozygotes for HC II deficiency only one patient had a well documented history of unexplained thrombosis. Therefore the question was raised whether heterozygotes for HC II deficiency can also be found among healthy volunteers. When defining a group of individuals suspected of HC II deficiency as those who have a 90% probability that their plasma HC II is below the 95% tolerance limits of the normal distribution in the relevant age group, 2 suspected HC II deficiencies were identified among the healthy volunteers. In one case the hereditary nature of the defect could be established. It is concluded that hereditary HC II deficiency is as prevalent among healthy volunteers as in patients with thrombotic disease. Further it is unlikely that heterozygosity for HC II deficiency in itself is a risk factor for the development of venous thrombosis.
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PMID:Hereditary heparin cofactor II deficiency and the risk of development of thrombosis. 360 11

125I-Antithrombin III metabolism studies were performed in 2 patients with ischemic and ulcerative colitis, respectively. Both patients had acquired antithrombin III deficiency and objectively diagnosed deep venous thrombosis. A decreased 125I-antithrombin III plasma disappearance halflife and an increased fractional catabolic rate was found in both patients. The transcapillary flux ratio was elevated in the patient with ischemic colitis. A follow-up study of the first patient during a period when no signs of an ischemic colitis were present and no medication was taken showed completely normal tracer data. The data are consistent with both gastrointestinal loss and intravascular consumption of antithrombin III. The antithrombin III deficiency could not be explained by other causes such as proteinuria, liver dysfunction, or obvious disseminated intravascular coagulation. Reduced antithrombin III plasma levels were considered to have contributed to the development of deep venous thrombosis in both patients.
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PMID:Antithrombin III metabolism in two colitis patients with acquired antithrombin III deficiency. 400 29

A new method is described for the preparation of highly purified human plasminogen and plasmin with specific activity of 32 CTA units per mg of protein. With this method, the purification of the urinary plasminogen + plasmin antigenic materials from patients with chronic glomerulonephritis, disseminated intravascular coagulation syndrome and severe toxemia of pregnancy was performed, and the resulting highly purified proenzyme and enzyme were analyzed by immunoelectrophoresis, separative agar electrophoresis, gel filtration and SDS-gel electrophoresis. Our findings indicated that urinary plasmin reflects more closely the extent of intraglomerular fibrinolysis, while urinary plasminogen reflects non-selective proteinuria in patients with chronic glomerulonephritis or severe toxemia of pregnancy.
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PMID:Studies on the purification and characterization of human urinary plasminogen and plasmin. 644 89

We describe 26 pregnancies in 19 patients with lupus nephritis. There were 4 spontaneous abortions, 2 therapeutic abortions, 4 stillbirths and 1 neonatal death. 10 deliveries were preterm and 2 fetuses were small for gestational age. 8 pregnancies were not accompanied by change of renal symptoms. Mild signs of renal involvement appeared during pregnancy in 4 patients. 6 patients showed an increase in proteinuria already present before pregnancy without renal function deterioration. A moderate worsening of renal function was observed in 3 patients. 4 patients, 3 of whom had an apparent onset of systemic lupus erythematosus during pregnancy, developed anuric acute renal failure after delivery or after late spontaneous abortion. 2 of them died from sepsis and disseminated intravascular coagulation while 2 had complete recovery of renal function. A high rate of complications was observed in patients not adequately treated during pregnancy. Renal biopsy before gestation was not predictive of the outcome of nephropathy during pregnancy, and change of histology in repeated biopsies was frequently observed.
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PMID:Lupus nephropathy and pregnancy. A study of 26 pregnancies in patients with systemic lupus erythematosus and nephritis. 669 Oct 1

A toxemia-like syndrome was induced in pregnant beagles by intraperitoneal inoculation of concentrates prepared from placentas of patients with preeclampsia-eclampsia and hydatidiform mole, which contained an agent, Hydatoxi lualba, that stained in a unique fashion with toluidine blue-O-. The pregnant dogs inoculated with either of these concentrates progressively developed hypertension, eyeground changes consistent with hypertensive retinopathy, proteinuria, disseminated intravascular coagulation, and hepatic dysfunction in addition to intrauterine growth retardation and intrauterine fetal death. Hepatic periportal hemorrhage and glomeruloendotheliosis, lesions usually seen in preeclampsia-eclampsia, were also noted to occur in pregnant beagles inoculated with these concentrates. A significant increased sensitivity to angiotensin II infusion was also noted. The toxemia-like syndrome did not develop in pregnant beagles when inoculated in a similar fashion with concentrates prepared from placentas from normal term pregnancies which were free of Hydatoxi lualba or in nonpregnant beagles inoculated with concentrates containing Hydatoxi lualba. Although the agent was not injected in pure form, the inoculation of concentrates containing Hydatoxi lualba appears to be required for the manifestation of the toxemia-like syndrome.
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PMID:Experimental induction of a toxemia-like syndrome in the pregnant beagle. 684 42

In three different disease entities associated with acquired antithrombin III (AT III) deficiency some of the pathogenetic mechanisms were studied. In liver cirrhosis (23 patients) the AT III level was closely correlated to the activity of hepatocellular synthesized clotting factors, indicating decreased AT III synthesis. In glomerular proteinuria (20 patients not on steroid therapy) the plasma level of AT III correlated inversely to the renal AT III clearance. In contrast to liver cirrhosis and proteinuria, in septicaemia (33 patients) the ratio between AT III antigen (radial immunodiffusion) and functional AT III (heparin cofactor assay using a chromogenic substrate) demonstrated an excess of AT III antigen probably due to inactive AT III-enzyme complexes. Therefore consumption of AT III appears to be an important cause of AT III deficiency in septicaemia. There was an inverse correlation between this ratio and the plasma AT III activity. It is well documented that congenital AT III deficiency predisposes to deep venous thrombosis (DVT) and sometimes to disseminated intravascular coagulation. A similar clinical relevance may be assumed for an acquired AT III deficiency, though so far a relationship between AT III deficiency and DVT has been only established in the nephrotic syndrome.
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PMID:[Pathogenetic mechanism and clinical relevance of acquired anti-thrombin III deficiency in internal medicine (author's transl)]. 702 26

Microangiopathic hemolytic anemia and thrombocytopenia secondary to disseminated intravascular coagulation is a well-described complication of widely metastatic carcinoma. The authors report four cases of gastric carcinoma, one case of colon cancer, and one case of adenocarcinoma of unknown primary in which the patient developed a syndrome analogous to thrombotic thrombocytopenic purpura, consisting of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure without definite evidence of disseminated intravascular coagulation. In contrast to previous reports, postmortem examination in three of the cases revealed no recurrence or only microscopic foci of residual tumor. In the remaining three, there was clinical and pathologic evidence of grossly disseminated carcinoma. Also in contrast to previous cases, all patients evidenced azotemia and proteinuria at the onset of the syndrome and ultimately uremia was a contributing cause of death. Coagulation profiles showed prolonged thrombin times and elevated fibrin degradation products in four instances and did not distinguish the patients with grossly metastatic disease from those with no tumor or only microscopic residua. Circulating immune complexes containing carcinoembryonic antigen were found in the patient with metastatic colon carcinoma. The syndrome was clinically identical whether or not grossly metastatic tumor was present, and it should not be attributed to advanced disease without definite clinical or pathologic evidence of a recurrence.
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PMID:Microangiopathic hemolytic anemia, thrombocytopenia, and renal failure in patients treated for adenocarcinoma. 728 73

The platelet count in 550 patients with gestational hypertension was significantly lower and the mean platelet volume significantly higher than in normal pregnant women. Both the platelet count and volume became increasingly abnormal when hypertension was accompanied by oedema, proteinuria or both, and women with severe pre-eclampsia or eclampsia had the lowest platelet counts and the highest mean platelet volume. The proportion of patients with thrombocytopenia and/or macrothrombocytosis also varied with the severity of the clinical presentation. Fibrinogen degradation products were found mainly in fully developed pre-eclampsia. These findings confirm the concept of a rapid platelet turnover caused by low-grade disseminated intravascular coagulation in gestational hypertension. The platelet pattern in essential hypertension is similar to that seen in normal pregnancy.
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PMID:Thrombocytopenia and macrothrombocytosis in gestational hypertension. 729 1

Hypertension is observed in 10 to 15% of pregnancies, but only 10% of affected women will suffer preeclampsia. The pathophysiology of preeclampsia is based on an early anomaly of placental implantation, leading to a cascade of events (secretion of vasopressive prostaglandins, anomalies of hemostatis) which can cause disseminated intravascular coagulation. The diagnosis of preeclampsia is based on hypertension and significant proteinuria (above 0.5 g/24 h), and paraclinical maternal and fetal examinations to follow the evolution and detect the appearance of maternal complications (retroplacental haematoma, Hellp syndrome and eclampsia) and (or) fetal complications (delayed growth, in utero fetal death, perinatal death). The aim of hypertensive treatment is to normalise blood pressure and to avoid maternal complications. Preventive treatment with aspirin reduces the frequency of recurrent preeclampsia and delayed growth of the fetus.
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PMID:[Arterial hypertension and pregnancy]. 749 63

The maternal mortality rate associated with eclampsia ranges from 100 to 6000 per 100,000, and the perinatal mortality rate ranges from 150 to 400 per 1000. Both eclampsia and its preceding condition, pregnancy-induced hypertension, occur in varying degrees in different parts of India. The warning signs of imminent eclampsia are 1) systolic blood pressure of 160 mmHg or more on two occasions six hours apart when the patient is on bed rest; 2) proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative assay; 3) oliguria or anuria; 4) cerebral or visual disturbances; 5) pulmonary edema or cyanosis; and 6) epigastric/right hypochondriac pain, impaired liver function, and thrombocytopenia and coagulation disorders. Eclampsia is classified as the acute fulminating type, which can occur without warning, and the insidious type. Most cases (61%) show onset of eclampsia during the prenatal period. Treatment of eclampsia involves 1) control of convulsions (through an injection of magnesium sulphate or diazepam or the intravenous administration of phenytoin); 2) correction of hypoxia and acidosis; 3) a gradual lowering of blood pressure with hydralazine hydrochloride, nifedipine, atenolol, labetalol, oxprenolol, or metoprolol); and 4) steps to effect delivery. Diagnosis of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) requires a complete blood count, blood film for platelet count and red blood cell fragmentation, and a coagulation screen for diagnosis of disseminated intravascular coagulation. Efforts to induce delivery in cases of prenatal eclampsia can take place 12-24 hours after convulsions have stopped. There is no reason to prolong pregnancy in the interests of the fetus, and in some cases Cesarean section may be required. Adequate prenatal care should allow the identification of almost every potential case of eclampsia and allow the prompt treatment of pre-eclampsia or termination of pregnancy when necessary. Medical staff must receive proper training to diagnose pre-eclampsia and treat the condition.
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PMID:Eclampsia. 765 39


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