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)

Pregnancy-related acute renal failure (ARF) can include reversible tubular necrosis as well as irreversible cortical necrosis. Though pathogenetic mechanism are not fully understood, disseminated intravascular coagulation (DIC) probably plays a primary role. We report 25 cases of pregnancy-related ARF: 13 were associated with preeclampsia or eclampsia and 12 with obstetric complications. The following parameters were studied: partial thromboplastin, prothrombin and thrombin time, fibrinogen, anti-thrombin III and FDP levels, platelet count, whole blood clot lysis time and area, fragmented red cells (schistocytes) in the blood smear, hemoglobin, aptoglobin and LDH concentrations. DIC was scored in arbitrary units ranging from 12 to 36 and related to the clinical picture, renal outcome and the treatment employed. Five patients had irreversible renal damage, while 19 recovered fully; one patient died and no renal histology was available. The DIC score did not seem to have a significant relation to the severity of renal damage.
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PMID:The role of intravascular coagulation in pregnancy related acute renal failure. 322 77

Determinations of coagulation/fibrinolysis parameters thrombin-antithrombin III complex (TAT) and D-dimers (cross-linked fibrin degradation product) were carried out in order to prove that preeclampsia is a chronic disseminated intravascular coagulation (DIC) state. Besides the parameters TAT and D-dimers, antithrombin III (ATIII), fibrin degradation products and platelets were measured as well. Even in normal pregnancy there is an activation of coagulation, reflected in a hypercoagulative state that is proceeding down to the formation of thrombin. This thrombin is, however, nearly completely inactivated by ATIII, so that no fibrin is formed. This inactivation is solely reflected by the increase of TAT in the blood. In preeclampsia, however, where no such rapid changes as in acute DIC occur, the increase of TAT is accompanied by a decrease of ATIII and platelet counts and an increase of D-dimers; this demonstrates much more clearly the chronic DIC nature of preeclampsia than the results from studies carried out so far.
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PMID:Preeclampsia as chronic disseminated intravascular coagulation. Study of two parameters: thrombin-antithrombin III complex and D-dimers. 331 18

Plasmas from patients with a wide variety of thrombotic and presumed prethrombotic conditions were examined for high molecular weight crosslinked fibrin degradation products (known as X-oligomers) using a two-site enzyme-linked immunospecific assay (ELISA). This assay employed a catcher-tag principle using two monoclonal antibodies (mabs) directed towards different epitopes on the complex X-oligomer fraction. In general, thrombotic events (pulmonary embolism, PE, myocardial infarction, MI, peripheral vascular disease, PVD, and disseminated intravascular coagulation, DIC) were accompanied by elevated levels of X-oligomers in the plasma. During pregnancy the value of X-oligomer assays was demonstrated to be a clear-cut marker for pre-eclampsia. Patients following a variety of forms of surgery present with heterogeneous plasma levels of X-oligomers and this may merely reflect the formation and lysis of the fibrin formed during and after surgery. The possible value of this ELISA procedure in monitoring thrombolytic therapy is discussed with a critical analysis of the data presented herein. While the assay of X-oligomer was demonstrated to be a valuable marker of fibrinolysis in plasma, more extensive data are required in order to assess whether such an assay is of diagnostic value in thrombosis-related conditions.
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PMID:Monoclonal antibodies to crosslinked fibrin degradation products (XL-FDP). II. Evaluation in a variety of clinical conditions. 334 98

Acute renal failure (ARF) is regarded as relatively uncommon in preeclampsia-eclampsia (PE-E) and, in any event, of moderate degree or reversible. Cortical necrosis is reported as rare, even in fatal cases. Little light has as yet been shed on the mechanisms responsible for ARF in PE-E. This paper describes 17 cases observed over the last 15 years, in which cortical necrosis (3 histological and 2 clinical diagnoses) was relatively frequent (29.4%). The severity of renal impairment did not appear to be related to chronological age, parity, period of pregnancy in which PE-E commenced and its duration prior to delivery, presence of frank eclamptic crises or the concomitance of earlier vascular or renal disease (p greater than 0.05). The superimposition of abruptio placentae (AP) was the only clinical factor significantly correlated with cortical necrosis (p greater than 0.05). The association PE-E + AP seems to be a particularly unfavorable prognostic sign for the kidney owing to the contribution of additional damage mechanisms (vasospasm, disseminated intravascular coagulation, hemorrhagic shock) furnished by AP, while PE-E itself prepares the ground for AP. The fact that PE-E is difficult to diagnose when AP is the onset symptom may be responsible for the underestimation of its contribution towards the induction of severe renal damage.
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PMID:Acute renal failure in preeclampsia-eclampsia. 342 11

In 1982 Weinstein described the Hellp-Syndrome in pre-eclampsia. Two personal case histories have led the authors to discuss the need to specify this syndrome. Apart from the classical elements of pre-eclampsia, which are: arterial hypertension, proteinuria and oedema, there are bowel symptoms in 86% of cases and on the biological level there is thrombocytopenia and a rise in the transaminases as well as a haemolytic anaemia. Some cases of rupture of the liver have been described. Treatment is that of pre-eclampsia. This involves treatment with cortisone and sometimes with heparin. Delivery of the fetus is, however, the only really effective treatment. The characteristic three elements of the Hellp-Syndrome seem to be linked to disseminated intravascular coagulation and have long been considered very serious factors in pre-eclampsia. On the other hand it does seem to be useful for the clinician to know about the Hellp-syndrome in order to estimate the seriousness of a case where there are vasculo-renal elements in the syndrome and in order to avoid diagnosis mistakes in cases where the symptoms are often deceptive.
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PMID:[Is it necessary to specify the HELLP syndrome?]. 345 19

We studied functional protein C activity, both anticoagulant and amidolytic, as well as protein C antigen in 30 normal subjects, several members of a family with congenital protein C deficiency, 18 patients with severe preeclampsia, 27 patients with coronary heart disease, including 15 patients with myocardial infarction and 12 with angina pectoris, 20 patients on stable oral anticoagulant therapy (thrombotest values: 3-12%) and three patients with disseminated intravascular coagulation. Protein C values measured by the coagulant assay were compared to those obtained with amidolytic and immunochemical assays. In all the groups studied, the activity assays (amidolytic and coagulant) correlated significantly with each other as well as with the immunochemical assay. In patients on oral anticoagulant therapy the coagulant assay gave lower protein C values than amidolytic and immunochemical assays. A good correlation was found between immunological and amidolytic protein C assays (r=0.90, p less than 0.001), immunological and coagulant protein C assays (r=0.93, p less than 0.001), and amidolytic and coagulant protein C assays (r=0.95, p less than 0.001) in all the samples studied without including the protein C values of patients on oral anticoagulant therapy. These results allow us to recommend the functional protein C coagulant assay in patients on stable oral anticoagulant therapy because only this assay evaluates the "in vivo" protein C function in these patients.
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PMID:Assay of protein C in human plasma: comparison of amidolytic, coagulation, and immunochemical assays. 379 19

A pulmonary artery catheter was placed in a parturient whose 33-week gestation was complicated by severe preeclampsia and pulmonary edema. Cesarean delivery was performed for both maternal and fetal indications. During the second postoperative day the patient developed disseminated intravascular coagulation; subsequently she experienced sudden cardiopulmonary arrest and died. Autopsy revealed multiple pulmonary thromboemboli and trivalvular nonbacterial thrombotic endocarditis.
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PMID:Nonbacterial thrombotic endocarditis associated with severe preeclampsia and pulmonary artery catheterization. A case report. 402 Jul 93

From the pre-natal follow-up it was remarkable that cases have been admitted relatively late. Hints to a possible development of preeclampsia could be seen from patients history or the routine check up, for example the registration of edema, fetal growth retardation and oligohydramnios. For early diagnosis of preeclampsia we recommend: Calculation of mean arterial blood pressure or its non-invasive measurement; determination of hematocrit, uric acid and total plasma protein (in particular hemorheologic measurements). Hypomagnesemia in preeclampsia, as described by some authors, was also seen in our cases. The complex symptomatology of preeclampsia could be attributed to a generalised disturbance of microcirculation, which leads to definite reactions of the organs concerned. The microcirculatory failure is caused by vasoconstriction, hemoconcentration, hyperviscosity and hypercoagulation (up to DIC and consumption coagulopathy). The resulting symptoms and syndromes can be: EPH, HELLP, hemolytic-uremic Syndrome, hepato-renal Syndrome, thrombocyte and antithrombin III deficiency etc. The drug of choice for treatment of preeclampsia is magnesium sulfate. Its application is based on long-term clinical experience and new aspects on the physiologic and pharmacologic role of magnesium. The recommendations of the German High Blood Pressure League to use calcium antagonists as a basis in the treatment of high blood pressure can be fulfilled particularly in pregnancy by the physiologic calcium antagonist Mg++. Magnesium sulfate should be given in a dosage of 24-72 g daily. The dose should also be made dependent from urinary output. Further treatment patterns of preeclampsia should be adjusted according to each case. The present results also support our hypothesis that magnesium deficiency (besides predisposing factors) could be responsible for the development of preeclampsia (present model shown in detail). Consequently, the early and long-term substitution of magnesium in pregnancy could help reduce preeclampsia.
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PMID:[Pathophysiology and clinical aspects of pre-eclampsia]. 404 84

In 80 pregnant women with pre-eclampsia and in 38 healthy pregnant women malondialdehyde production by blood platelets, platelet survival and several haemostatic variables were determined. It was demonstrated that due to the enhanced platelet turnover pre-eclampsia was invariably accompanied by a thrombophilic state which in severe cases developed into chronic consumption coagulopathy.
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PMID:[Thrombophilic states in late gestosis]. 608 23

Renal morphological changes are described in four cases of idiopathic acute fatty liver of pregnancy. Light microscopy showed mild glomerular hypercellularity together with thickening and narrowing of capillary loops. In two cases the tubules showed lipid accumulation which included free fatty acids. Electron microscopy showed mesangial cell interposition between the basal lamina and endothelial cells. Glomeruli contained electron dense material in a subendothelial location. Immunoperoxidase stains showed diffuse segmental deposits of fibrin/fibrinogen and IgM in relation to glomerular capillary loops. IgG and C3 were found in three and two cases respectively. Pathogenetic mechanisms including disseminated intravascular coagulation, immune complex deposition and alterations in lipid metabolism are discussed. Coexistent preeclampsia is considered to be an unlikely explanation for the changes. There is a possibility that these renal changes comprise an early feature of idiopathic acute fatty liver of pregnancy.
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PMID:Renal morphological changes in idiopathic acute fatty liver of pregnancy. 638 13


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