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)

Fifteen cases were reviewed over a five-year period at a perinatal centre with intrauterine demise of one member of a multiple gestation. Nine cases were monozygotic twin pairs, two were dizygotic, and two were triples . Gestational age ranged from 27 to 39 weeks. The management protocol consisted of delivery in all cases after confirmation of the diagnosis. In 4 cases delivery was immediate because of spontaneous labor. In the other cases elective delivery was performed if the gestational age was 37 weeks or greater or there was evidence of preeclampsia or if amniocentesis revealed a mature lecithinsphingomyelin (L/S) ratio. Steroids were given if the L/S was immature or the attempt at amniocentesis was unsuccessful and delivery was performed 48 hours after initiation of steroid therapy. Cesarean section was the mode of delivery in 14 of the 15 cases. All of the cotwins and cotriplets survived. One survivor of a monozygous twin pair has multicystic encephalomalacia possibly implicating perinatal arterial occlusion or in utero disseminated intravascular coagulation (DIC). The intrauterine deaths are categorized into possibly avoidable deaths (2/15), unavoidable due to congenital anomalies (3/15), and unknown or unavoidable deaths (8/15).
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PMID:Intrauterine fetal demise in multiple gestation. 674 17

In order to choose the best adapted test for pre-eclampsia monitoring, platelet production time (PPT) was measured simultaneously with uricemia, factor VIII complex, beta-thrombogobulin, and other tests of platelet activation including platelet volume, density and platelet very dense body content. In the pre-eclamptic group (11 patients). In the PPT was significantly reduced in comparison with normal pregnancies (6 patients). In the pre-eclamptic group, there was good and significant correlation between PPT and the VIIIrAg/VIIIc ration (r = 0.87) and between PPT and uricemia (r = 0.79). The correlations between PPT and the other tests are poor and non-significant. Thus, for clinical purposes, the VIIIrAg/VIIIc ratio and uricemia are convenient parameters, and give very reliable information on the severity of the consumption coagulopathy which characterizes pre-eclamptic pregnancies.
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PMID:Platelet production time, uricemia, and some hemostasis tests in pre-eclampsia. 677 20

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

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

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60

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

Retinal detachment is a rare complication of preeclampsia, eclampsia and abruptio placentae. We report a case of bilateral retinal detachment in association with severe preeclampsia complicated with abruptio placentae, intrauterine fetal death and disseminated intravascular coagulation. In obstetric complications, placental thromboplastin may release into maternal circulation and activate the extrinsic coagulation system with resultant disseminated intravascular coagulation. This may be responsible for choroidal ischemia and consequent serous retinal detachment.
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PMID:Retinal detachment in association with preeclampsia and abruptio placentae. 763 40

Sixty cases of severe eclampsia were treated in an intensive care unit between January 1989 and September 1993. Mean age was 26, and 70% of patients were primipara. The pregnancy has been unsupervised in almost all cases. All had visceral lesions and/or hematologic problems and there was impaired conscious level in 9 cases out of 10. Medical treatment involved the control of seizures and of hypertension. Cesarean section was performed in 34 cases. The maternal death rate was 23.3%. Our experience indicates that mortality depends upon visceral lesions (cerebral, disseminated intravascular coagulation, acute pulmonary edema, Hellp syndrome). Better awareness of severity factors in preeclampsia improves both maternal and fetal prognosis by precisely indicating the best time for fetal extraction.
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PMID:[Maternal prognostic factors in severe eclampsia]. 764 67

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

A previously healthy 37-year-old Latin American female presented at 17 6/7 weeks gestation with clinical manifestations of preeclampsia. Ultrasound revealed a growth-retarded fetus with hypoechoic bowel, a thickened cystic placenta, bilateral multicystic adnexal masses, and oligohydramnios. The patient had laboratory evidence of hyperthyroidism and the maternal serum alpha-fetoprotein was 12.3 multiples of the mean. Subclinical disseminated intravascular coagulation rapidly ensued and an induction of labor was performed. This was productive of a 110-g female fetus with a markedly distended abdomen and syndactyly. The placenta weighted 650 g with gross hydropic changes throughout. The clinical aspects of this case and review of the literature on partial molar pregnancies will be discussed.
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PMID:Partial hydatidiform molar pregnancy presenting with severe preeclampsia prior to twenty weeks gestation: a case report and review of the literature. 774 35


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