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)

A 44-year-old Spanish woman travelled in Kenya without doing correct malarial prophylaxis. Upon her return to Spain, she suffered from Plasmodium falciparum malaria. She was initially treated with chloroquine for three days, but her state worsened and she was admitted to our intensive care unit. On admission, parasitaemia was 22%. She had hyperpyrexia, obtundation, hypotension, tachycardia, tachypnoea, jaundice, digestive haemorrhage, petechiae in her soles, oliguria with elevation of serum uraemia and creatinine, anaemia, thrombocytopaenia, hypoproteinaemia, hyponatraemia, hypocalcaemia, metabolic acidosis and parameters of disseminated intravascular coagulation. She was given quinine, sulfadoxine-pyrimethamine and clindamycin. An exchange transfusion was performed, during which an acute pulmonary oedema appeared, initially with high pulmonary artery wedge pressure. She required mechanical ventilation for 16 days and haemodialysis for 11 days. She remained in coma and had seizures which required diazepam, phenitoin and thiopentone. She received a total amount of 22 units of packed erythrocytes, 55 of platelets and 15 of plasma. After the first week, she had nosocomial infection due to Escherichia coli, Staphylococcus and Pseudomonas aeruginosa and was treated with the corresponding antibiotics. She cured completely. This case report gives us the possibility of discussing on frequent problems in the prevention and treatment of malaria, and on the treatment of severe, life-threatening malaria in the setting of the intensive care unit.
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PMID:[Multiple organ failure in Plasmodium falciparum malaria]. 853 25

Adult onset Still's disease (AOSD) is a well characterized rheumatoid disorder with frequent liver involvement. This is usually asymptomatic but severe hepatic failure has occasionally been reported. We describe a 44-year-old woman who developed acute liver failure 2 months after presenting symptoms of AOSD. Full etiologic evaluation was done and all other causes of liver failure were excluded. She underwent emergency orthotopic liver transplantation but developed disseminated intravascular coagulation with acute renal failure, seizures, and coma, and died after 48 hours.
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PMID:Fulminant hepatic failure in adult onset Still's disease. 873 Jan 49

Cantharidin, known popularly as Spanish fly, has been used for millennia as a sexual stimulant. The chemical is derived from blister beetles and is notable for its vesicant properties. While most commonly available preparations of Spanish fly contain cantharidin in negligible amounts, if at all, the chemical is available illicitly in concentrations capable of causing severe toxicity. Symptoms of cantharidin poisoning include burning of the mouth, dysphagia, nausea, hematemesis, gross hematuria, and dysuria. Mucosal erosion and hemorrhage is seen in the upper gastrointestinal (GI) tract. Renal dysfunction is common and related to acute tubular necrosis and glomerular destruction. Priapism, seizures, and cardiac abnormalities are less commonly seen. We report four cases of cantharidin poisoning presenting to our emergency department with complaints of dysuria and dark urine. Three patients had abdominal pain, one had flank pain, and the one woman had vaginal bleeding. Three had hematuria and two had occult rectal bleeding. Low-grade disseminated intravascular coagulation, not previously associated with cantharidin poisoning, was noted in two patients. Management of cantharidin poisoning is supportive. Given the widespread availability of Spanish fly, its reputation as an aphrodisiac, and the fact that ingestion is frequently unwitting, cantharidin poisoning may be a more common cause of morbidity than is generally recognized. Cantharidin poisoning should be suspected in any patient presenting with unexplained hematuria or with GI hemorrhage associated with diffuse injury of the upper GI tract.
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PMID:Poisoning from "Spanish fly" (cantharidin). 876 16

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

Hemorrhagic shock and encephalopathy syndrome (HSES) is a sudden-onset symptom complex occurring in previously healthy infants and children. It was first described in 1983 in the United Kingdom in 10 infants. Subsequently, > 140 cases have been reported worldwide, although no cases have been previously reported in the forensic literature. Typically the child presents with fever, shock, encephalopathy with coma and seizures, evidence of hemorrhage, and diarrhea. Laboratory investigation reveals falling hemoglobin and platelet counts, renal impairment, evidence of disseminated intravascular coagulation, metabolic acidosis, and raised serum transaminases. Microbiological cultures are uniformly negative. The condition has a high mortality and morbidity. The etiology is unknown and may be multifactorial. However, hyperpyrexia appears to play a central role in pathogenesis. The diagnosis of HSES in the deceased child is one of exclusion and requires a careful antemortem history as well as a thorough autopsy with toxicological and microbiological investigations. A case of HSES is reported and the literature reviewed.
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PMID:Hemorrhagic shock and encephalopathy syndrome. An unusual cause of sudden death in children. 909 7

We describe a male infant with early myoclonic encephalopathy (EME) associated with the congenital nephrotic syndrome, microcephaly, multiple minor anomalies, and cerebellar hypoplasia. He had erratic and massive myoclonus, and partial seizures from the neonatal period. Electroencephalography showed the so-called suppression-burst pattern. He died of disseminated intravascular coagulation caused by the congenital nephrotic syndrome at the age of two months. Our patients is the first reported case with EME associated with the congenital nephrotic syndrome.
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PMID:A case of early myoclonic encephalopathy with the congenital nephrotic syndrome. 910 63

A case of amniotic fluid embolism during the delivery of an at term pregnancy is reported. The 34-year old primipara with an unremarkable medical history suddenly suffered from a seizure in the second stage of labor. Shortly prior to this event, a prolonged fetal bradycardia was recorded. After forceps delivery a massive postpartum haemorrhage as the result of a consumption coagulopathy occurred. Immediate resuscitation with artificial ventilation improved the condition of mother and child. The substitution of packed red cells and platelets, fresh frozen plasma and other blood derivates was necessary. Mother and child survived without any physical damage or neurological deficit. Because of the clinical pattern we diagnosed an amniotic fluid embolism.
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PMID:[Clinical aspects and therapy of amniotic fluid embolism. Illustration based on a case report]. 941 May 22

The clinical characteristics of and outcome for 75 children with meningococcal septic shock were studied. In addition, a new prognostic scoring system was developed. The median age of the patients was 3.2 years (range, 3 weeks to 17.9 years). The most common phenotype of Neisseria meningitidis was B:4:P1.4 (27%). A mortality rate of 21% was observed. Ten (17%) of the 59 survivors had serious sequelae. Calcium levels were significantly lower in patients with seizures. Disseminated intravascular coagulation occurred in 58% of the patients who were tested. Logistic regression analysis identified four laboratory features independently associated with mortality: serum C-reactive protein level, base excess, serum potassium level, and platelet count. These features were used to develop a novel scoring system with a predictive value for death and survival of 71% and 90%, respectively. The outcome was predicted correctly for 86% of the patients, which is higher than rates previously reported for scoring systems.
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PMID:Meningococcal septic shock in children: clinical and laboratory features, outcome, and development of a prognostic score. 931 53

Two children developed multiorgan dysfunction with disseminated intravascular coagulation 9 days after lamotrigine was added to their antiepileptic therapy, which included valproic acid. During the episodes, rhabdomyolysis was detected in one of them, while being seizure-free, suggesting that this adverse reaction may involve muscular tissue.
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PMID:Multiorgan dysfunction and disseminated intravascular coagulation in children receiving lamotrigine and valproic acid. 937 37

Thromboembolic (TE) events have been frequently reported in beta-thalassemic patients in association with known risk factors such as diabetes, complex cardiopulmonary abnormalities, hypothyroidism, liver function anomalies, and postsplenectomy thrombocytosis. In a recent survey involving 9 Italian thalassemic centers, we identified 32 patients with TE episodes in a total of 735 subjects, of whom 683 had thalassemia major and 52 thalassemia intermedia, corresponding to 3.95 and 9.61%, respectively. There was a great variation in localization: the main one (16/32) was CNS, with a clinical picture of headache, seizures and hemiparesis. Other localizations were the pulmonary (3 patients), mesenteric (1 patient) and portal (2 patients) sites. There were 6 cases of deep venous thrombosis (2 in the upper limbs, 4 in the lower ones). Intracardiac thrombosis was found in 2 subjects and clinical and laboratory signs of DIC were observed in 2 others during pregnancy. Since our patients with TE events present a statistically significantly higher incidence of associated dysfunction (cardiomyopathy, diabetes, liver function anomalies, hypothyroidism) than those without TE events (50 vs. 13.8%), we suggest close monitoring of those patients who are at higher risk of developing TE events because of the presence of one or more of these predisposing factors.
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PMID:Thromboembolic events in beta thalassemia major: an Italian multicenter study. 985 99


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