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)

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

The metabolic and functional alterations which occur during the acute phase of nephrotoxic nephritis (NTN) in rats, a model of immune-mediated glomerulonephritis, result from a cooperative interaction between PMNs and platelets (PLTs). In consequence, we hypothesized that fibrinogen (Fg) might play a critical role in this process and, accordingly, we found that defibrination of animals decreased both the acute phase proteinuria in NTN (approximately 70%) as well as the influx of PLTs and PMNs into the glomerulus (approximately 40-50%). In contrast, blockade of the PLT Fg receptor, alpha IIb beta 3, with the RGD peptidomimetic SC-49992 decreased proteinuria (approximately 90%) without substantially altering the influx of PMNs or PLTs. Immunocytochemistry showed a marked increase in beta 3 integrin expression in inflamed glomeruli which was prevented either by PMN or PLT depletion before disease induction. FACS and immunocytochemical analysis of glomerular cell dissociates demonstrated that beta 3 integrin expression was predominantly on intraglomerular PLTs. In vitro, activated PLTs stimulated the PMN respiratory burst, an interaction which could be inhibited by Fg receptor blockade. In sum, acute NTN is accompanied by a marked increase in glomerular beta 3 integrin expression predominantly due to the influx of PLTs which localize to the glomerulus in a PMN-dependent fashion. Fg appears to serve a major role as a coactivating stimulus for PLT-PMNs in situ via alpha IIb beta 3, potentially mediating the PMN respiratory burst which contributes to proteinuria. Fg may also play a subsidiary role in PMN/PLT comigration.
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PMID:Fibrinogen mediates platelet-polymorphonuclear leukocyte cooperation during immune-complex glomerulonephritis in rats. 808 78

In 1982 Weinstein coined the term HELLP syndrome to describe a special group of pre-eclamptic women who had evidence of hemolysis, elevated liver enzymes and low platelets. The question of whether the HELLP syndrome exists as a distinct entity or is a part of a spectrum of pregnancy complications has long been a source of speculation and debate among obstetricians and internists. A review of the literature indicates that the syndrome occurs in post-partum from 20% to 30% of the cases; maternal mortality from 1% to 4% and perinatal mortality from 5% to 40%. Hypertension and proteinuria are frequently associated with HELLP syndrome, but may also be absent. The syndrome is a group of clinical and pathological manifestations resulting from an insult that leads to intravascular platelet activation (thrombocytopenia) and micro-angiopathic hemolytic anemia (elevated total bilirubin and LDH). Endothelial damage and vasospasm are responsible of hepatic hypoperfusion that results in liver damage, as indicated by a rise in circulating liver enzymes. Since natural evolution of HELLP syndrome is the disseminated intravascular coagulation (CID), the interruption of pregnancy is mandatory and irrespective of the gestational age. This is the reason of an high incidence of cesarean section. Visser and Wallemburg (1995) treated 128 pre-eclamptic patients with HELLP syndrome with volume expansion and pharmacologic vasodilatation under invasive haemodynamic monitoring; they tried to delay delivery with the aim of enhancing fetal maturity. A complete reversal of HELLP occurred in 43% of patients. Further investigations will be necessary to confirm this interesting experience.
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PMID:[The HELLP syndrome. Notes on its pathogenesis and treatment]. 876 57

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

Data from 1981 to 1993 (excluding 1990-1991 due to Iraqi invasion) obtained from the Maternity Hospital in Kuwait were analyzed to examine pregnancy outcomes of eclamptic women and the risk factors for eclampsia in Kuwait. During the study period, 101 of 167,080 mothers had eclampsia for an incidence rate of 6/10,000. Eclampsia incidence did not change significantly during the study period. The incidence was 33/1000 for preeclampsia and 32/1000 for hypertension. Strong, significant risk factors for eclampsia included primiparity (relative risk [RR] = 8.93), age 30 years or younger (RR = 3.86), multiple pregnancy (RR = 4.15), preeclampsia (RR = 8.69), and low birth weight of 2500 g or less (RR = 13.96). Eclamptic women were significantly more likely to experience stillbirth, early neonatal death, and cesarean section. Maternal complications included need for intubation, disseminated intravascular coagulation, postpartum hemorrhage, maternal death, persistent increase in blood pressure, and proteinuria 1 week postpartum. One woman died from eclampsia for a maternal mortality rate of 0.99%, which is significantly higher than that for preeclampsia and for hypertension (0.0405 and 0.0396%, respectively). These findings show that risk factors for eclampsia are primiparity, young maternal age, multiple pregnancy, and presence of preeclampsia, and that eclamptic mothers experienced poorer pregnancy outcomes than other mothers.
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PMID:Eclampsia in Kuwait 1981-1993. 888 46

A 29-year-old woman with a triplet pregnancy received emergency caesarean section in the 33rd week of pregnancy. She lost 2 babies, one of whom was a fetal death and the other a neonatal death. Three weeks before delivery, she was admitted to hospital suffering from vomiting, diarrhea and polyuria. There were no laboratory abnormalities such as a slightly elevated levels of liver enzymes, nor any clinical symptoms of preeclampsia. At the end of the operation, disseminated intravascular coagulation (DIC) occurred and HELLP syndrome was diagnosed. However, the hemoglobin level was in the normal range at this point. On the 2nd postoperative day, hemolytic anemia developed in spite of the resolution of other problems. We suggested that the hemolysis, which may have been caused by a latent hemoconcentration and a membrane disorder of the red cells, was an osmotic hemolysis. This case was unique for the following reasons; 1) a lack of symptoms of hypertension, proteinuria and edema, 2) complications due to diabetes insipidus, 3) postpartum severe hemolysis following latent hemoconcentration, and 4) slow progress of the condition after onset. Early detection of HELLP syndrome is difficult. It should be considered in the management of patients with unrecognizable hemoconcentration and nonspecific complications.
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PMID:[HELLP syndrome in triplet pregnancy complicated by DIC and transient diabetes insipidus]. 951 34

Apparently healthy Wistar rats of body weight 250-300 g were chosen for the experiments. A group of 6 rats were assigned for each fraction. The dose of Russell's viper venom (RVV) fraction used for in vivo experiments was 0.75 microgram/g body weight. Of each batch of 6 rats 3 were sacrificed on the third day and the remaining 3 on the fifth day after the administration of test venom fractions. Daily urine output with proteinuria and serum creatinine were determined on the day they were sacrificed. Kidneys from the rats were also examined under light microscopy after hematoxylin and eosin staining. In the in vitro experiment, kidney slices (1 mm thickness) from normal rat was incubated with RVV fractions of 5 mg/ml concentration. The predominant renal lesions observed in both sets of animal experiments were tubular degeneration and necrosis. The changes were mostly confined to proximal tubules. Glomerular changes were mild. Similar tubulotoxic effects were produced by whole RVV as well as single fractions. Therefore, it is possible that RVV contains a common nephrotoxic (protein) component which is present in all fractions of the venom. The renal damage caused by RVV seemed to be due to both systemic effects (mainly DIC and renal ischemia) and direct tubulotoxic effects of the venom.
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PMID:Russell's viper venom fractions and nephrotoxicity. 956 25

Eclampsia is defined as the occurrence of seizures in pregnancy or within 10 days of delivery, accompanied by at least two of the following features documented within 24 hours of the seizure: hypertension, proteinuria, thrombocytopenia or raised aspartate amino transferase. Eclampsia complicates approximately one in 2,000 pregnancies in the United Kingdom and it remains one of the main causes of maternal death. Up to 38% of cases of eclampsia can occur without premonitory signs or symptoms of pre-eclampsia-that is, hypertension, proteinuria, and oedema. Only 38% of eclamptic seizures occur antepartum; 18% occur during labour and a further 44% occur postpartum. Rare cases of eclampsia have occurred over a week after delivery. Outcome is poor for mother and child. Almost one in 50 women suffering eclamptic seizures die, 23% will require ventilation and 35% will have at least one major complication including pulmonary oedema, renal failure, disseminated intravascular coagulation, HELLP syndrome, acute respiratory distress syndrome, stroke, or cardiac arrest. Stillbirth or neonatal death occurs in approximately one in 14 cases of eclampsia. Up to one third of eclamptic seizures occur out of hospital. For this reason, initial management may involve accident and emergency departments. Early involvement of senior obstetric staff is crucial. Optimal emergency management of seizures, hypertension, fluid balance and subsequent safe transfer is essential to minimise morbidity and mortality.
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PMID:Management of eclampsia in the accident and emergency department. 1065 82

Objective: Acute fatty liver of pregnancy (AFLP) is an uncommon, potentially fatal disorder that usually occurs in the late third trimester of pregnancy. We present the first reported case of acute fatty liver in the second trimester of pregnancy.Methods: We report the clinical and laboratory findings in a patient with AFLP who presented in the second trimester of pregnancy.Results: A 37-year-old G5P4 woman presented at 22 weeks gestation (by 18 weeks ultrasound) with nausea and vomiting. She was normotensive, had no proteinuria, had elevated SGOT and SGPT (266 and 261, respectively), negative hepatitis studies and a normal platelet count. She was managed conservatively for presumed cholelithiasis until 24 weeks gestation when she was transferred to our facility because of worsening SGPT and SGPT (368 and 505, respectively), jaundice (total bilirubin of 8.9 mg/dL), hypoglycemia, and laboratory evidence of disseminated intravascular coagulation (DIC) (PT = 18.6, PTT = 56, hypofibrinogenemia and presence of fibrin split products). Ultrasound showed singleton fetus (EFW 450 g) with total placenta previa. Computed tomography scan of the abdomen revealed decreased hepatic density consistent with AFLP. Delivery of a nonviable fetus was effected after transfusion of fresh frozen plasma. Postoperatively, the patient had rapid resolution of DIC, jaundice, and hypoglycemia; liver transaminases normalized 5 days postoperatively and the patient was discharged home in good condition 5 days later.Conclusion: It has been traditionally stated that AFLP occurs in the late third trimester of pregnancy. This case demonstrates that, even in the second trimester of pregnancy, the diagnosis of AFLP should be considered as a cause of deteriorating liver function, jaundice, and DIC.
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PMID:Acute fatty liver in the second trimester of pregnancy. 1083 61

Few case reports have shown the presence of metastatic tumor cells in renal glomeruli. We report one case with intraglomerular metastasis proved at renal biopsy. A 60-year-old man suffered from weight loss and fever of unknown origin. Urinalysis revealed proteinuria with cellular and granular casts. Because vasculitis was suspected, renal biopsy was performed. Presence of tumor cells occupying the glomerular capillary lumina was shown by means of light microscopy and electron microscopy. Laboratory findings revealed elevated leukocyte count (28.9 x 10(3)/mm(3)), serum granulocyte colony-stimulating factor (G-CSF) (77 pg/mL), and serum CA 19-9 (21,885 U/mL). The patient soon developed disseminated intravascular coagulation and died. Autopsy findings revealed pancreatic cancer showing positive staining for G-CSF and CA 19-9. Tumor cells in the glomerular capillary lumina showed positive staining for CA 19-9 and proliferating cell nuclear antigen (PCNA). These results suggest that the pancreatic tumor cells producing G-CSF were entrapped in the glomerular capillary lumina where they proliferated. This may have been the first step in renal metastasis.
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PMID:Intraglomerular metastasis from pancreatic cancer. 1138 3


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