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)

This clinical-pathological conference took place at the Sourasky Medical Center, Tel Aviv, on February 21, 2001. We present the case of a young and previously healthy soldier who developed multi-organ failure with predominant liver dysfunction following exertional heatstroke. The patient's clinical course consisted of an early phase of transient encephalopathy, associated with hyperthermia, hypophosphatemia, mild laboratory indications of renal failure, rhabdomyolysis and consumption coagulopathy. Following an intermediate convalescing phase that lasted a single day the patient deteriorated into a catastrophic course with hemodynamic instability, fulminant hepatic failure, respiratory distress, kidney failure, rhabdomyolysis, coagulopathy and coma. He died 4 days later. In this article we elaborate on the association of heatstroke with multiple organ dysfunction syndrome in general, and fulminant liver failure in particular. The nature of hypophosphatemia and the possible role of additional injury from acetaminophen are discussed.
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PMID:[Multi-organ failure in a young soldier: a clinical-pathological meeting]. 1190 96

We report here the case of a patient with fluoxetine and selegiline induced serotonin syndrome, which presented as encephalopathy, generalized myoclonias, fever, stiffness and sweating, complicated with acute renal failure, rhabdomyolysis and disseminated intravascular coagulation findings. The patient died 6 days after admission. This syndrome is discussed, with an analysis of its causes, pathophysiology and therapy. A special emphasis is placed on the clinical issues and differential diagnosis with the malignant neuroleptic syndrome and other clinical entities with which it could be mistaken. General recommendations are provided to avoid this poorly characterized syndrome that, as in our patient, may have a fatal outcome.
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PMID:[Serotonin syndrome: report of a fatal case and review of the literature]. 1200 30

Acute fatty liver of pregnancy is an uncommon, potentially fatal disorder. Between 1998 and 2000, two patients with acute fatty liver of pregnancy presented at the Christian Medical College Hospital, Vellore. Both patients were in the thirty-sixth week of pregnancy. jaundice and encephalopathy were the predominant symptoms. Both the mothers died after they delivered a stillborn Infant each. The maternal deaths were due to multiorgan failure and/or postpartum haemorrhage and sepsis. The route of delivery was vaginal in both the patients. Extrahepatic and metabolic complications in both cases Included renal failure, sepsis, hypoglycaemia, disseminated intravascular coagulation and gastrointestinal bleeding. Liver biopsy done in both patients was consistent with the diagnosis of acute fatty liver of pregnancy. To the best of our knowledge, this is the first report from India on acute fatty liver of pregnancy.
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PMID:Acute fatty liver of pregnancy: a report of two cases. 1254 67

In order to test the practicability and safety of whole-body cooling in term neonates with moderate-to-severe hypoxic-ischaemic encephalopathy (HIE) and to report outcomes, a prospective pilot study was carried out in 25 term infants (median postmenstrual age 38 weeks, range 36 to 41 weeks; 20 males, five females). Whole-body cooling, to a target core temperature of 33 to 34 degrees C, started within 6 hours of birth and was maintained for 72 hours. Of the 25 newborn infants (19 Sarnat II and six Sarnat III, 18 outborn), 18 survived, including 13 (72%) with normal cerebral signal by MRI. Temperature instability occurred during cooling in 15 infants, but neither severe haemodynamic instability nor renal failure was seen. Thrombocytopenia developed in 12 infants, including seven with biological disseminated intravascular coagulation. One patient had hypoxaemia with right-to-left shunting through the ductus arteriosus, and seven had limited meningeal or subdural bleeding. Whole-body cooling is feasible in term neonates, with no life-threatening adverse events. Improvements are needed to obtain stable hypothermia for 72 hours.
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PMID:Whole-body cooling after perinatal asphyxia: a pilot study in term neonates. 1255 98

Hepatitis E causes large-scale epidemics in endemic areas. The disease, during epidemics, has increased incidence and severity in pregnant women. Sporadic acute viral hepatitis (AVH) is common in endemic areas. The relationship of sporadic AVH and pregnancy has not been well studied. Over a 3-year period we prospectively studied 76 pregnant women and 337 non-pregnant women of childbearing age with sporadic acute viral hepatitis for aetiology, clinical course and outcome of disease. The aetiology in sporadic AVH was hepatitis A virus (HAV) in six (1.5%), hepatitis B virus (HBV) in 62 (15%), hepatitis C virus (HCV) in seven (1.7%), hepatitis D virus (HDV) co-infection in six (1.5%), hepatitis E virus (HEV) in 205 (49.6%), and hepatitis non-A-to-E (HNAE) in 127 (30.7%). Sixty-five (85.5%) pregnant women and 140 (41.5%) nonpregnant women had hepatitis E. The proportion of pregnant women was 31.7% in HEV group and 5.3% in non-HEV group [P < 0.001; OR=8.3 (95%C1 4.2-16.3)]. The prevalence of HEV in pregnant women in first trimester (76.9%), second trimester (88.9%), third trimester (83.8%) and puerperium (100%) did not differ significantly (P=0.09). Forty-seven (61.8%) of the 76 pregnant women developed fulminant hepatic failure (FHF), 69.2% in HEV group and 10% in non-HEV group (P < 0.001). Thirty-four (10.1%) nonpregnant women developed fulminant hepatic failure, 10% in HEV group and 9.7% in non-HEV group (P=0.86). FHF had occurred in four (40%) of 10 patients with HE in first trimester as against 41 (74.5%) of 55 patients in second trimester and beyond (P=0.015). Amongst the major complications of fulminant hepatic failure, cerebral oedema (53.2%) and disseminated intravascular coagulation (21.3%) occurred more often in pregnant women than in nonpregnant women (29.4% and 2.8%; P=0.03 and 0.016, respectively) while infections occurred more often in nonpregnant women (36.1%) than in pregnant women (10.6%; P=0.003). Fifty (61.7%) patients with FHF died [25 (53.2%) pregnant women and 25 (69.5%) nonpregnant women (P=0.06)]. Cerebral oedema and HEV aetiology were independent variables of survival in patients with FHF. Patients with cerebral oedema had worse prognosis and patients with HEV aetiology had best chances of survival. Hence HEV was the most common cause of sporadic AVH in this endemic area. High proportion of pregnant women and increased severity of disease in pregnancy were limited to patients with hepatitis E. Sporadic AVH caused by agents other than HEV did not show any special predilection to or increased severity in pregnancy. FHF in pregnant women caused by HEV was an explosive disease with short pre- encephalopathy period, rapid development of cerebral oedema and high occurrence of disseminated intravascular coagulation and may represent a severe manifestation of a Schwartzmann-like phenomenon.
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PMID:Aetiology, clinical course and outcome of sporadic acute viral hepatitis in pregnancy. 1255 14

A hundred and thirty five patients admitted to Moscow Tuberculosis Hospital No. 7 for disseminated and progressive forms of tuberculosis were examined. Among neurological disorders in tuberculosis, acute toxic encephalopathy (ATE) should be placed in the first place in terms of their severity, problems of diagnosis and treatment. In patients with acutely progressive forms of tuberculosis, the development of ATE is brought about by two factors: 1) significant tuberculous toxemia concurrent, in 37% of cases, with severe alcoholic intoxication that leads to generalized toxic and allergic vasculitis and as a result DIC syndrome; 2) cerebral hypoxia with dyscirculatory disorders due to progressive cardiopulmonary failure. The status of patients with tuberculosis and ATE is generally critical or extremely critical. These are actually resuscitative patients. Most patients have disseminated bilateral lung lesions with multiple decay cavities, with massive bacterial isolation found at sputum bacterioscopy. With this, mycobacterial resistance to at least one antituberculous drug was found in 83% of cases. Primary multidrug resistance was detected in 29.6% of patients. The diagnosis of ATE in patients with tuberculosis is difficult and requires that tuberculous meningitis shall be excluded. Acute progression, no spinal fluid changes, significant signs of cooagulopathy and thrombcytopathy with multiorgan failure and progressive DIC syndrome may diagnose ATE in patients with acutely progressive tuberculosis. The specific features of treatment in patients with tuberculosis and ATE are intensive antituberculous therapy with predominantly parenteral administration of drugs and intensive therapy for the DIC syndrome. Despite the treatment, 48 (35.6%) patients died from progressive tuberculosis and ATE, in 40 (29.6%), therapeutic efficiency was low due to multidrug myobacterial resistance.
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PMID:[Acute toxic encephalopathy in patients with tuberculosis]. 1261 36

Coagulation disorders are common in cancer patients. In patients with solid tumors, a low-grade activated coagulation can result in systemic and cerebral arterial or venous thrombosis. Cancer treatments may also contribute to this coagulopathy, which usually, but not exclusively, occurs in the setting of advanced malignant disease. There may be TIAs or cerebral infarctions. Because of the widespread distribution of cerebral thromboses, there may be a superimposed encephalopathy; sometimes this is the only sign. Concurrent systemic thrombosis is present in many patients and is a useful clue to the diagnosis. In cerebral venous occlusion, the initial symptom is usually a headache. Except for cerebral intravascular coagulation that is unassociated with NBTE, neuriomaging studies usually demonstrate one or more parenchymal infarctions. MRI or MRV may demonstrate venous thrombosis. The laboratory evidence of coagulopathy is difficult to distinguish from the asymptomatic coagulopathy that often accompanies advanced cancer, and the test results must be interpreted cautiously. NBTE can be diagnosed by transesophageal echocardiography. There is no established treatment for the thrombotic coagulopathy associated with cancer, but anticoagulation should be considered. In leukemia and lymphoma, the coagulopathy is typically acute DIC that can lead to systemic and brain hemorrhages. It is especially common in acute myelogenous leukemias. The clinical signs of cerebral hemorrhage are fulminant and may be fatal. The bleeding usually occurs in the brain or subdural compartment, and rarely in the subarachnoid space. The diagnosis can be suspected by the clinical setting and by systemic thrombosis or hemorrhage. It can be established by examination of the peripheral smear, the platelet count, and tests of coagulation function. Therapy of acute DIC is controversial and should be individualized for the clinical setting. Cerebrovascular disorders can complicate metastatic or primary tumor in the brain, skull, dura, or leptomeninges. The clinical signs of infarction are indistinguishable from other causes of stroke, except that tumor-related venous occlusion will usually first produce signs of increased intracranial pressure. The diagnosis of tumor-related infarction can usually be established by neuroimaging studies that show infarction and may show extracerebral sites of tumor. CSF examination is useful in diagnosing leptomeningeal metastasis. A search for lung or cardiac tumor should be performed when embolic tumor infarction is suspected. Primary or metastatic tumors in the brain or dura may hemorrhage, producing the initial clinical signs of the brain tumor or a change in chronic signs induced by the tumor. There are helpful clues to a neoplastic hemorrhage on brain CT or MRI scans. The brain hemorrhage may require evacuation and the underlying tumor will usually require additional antineoplastic treatment. Hyperleukocytosis (extreme elevation of the cell count) in acute myelogenous leukemia is a less common cause of brain hemorrhage in recent years because of improved methods to lower the cell count. Cerebral arterial or venous thrombosis is sometimes the result of cancer therapy. The attribution of thrombosis to chemotherapy in many published cases is only speculative, because carefully conducted prospective studies that include investigation for other thrombotic causes are not available. The best-known associations with thrombosis are L-asparaginase, which is typically used in the induction therapy of acute lymphocytic leukemia, and combination hormonal therapy and chemotherapy for breast cancer. Radiation to the head and neck, typically administered for head and neck epithelial cancers or lymphoma, may result in delayed carotid atherosclerosis. The distribution of stenosis or occlusion is within the radiation portal and is typically more extensive than is atherosclerosis that develops in the absence of radiation. Small clinical series suggest that surgical treatment is equally effective as in nonirradiated carotid atherosclerosis. In children, the cerebral vessels can be affected by brain radiation resulting in stenosis or occlusion. Brain hemorrhages can result from chemotherapy effects on the hemostatic system or a microangiopathic anemia. Hemorrhages from radiation-induced vascular abnormalities are rare. Opportunistic infections, especially fungal infections, can complicate cancer or its treatment. Septic cerebral emboli may result in focal cerebral signs, seizures, or encephalopathy. Sometimes there is an associated hemorrhagic vasculitis or cerebritis. Rarely, mycotic aneurysms may bleed. A high index of suspicion is needed to diagnose fungal infection because of the difficulty in culturing the organism from the blood or CSF. A clinician can usually establish the cause of stroke in the cancer patient by performing a careful review of the clinical setting--including the type and extent of cancer and the type of antineoplastic therapy--in which the stroke occurred. Systemic thrombosis, embolism, or hemorrhage can be a clue to the cause, and appropriate neuroimaging and coagulation studies to aid in the diagnosis are available. Therapy may ameliorate symptoms or prevent further episodes. The identification of one of these unusual stroke syndromes that leads to the diagnosis of an occult and treatable cancer can be particularly rewarding.
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PMID:Cerebrovascular complications in cancer patients. 1269 Jun 49

Intravascular lymphomatosis (IVL) is a rare angiotrophic large cell lymphoma producing vascular occlusion of arterioles, capillaries, and venules. Antigenic phenotyping shows that these lymphomas are mostly of B cell type, and less commonly T cell or Ki-1 lymphomas. The central nervous system and skin are the two most commonly affected organs; patients usually present with progressive encephalopathy with mental status changes and focal neurological deficits and skin petechia, purpura, plaques, and discolouration. Other involved organs include adrenal glands, lungs, heart, spleen, liver, pancreas, genital tract, and kidneys. Bone marrow, blood, cerebrospinal fluid, and lymph nodes are typically spared. Fever of unknown origin is another common presentation. Only one case of IVL presenting with disseminated intravascular coagulation and anasarca (generalised oedema) has been reported in the literature. This report describes a postmortem case of a patient with IVL who initially presented with disseminated intravascular coagulation complicated by intracerebral haemorrhage.
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PMID:Intravascular lymphomatosis. 1278 76

From the middle of 1990's, there repeated in winter season an outbreak of encephalopathy in Japan that appeared to be associated with influenza. A national survey was conducted, and a total of 507 patients was diagnosed as having influenza-associated encephalopathy during 1998-2002 on the basis of virologic analysis. Type A influenza was more pathogenic than type B, and A: H3 type was more invasive than A: H1 type. Encephalitis developed mainly in children below 5 years of age, either on the day that influenza signs appeared or on the next day. We hypothesized that the replicated viruses at nasopharyngeal epithelium disrupt the olfactory mucosa. Via olfactory nerve system, the stimuli may be transmitted to the brain eventually to activate glial cells, and to induce the production of pro-inflammatory cytokines. The cytokine storm results in neural cell damage as well as apoptosis of glial cells due to TNF-induced mitochondrial respiratory failure. The disruption of blood-brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF.
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PMID:[Influenza-associated encephalopathy--pathophysiology and disease mechanisms]. 1461 37

Systemic-onset juvenile rheumatoid arthritis (SoJRA) constitutes about 10-20% of all JRA. However more than two-thirds of the mortality seen in JRA patients is accounted for by SoJRA. Macrophage activation syndrome (MAS), which can also be considered as a form of secondary hemophagocytic lymphohistiocytosis, is a major cause of morbidity and mortality in children with SoJRA. MAS is characterized by persistent high fever, pancytopenia, mild to serious derangements of liver cell function, encephalopathy, and disseminated intravascular coagulation. Renal involvement in MAS is a rarely recognized feature. In 2 recently reported case series of MAS in SoJRA, renal involvement appeared to be associated with poor prognosis. We describe 3 children with SoJRA who had renal involvement complicating MAS and had a favorable outcome.
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PMID:Favorable outcome in patients with renal involvement complicating macrophage activation syndrome in systemic onset juvenile rheumatoid arthritis. 1546 77


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