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)

Acute encephalopathy is the most serious complication of pediatric viral infections, such as influenza and exanthem subitum. It occurs worldwide, but is most prevalent in East Asia, and every year several hundreds of Japanese children are affected by influenza-associated encephalopathy. Mortality has recently declined, but is still high. Many survivors are left with motor and intellectual disabilities, and some with epilepsy. This article reviews various syndromes of acute encephalopathy by classifying them into three major categories. The first group caused by metabolic derangement consists of various inherited metabolic disorders and the classical Reye syndrome. Salicylate is a risk factor of the latter condition. The second group, characterized by a systemic cytokine storm and vasogenic brain edema, includes Reye-like syndrome, hemorrhagic shock and encephalopathy syndrome, and acute necrotizing encephalopathy. Non-steroidal anti-inflammatory drugs, such as diclofenac sodium and mephenamic acid, may aggravate these syndromes. Severe cases are complicated by multiple organ failure and disseminated intravascular coagulation. Mortality is high, although methylprednisolone pulse therapy may be beneficial in some cases. The third group, characterized by localized edema of the cerebral cortex, has recently been termed acute encephalopathy with febrile convulsive status epilepticus, and includes hemiconvulsion-hemiplegia syndrome and acute infantile encephalopathy predominantly affecting the frontal lobes. Theophylline is a risk factor of these syndromes. The pathogenesis is yet to be clarified, but an increasing body of evidence points to excitotoxicity and delayed neuronal death.
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PMID:Acute encephalopathy associated with influenza and other viral infections. 1778 37

Of the approximately one in 1000 pregnant women who develop the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP), 2 to 3 per cent develop hepatic complications, including liver failure for which liver transplantation (LT) may be required. Between February 1, 1984, and December 31, 2006, eight women without a history of liver disease underwent LT for complications of HELLP syndrome. All received cadaveric grafts with a mean interval from delivery to LT of 7 days. The mean admission Child-Turcotte-Pugh score was 13.1 (class C), and the mean model for end-stage liver disease score was 40. Manifestations of liver failure included encephalopathy (seven patients), renal failure (four), disseminated intravascular coagulation (three), and respiratory failure (one). There were no intraoperative deaths. Complications of LT included biliary leaks (three patients), reoperation (three), and retransplantation (two). There was one death from sepsis on postoperative day 91 and one death from cholangitis/sepsis more than 5 years postoperatively. After LT, 1-, 5-, and 10-year patient survival rates were 88 per cent, 88 per cent, and 65 per cent; 1-, 5-, and 10-year graft survival rates were 64 per cent, 64 per cent, and 48 per cent. This is the largest single-center report of LT for HELLP. Early recognition and transfer to a transplant center will yield best results with this challenging complication of pregnancy.
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PMID:Liver transplantation for HELLP syndrome. 1798 71

The patient in this study was a 43-year-old woman who had become unconscious after contracting influenza virus type A infection. Brain CT showed severe brain swelling. Brain MRI also showed brain edema with no specific abnormality on T2-weighted images. We diagnosed her as having influenza type A virus-associated encephalopahty and treated her with Oseltamivir, methylprednisolone pulse therapy, and a high dose of intravenous immunoglobulins. In addition, we treated her with hypothermia and a high dose of intravenous ATIII because of the severe brain swelling and possibility of DIC. After the treatments, brain swelling had improved, and she regained consciousness without any sequelae. Adult influenza virus-associated encephalopathy is rare. We were able to successfully treat our patient with primary multidisciplinary treatments without causing sequelae.
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PMID:[Case of adult influenza type A virus-associated encephalopathy successfully treated with primary multidisciplinary treatments]. 1809 96

Influenza-associated encephalopathy (IAE) usually occurs in children aged <5 years. Adult cases of IAE are very rare and, thus far, no definite adult autopsy case has been reported. Here, we present the first definite adult autopsy case of IAE. A 76-year-old man presented with sudden coma a day after the onset of fever caused by infection with influenza type A virus. Soon after admission, his condition was complicated by DIC, shock, and multiple organ failure, and he was diagnosed with IAE. Oseltamivir administration and steroid pulse therapy were performed but these proved to be ineffective. The patient died about 24 hours after the onset of encephalopathy. The autopsy revealed massive brain edema and diffuse increase of amoeboid glias without inflammatory cell infiltration. Influenza type A/Hong Kong virus (H3) was isolated from his lungs. Serum IL-6 level was extremely high (35,800 pg/ml; normal, 0.221-4.62 pg/ml). The clinical course, and the laboratory and pathological findings of this adult case resembled those of a typical childhood-onset IAE, suggesting the same pathogenesis. During the influenza season, IAE should be taken into account for differential diagnosis in adult patients with altered mental status and fever.
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PMID:[Elderly autopsy case of influenza-associated encephalopathy]. 1908 26

A case of fulminant disseminated varicella is reported in a 28-year-old immunocompetent man. He developed hepatitis, severe pneumonia, rhabdomyolysis and disseminated intravascular coagulation, followed by encephalopathy and multiorgan failure despite acyclovir therapy. He spent a total of 3.5 months in intensive care and rehabilitation units. Real-time PCR yielded a rapid diagnosis of varicella-zoster virus (VZV) infection and was used to monitor plasma viral load for 56 days. Plasma viral load peaked at 7.1 log(10)/ml on day 4 after symptom onset, then gradually declined and became undetectable after between 1 and 2 months; viral load in lung fluid followed a similar pattern. The glycoprotein E variant associated with increased VZV virulence was not detected, and the VZV thymidine kinase gene bore no major mutations associated with acyclovir resistance. This case serves as a reminder that varicella can be life-threatening in adults and that vaccination of individuals at risk remains essential.
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PMID:Disseminated varicella with multiorgan failure in an immunocompetent adult. 1923 68

We report a 4-year-old boy with fulminating meningitis caused by Haemophilus influenzae (Hib). He suddenly developed fever, vomiting and then somnolence. As bacterial meningitis was suspected, treatment with antibiotics was started at 12 hours after the onset. However, there was a rapid progression of severe brain edema and brain hernia, leading to clinical brain death. His clinical course and neuroradiological findings mimicked those in patients with acute encephalopathy, with cytokine profiles in cerebrospinal fluid demonstrating a marked increase of inflammatory cytokines. From a review of the literature, fulminating Hib meningitis may be classified into two disease types: DIC plus multiple organ failure and acute brain swelling types. The present case belongs to the latter type, in which cytokine storm seems to play an important pathogenic role.
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PMID:[Fulminating meningitis caused by Haemophilus influenzae with rapid progression of severe brain edema similar to acute encephalopathy]. 1992 44

HELLP is a syndrome with haemolysis, elevated liver enzymes and thrombocytopenia. It occurs in 1 to 6 per 1,000 parturient. Approximately 10% of the cases occur post partum. A 16-year-old woman delivered twins in the 34th gestational week. During the following hours, she developed symptoms of hypovolaemic shock. Blood sample values were critical and the patient was diagnosed with HELLP with DIC. She developed liver shock with encephalopathy and acute renal failure. Her condition stabilized on the 8th day of admission and the woman was extubated on the 16th day. She was discharged without complications on the 22 th day.
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PMID:[Sixteen-year-old woman with multiorgan dysfunction after HELLP]. 2019 53

We recently treated a patient with adult-onset Still's disease who developed macrophage activation syndrome (MAS) secondary to disseminated histoplasmosis while being treated with adalimumab. The gastroenterology service was consulted early, before diagnosis, as the patient presented with elevated liver enzymes and disseminated intravascular coagulation. MAS is an exaggerated immune response that can develop as a primary condition or secondary to infections, drugs and various diseases, resulting in liver dysfunction, encephalopathy, pancytopenia and disseminated intravascular coagulation. The development of MAS has also been reported in patients with inflammatory bowel disease and post-liver transplantation and has been triggered by medications used by gastroenterologists, particularly sulfasalazine and anti-tumor necrosis factor biologic modifiers. Therefore, we present a review on etiology, pathogenesis, clinical and laboratory features, and treatment of MAS with a focus on gastrointestinal aspects and presentations. MAS is a life threatening condition with a high mortality rate if untreated. Therefore it is important to recognize this condition early. As these patients may occasionally present to gastroenterologists we hope this review will increase awareness of this rare, but serious syndrome.
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PMID:Macrophage activation syndrome: why and what should a gastroenterologist know. 2092

It is important to consider that between Jul-October 2009 in the pathologic center of infectious diseases (Tbilisi State Medical University Department of Infectious Diseases) among hospitalized patients with hemorrhagic colitis 25 patients developed HUS syndrome. Most of patients were rural residents 20 (80%), only 5 (20%) were urban. 11 (44%) patients were children, 14 (56%) were adults. Male and female rate was equal. All the patients related the onset of the disease with the consumption of notwashed raw fruits or vegetables, nonpasteurized dairy products, food from street vendors, soft cheeses made from raw milk and untreated water in areas lacking adequate chlorination. The onset of the disease was not acute: low grade fever (37,5-37,8(0)C), severe diffuse pain in abdomen accompanied with cramps, frequent bowel movement with loose, watery stools 5-6 times a day. On the 2-3rd days of disease condition was worsened by increased of intoxication and frequent bowel movement with bloody stools about 10-15-20 times a day. On the 3-4 rd days of the onset of the diarrhea developed oliguria, anuria, edema. Among other complications important were: polyserosit - 8 (32%), encephalopathy - 2 (8%), disseminated intravascular coagulation - 3 (14%), ileus -1 (4%,) acute reactive phsycosis - 1 (4)%. In 15 (60%) cases became necessary to carry out hemodialysis. died 5 patients, lethality is - 5 (20%). Treatment options included: pathogenetic and symptomatic. Thus, increased rate of patients in the recent years indicates to circulation of shiga-toxin producing E.Coli in Georgia.
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PMID:Enterohemorrhagic E. coli and hemolytic uremic syndrome in Georgia. 2097 74

Hemorrhagic shock and encephalopathy syndrome (HSES) is characterized by abrupt onset of hyperpyrexia, encephalopathy(seizure and coma), shock, diarrhea, disseminated intravascular coagulation, and renal and hepatic failure. HSES occurs in infants and prognosis is quite poor; early death in 35-82%, severe neurological squeal in 20-30%, and normal in only 10-20%. The underlying pathogenesis is still unknown. Although previous reports revealed that lowered plasma alpha1-antitrypsin level or elevated cytokine levels including IL-6 and TNF-alpha, the results are controversial.
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PMID:[Hemorrhagic shock and encephalopathy syndrome (HSES)]. 2140 Aug 39


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