Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autologous intraoperative transfusion employing the Haemonetics Cell Saver is reported in 725 patients from a general hospital population, of which 75% were cardiovascular patients. The remaining cases included various orthopedic procedures, splenectomy, craniotomy, ectopic pregnancies, Caesarian sections, and exploratory laparotomy. On occasion, this method was utilized in trauma and in pediatric surgery. The product of washed red blood cells gave an average yield of 573 cc per case with an average hematocrit of 55 cc/dl available for autologous infusion. In 100 consecutive open heart procedures operated prior to the Cell Saver period, an average of 1.97 units of bank blood was utilized during operation, as compared with 0.75 units in 100 consecutive cases studied employing the Cell Saver (p less than 0.0001). Homologous blood utilization during cardiac surgery declined more than 50% with the use of the Cell Saver. Quality control was monitored scrupulously and included special precautions against air embolism, abnormal coagulation, and sepsis. The overall mortality rate was 2.8%, and in no instance was mortality or morbidity ascribable to the autologous transfusion. Numerous advantages offered by autotransfusion include prevention of sensitization of the recipient to various antigens in donor erythrocytes, leucocytes, platelets, and plasma, and avoidance of transfusion-transmitted diseases, especially viral hepatitis. Additionally, autologous blood, the only perfectly compatible product, provided immediate availability while conserving blood bank resources. In circumstances in which the intraoperative blood loss exceeded 1000 cc in the adult, its use was observed to be cost-effective. In the present study, autotransfusion proved safe, efficient, and in some instances life saving.
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PMID:Intraoperative autotransfusion. Experience in 725 consecutive cases. 640 2

Circulating immune complexes were studied using 3.5% polyethyleneglycol precipitation in 312 children with various diseases whose ages ranged from 1 month to 14 years. One hundred and one patients (32.6%) were positive and the groups with the highest percentage were those with viral hepatitis (90%), sepsis (80.7%), collagen diseases (76.4%) and Schonlein-Henoch purpura (57.1%). We found immune complexes less frequently in idiopathic thrombocytopenic purpura than in published series of adult cases, possibly due to the fact that the diseases in children is due to a different pathogenetic mechanism. The composition of the immune complexes was tested by 1% agarose immunodiffusion against a panel of antisera. IgG and IgM were found most frequently, and IgA was very uncommon except in some cases of hepatitis. C4 was the most frequently found complement component, followed by C3. Important differences between the various diseases studied were noted. Our results are very similar to those previously published by other authors. Whereas serum autoantibodies and autoimmune diseases are less common in children than in adults, circulating immune complexes seem to have a similar frequency in children to that already reported for adults. It is difficult to assess the significance of circulating immune complexes. They might be (a) a mere "marker" of no pathogenic significance (b) a mechanism of tissue damage by intravascular deposition, or (c) they might interfere with the cell membrane receptors of macrophages, producing a defect in phagocytosis. However, we were unable to demonstrate an increased number of infections in these patients.
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PMID:[Incidence of circulating immune complexes in pediatric diseases. Comparative study with adults]. 645 Nov 57

Among 103 patients with fulminant hepatic failure due to viral hepatitis, paracetamol overdose, or halothane anaesthesia, treated over a 2-year period, 23 had bacteraemia. Gram-positive organisms, mainly streptococci and Staphylococcus aureus, were isolated from 61% of patients. Escherichia coli, the main type of gram-negative organism isolated, was found in 26% of patients and was associated with a fatal outcome more often than gram-positive bacteria. The type of organism isolated was not related to the aetiology of the hepatic necrosis, the presence of renal failure, or the clinical outcome. In the 23 patients with bacteraemia the same organism was isolated from other sites of infection, including sputum in four, urine in two, and the central venous catheter and arteriovenous shunt in one. Bacteraemia usually occurred 3 days after admission or on average 2 days after clinical deterioration to grade IV encephalopathy had begun. In 11 patients, the infection had an adverse effect on their clinical course, in three patients being implicated as a cause of the encephalopathy. Although in four patients the development of infection after all signs of encephalopathy had cleared may have been a major factor in their death, two of these patients had evidence of severe sepsis, pneumococcal peritonitis, and renal abscesses from which Candida albicans was cultured. An awareness of infection as a complication both of the acute stage of the illness and during recovery is essential if early detection and treatment are to be effective.
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PMID:Bacteraemia in patients with fulminant hepatic failure. 717 37

In clinical studies, frequent hepatic dysfunction associated with crises in sickle cell disease has been noted, but whether irreversible morphologic changes arise from these transient episodes is uncertain. We studied 70 patients with sickle cell disease (57 SS, 12 SC and one S-thalassemia (S-thal) hemoglobin) autopsied at The Johns Hopkins Hospital. They ranged in age from five months to 75 years (average 21 years) and 35 (50 percent) were female, In 64 patients (91 percent), livers were enlarged and had distention of Kupffer cells with phagocytized sickled red cells; this was massive in 10. In 19 patients (27 percent) the sinusoids were markedly distended with sickled red cells and appeared obstructed. Focal parenchymal necroses were present in 24 patients (34 percent) and were explained in 12, eight by cardiac dysfunction and four by sepsis. Reparative changes, portal fibrosis and regenerative nodules were each found in 14 patients (20 percent), only one of whom had a known history of viral hepatitis despite the frequency of transfusions. Cirrhosis of unknown cause was present in seven patients and cardiac cirrhosis in one. Cirrhosis with hemochromatosis was present in three patients and 30 others had parenchymal iron accumulation. Thus, unexplained hepatic necroses, portal fibrosis, regenerative nodules and cirrhosis were frequently encountered in these patients. This spectrum of liver disease appears to be best understood as a consequence of recurrent vascular obstruction, necrosis and repair arising as a component of sickle cell disease.
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PMID:The liver in sickle cell disease. A clinicopathologic study of 70 patients. 744 49

Hepatic dysfunction following bone marrow transplantation (BMT) may present complex management issues. The incidence and aetiology of abnormal liver function following allogeneic and autologous BMT was reviewed over a 2 year period in Royal Perth Hospital and these findings were related to management decisions and patient outcome. Abnormal serum liver biochemistry during the first 12 post-transplant months occurred in all allogeneic (n = 31) and 14 of 23 (61%) autologous transplant patients; 13 (41%) allogeneic and three (13%) autologous patients developed severe hepatic dysfunction. In allogeneic transplants, the most common causes of liver disease were graft-versus-host disease (33%), drug hepatotoxicity (19%) and posttransplant viral hepatitis (15%); in autologous patients, disease recurrence (28%) and sepsis (17%) were the most frequent identifiable cause of abnormal liver function. The aetiology of abnormal liver biochemistry was not determined in 13 instances, but this did not adversely affect patient outcome. Percutaneous liver biopsy or endoscopic cholangiography were only required in three patients. Liver disease contributed to death in two allogeneic patients with multiple causes for liver dysfunction, and in one patient with refractory severe hepatic graft-versus-host disease. It was concluded that hepatic dysfunction is common after BMT, the cause of which can be determined in many cases with simple non-invasive tests used in conjunction with the clinical setting. Specific treatment, where necessary, is then able to be commenced in a majority of patients without the need for invasive investigation.
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PMID:Liver disease complicating bone marrow transplantation: a clinical audit. 762 96

While orthotopic liver transplantation (OLT) has become the treatment of choice for most irreversible end-stage liver diseases, its role in patients with hepatitis B (HBV) infection is controversial. A high risk of reinfection of the transplanted graft, associated with significant morbidity and mortality, has been reported. Although passive and active immunization can delay reappearance of the virus in the allograft, there is not yet an effective therapy for recurrent HBV infection in liver transplant recipients. Between October 1985 and March 25, 1991, 28 OLT in 25 patients with acute and chronic HBV infections were performed. Twelve of the patients were HBV DNA-negative, six were HBV DNA-positive, and seven were not tested prior to transplantation. Only the 19 patients surviving more than 100 days after transplantation were considered to have sufficient duration of follow-up (mean 734 days; range 500-1545) to include in analysis of recurrence. Five (26%) were free of recurrent disease at the time of last follow-up (mean 1031 days, range 526 to 1770 days. Recurrent HBV in the allograft, as defined by positive immunoperoxidase stains of biopsy sections for viral antigens, was detected in 74% (13 male, 1 female; 7 Asian, 7 white) at a mean of 134 days posttransplantation. Histological changes of viral hepatitis, first appearing an average of 157 days (range 95-326) posttransplantation, were evident in 13 of 14 with positive immunostaining. Twelve of the 14 patients were treated, on an open trial basis, with intravenous and oral prostaglandin E (PGE) because of deteriorating clinical condition. Eleven of the twelve responded to PGE with an initial drop in serum transaminases, improvement in coagulopathy and resolution of encephalopathy. One patient failed to respond and died of a myocardial infarction within 9 days of institution of therapy. Three of the eleven patients with an initial response relapsed and died in liver failure as a direct result of recurrent HBV after 13, 16, and 37 days of treatment in association with generalized sepsis. Eight of the 12 patients (67%) had a sustained favorable response to PGE therapy (mean follow-up 737 days, range 403-1545). All patients with a sustained response had accompanying improvement in histology and reduction in viral antigen staining in hepatocytes. Treatment with PGE appeared to be of benefit in recurrent HBV infection of the transplanted liver with an initial response rate of 92% and a sustained response rate of 67%.
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PMID:Prostaglandin E in the treatment of recurrent hepatitis B infection after orthotopic liver transplantation. 804 36

Carbamazepine is a drug commonly used in the treatment of neuropathic pain. It is an iminostilbene derivative that is extensively metabolized by the liver. We describe a 66-year-old man with dysesthetic pain from cervical myelopathy who developed cholestatic hepatitis, skin rash, and eosinophilia after carbamazepine was administered for 5 weeks (total dose of 18.9gm). Withdrawal of carbamazepine led to complete resolution of both clinical and biochemical abnormalities within 3 weeks. Clinicians should be alert to this rare complication because it can be confused clinically with biliary tract sepsis and viral hepatitis.
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PMID:Carbamazepine-induced hepatitis in a patient with cervical myelopathy. 860 Aug 77

Of all foodborne infectious diseases, infection with Vibrio vulnificus is one of the most severe; the case-fatality rate for V. vulnificus septicemia exceeds 50%. In immunocompromised hosts V. vulnificus infection can cause fever, nausea, myalgia, and abdominal cramps 24-48 hours after eating contaminated food; because the organism can cross the intestinal mucosa rapidly, sepsis and cutaneous bullae can occur within 36 hours of the initial onset of symptoms. Cases are most commonly reported during warm-weather months (April-November) and often are associated with eating raw oysters. During April 1993-May 1996, a total of 16 cases of V. vulnificus infection were reported in Los Angeles county. Fifteen (94%) of these patients were primarily Spanish-speaking, 12 (75%) had preexisting liver disease (associated with alcohol use or viral hepatitis), all were septicemic, and all had eaten raw oysters 1-2 days before onset of symptoms. In May 1996, three deaths related to V. vulnificus infection among primarily Spanish-speaking persons were reported to the Los Angeles County Department of Health Services (LACDHS). This report summarizes the findings of the investigations of these fatal cases and illustrates the importance of prevention strategies for persons with preexisting liver disease.
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PMID:Vibrio vulnificus infections associated with eating raw oysters--Los Angeles, 1996. 896 88

To assess the impact of chronic viral hepatitis on host immune response, we analyzed the incidence of acute rejection and the frequency of infections in 86 patients infected with hepatitis B and C viruses and had developed clinical evidence of chronic liver disease and 1283 control patients who were transplanted at our center during the same period, but had no evidence of chronic viral hepatitis. To compare the mean number of rejections and the mean number of infections between the two groups, we used multivariate linear regression analysis, which allowed us to adjust simultaneously for the effects of 10 other risk variables with potential impact on graft rejection and posttransplant infection. During a mean follow up of 5.3+/-5.2 years, 62% of hepatitis patients and 54% of control patients had experienced an acute rejection (P=NS). The mean rejections/patient in the hepatitis group was 1.3+/-0.14 versus 1.03+/-0.03 in control (P=NS). In the linear regression analysis, the number of acute rejections in the hepatitis group was 0.16 higher than in control (P=NS). With reference to infection, 84% of hepatitis patients experienced an infectious complication in the posttransplant period, compared with 75% in the control (P=0.05). The mean number of infections/patient was 5.7+/-0.73 in the hepatitis group compared with 3.9+/-0.14 in the control group (P=0.002). The linear regression model had shown that the hepatitis group had a relative increase of 1.18 infections/pt, compared with control. Of the different sites of infection, the hepatitis group had a significant increase in bloodstream (0.48+/-0.08 vs. 0.25+/-0.02) P=0.003; pulmonary (0.60+/-0.09 vs. 0.38+/-0.03) P=0.03; and CNS infections (0.08+/-0.03 vs. 0.02+/-0.004) P=0.05 compared with control. Among the different microorganisms causing infection, the hepatitis patients had a significant increase in gram negative bacterial infections compared with the control group (74% vs. 61%) P=0.04. Our data suggest that chronic viral hepatitis is associated with a significant increase in overall infections, and that of potentially fatal infections involving CNS, lungs and bloodstream. Since there is no significant increase in the rate of graft rejection, one could consider a cautious reduction in the doses of maintenance immunosuppressive agents in renal transplant patients with chronic viral hepatitis. The reduced immunosuppression may in turn lower the death rate from sepsis and progressive hepatic failure.
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PMID:Chronic viral hepatitis enhances the risk of infection but not acute rejection in renal transplant recipients. 899 Mar 59

The liver is implicated in many processes, and its failure induces severe consequences for metabolism, immune response, detoxification and antimicrobial defenses. The mechanisms involved in liver injury are complex and interactive, and can be artificially separated as chemical and immune injuries. The biochemical mechanisms concern various chemicals that are detoxified in the liver via cytochrome P-450 and conjugation. Toxic metabolites may alter plasma membrane, mitochondria, intracellular ion homeostasis, or degratative enzyme activity. Immune mechanisms involve cell cooperation, and are mediated by cytokines, nitric oxide, and complement. Pathologic apoptosis is potentially an important mechanism of acute liver injury. Specific attention is paid here to the more frequent causes of acute liver failure: hypoxia/reoxygenation, liver congestion, acetaminophen poisoning, posttransplant acute liver rejection, severe sepsis, viral hepatitis, and alcoholic liver disease. Knowledge of the intimate mechanisms of liver injury at the cellular level may lead to adaptation of therapeutic strategies that will prevent end-stage liver failure.
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PMID:Mechanisms of liver damage. 902 49


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