Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and twenty patients with a mean age of 38 years (range 12-85 years; M 91, F 37) were studied over a period of 5 years in a teaching hospital in Dhaka. Sixty-two patients presented with probable anuria with 1-4 days' duration, 63 patients presented with oliguria, and 3 were nonoliguric. The causes of acute renal failure were medical (94), surgical (22), obstetrical (13). Of the medical cases, the causes were gastroenteritis in 42 cases, gastroenteritis with CNS involvement in 11 cases, rapidly progressive glomerulonephritis in 10 cases, acute viral hepatitis in 8 cases, and septicemia in 8 cases. Of 22 surgical cases, postoperative acute renal failure was the cause in 9, road traffic accident in 6, and renal calculus disease in 7. There were 13 cases in the obstetrics group, of whom 9 were due to abortion, 2 were due to preeclampsia, and the other 2 were postoperative. The mean blood urea of all cases was 35 mmol/L and serum creatinine was 988 mumol/L. Dialysis was required in 105 cases; of these, 72 were medical cases, 21 were surgical cases, and 12 were obstetric cases. The overall survival rate was 75%. The improved survival is probably due to timely referral and prompt medical management.
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PMID:Outcome of acute renal failure in adults in a teaching hospital in Bangladesh. 829 Jul 6

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

Adhesion molecules are cell surface glycoproteins that are critical for the localization of leukocytes at sites of inflammation. This review discusses the current knowledges of adhesion molecule expression in normal liver and its upregulation on individual liver cell types during liver inflammation. Cytokines, chemokines, complement factors, and lipid-derived mediators are critical for increased gene transcription and activation of constitutively expressed adhesion molecules. The specific role of selectins, integrins, and members of the immunoglobulin gene superfamily in sinusoidal and venular leukocyte sequestration, transendothelial migration, and adherence to target cells in the liver is described. Increased understanding of these basic mechanisms of communication between resident liver cells and infiltrating leukocytes (neutrophils, lymphocytes, macrophages) not only advances our insight into the pathophysiology of hepatic inflammation but also identifies promising new targets for therapeutic interventions and expands the spectrum of diagnosis and treatment of liver diseases, including alcoholic hepatitis and cirrhosis, viral hepatitis, ischemia-reperfusion injury (transplantation, tumor resection, shock), sepsis- or endotoxin-induced liver injury, acute and chronic rejection, primary biliary cirrhosis, and primary sclerosing cholangitis.
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PMID:Cellular adhesion molecules: regulation and functional significance in the pathogenesis of liver diseases. 934 Oct 49

The presence of jaundice in the neonate, infant or young child presents a broad differential diagnosis. The 'disease' may be benign, as in breast-milk jaundice, or potentially fatal, as in hereditary fructose intolerance. The cause of the jaundice may be a primary hepatic disorder, such as extrahepatic biliary atresia, or secondary to a non-hepatic cause, such as haemolysis or sepsis. There may be significant hepatic injury and dysfunction, as in fulminant viral hepatitis, or simply elevation of plasma bilirubin, as in Gilbert's syndrome. In this chapter we will discuss the familial hyperbilirubinaemia syndromes. This diverse group of disorders is characterized by hepatic dysfunction in the absence of hepatocellular injury. The first section of the chapter will discuss the unconjugated hyperbilirubinaemias: Crigler-Najjar syndrome I, Crigler-Najjar syndrome II and Gilbert's syndrome. The discovery of the gene for bilirubin uridine diphosphate glucuronosyltransferase has increased our understanding of the genetic heterogeneity and clinical presentation of the Crigler-Najjar syndromes. The remainder of the chapter will discuss the conjugated hyper-bilirubinemias: Rotor syndrome and Dubin-Johnson syndrome. These rare diseases share many clinical features; however, they can be readily distinguished by biochemical markers in the urine and bile.
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PMID:The hereditary hyperbilirubinaemias. 989 77

Tacrolimus is an effective immunosuppressant in the rescue of liver allograft patients in whom conventional immunosuppression failed. Efficacy and safety were examined in a multicenter trial of liver transplant recipients converted to tacrolimus because of rejection despite cyclosporine (CyA) therapy or intolerance to CyA. Six hundred seventy-seven patients were enrolled onto the study; 475 patients for rejection, 197 patients for intolerance, and 5 patients treated compassionately. The mean daily dose of tacrolimus was less in the intolerance (Int) patients throughout the study: 0.22 versus 0.17 mg/kg at 1 week and 0.14 versus 0.11 mg/kg at 24 months in rejection (Rej) and Int patients, respectively. Mean blood levels paralleled dosing in both groups, but were greater in the Rej patients (10.7 v 8.3 ng/mL at 18 months). Kaplan-Meier estimates of patient and graft survival were similar in the two groups. Patient survival rates were 80.1% and 81.5%, and graft survival rates were 72.7% and 73.9% at 24 months in the Rej and Int patients, respectively. Most adverse events occurred with a similar incidence in the two groups. Those with a 4% or greater incidence were fever, viral hepatitis, and pneumonia. The incidence of sepsis, gastrointestinal hemorrhage, kidney failure, and convulsion was greater in the Int group. The incidence of abnormal liver function test results, hyperglycemia, headache, and abnormal kidney function was greater in the Rej group. Mean liver function test results decreased with time postrescue in both groups. Mean serum creatinine level increased from baseline to 18 months postrescue in both groups (1.44 to 1.51 mg/dL for Int patients, 1.14 to 1.48 mg/dL for Rej patients). We conclude tacrolimus is safe and effective rescue in liver transplant recipients with rejection or CyA intolerance.
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PMID:Tacrolimus rescue in liver transplant patients with refractory rejection or intolerance or malabsorption of cyclosporine. The US Multicenter FK506 Liver Study Group. 1054 38

Acute hepatic failure (AHF) in India almost always presents with encephalopathy within 4 weeks of the onset of acute hepatitis. Further subclassification of AHF into hyperacute, acute and subacute forms may not be necessary in this geographical area, where the rapidity of onset of encephalopathy does not seem to influence survival. Viral hepatitis is the cause in approximately 95-100% of patients, who therefore constitute a more homogeneous population than AHF patients in the West. In India, hepatitis E (HEV) and hepatitis B (HBV) viruses are the most important causes of AHF; approximately 60% of cases are caused by to these viruses. Hepatitis B virus core mutants are very important agents in cases where hepatitis B results in AHF in this country. Half of the patients with AHF admitted to our centre are female, one-quarter of whom are pregnant. Therefore, pregnant females who contract viral hepatitis constitute a high-risk group for the development of AHF. However, the outcome of AHF in this group is similar to that in non-pregnant women and men. No association with any particular virus has been identified among sporadic cases of AHF. In our centre, approximately one-third of AHF patients survive with aggressive conservative therapy, whereas two-thirds of deaths occur within 72 h of hospitalization. Cerebral oedema and sepsis are the major fatal complications. Both fungal and gram-negative bacteria are major causes of sepsis. Among patients with AHF, despite the presence of sepsis, its overt clinical features (i.e. fever, leucocytosis) may be absent and objective documentation of the presence of sepsis in such patients is achieved by repeated culture of various body fluids. It should be possible to develop simple, clinical prognostic markers for AHF in this geographical region, in order to identify patients suitable for liver transplantation.
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PMID:Acute hepatic failure in India: a perspective from the East. 1084 29

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.
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PMID:Acute liver failure. 1113 56


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