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)

Syncytial giant cell hepatitis in the neonatal period has been associated with many different etiologic agents and may present initially as cholestasis. Infectious causes are most common and include: (1 ) generalized bacterial sepsis, (2) viral agents, (3) toxoplasmosis, (4) syphilis, (5) listeriosis, and (6) tuberculosis. Viral hepatitis may be due to cytomegalovirus, rubella virus, herpes simplex, HHV-6, varicella, coxsackievirus, echovirus, reovirus 3, parvovirus B19, HIV, enteroviruses, paramyxovirus, and hepatitis A, B, or C (rare). Giant cell hepatitis may result in fulminant liver failure with massive hepatocyte necrosis and severe liver dysfunction leading to death, resolution with severely compromised liver function, or liver transplantation. The authors report a 6-week-old male who had an unremarkable perinatal period, became jaundiced after developing diarrhea, and subsequently developed liver dysfunction with massively increased liver enzymes and a coagulopathy. Open wedge and core liver biopsies were performed to determine if the patient should be listed for liver transplantation. Giant cell hepatitis with a significant mixed lymphocytic and neutrophilic infiltrate was present on both the wedge and core biopsies. The residual 60% of hepatocytes had ballooning degeneration and many possessed pyknotic nuclei. The hepatocytes were arranged in a pseudoacinar pattern. Electron microscopy showed paramyxoviral-like inclusions in the giant cells, characterized as large inclusions with fine filamentous, beaded substructures (18-20 nm). Paramyxoviridae are nonsegmented, negative-sense, single-stranded RNA viruses. This family is divided into the Paramyxovirinae subfamily containing respirovirus (Sendai virus, parainfluenza virus type 3), rubulavirus (mumps, parainfluenza virus type 2), and morbillivirus genera (measles); and Pneumovirinae subfamily (pneumovirus genus [respiratory syncytial virus]). Supportive care to determine if hepatic function resolves following the viral episode, liver transplantation with fulminant liver failure, and ongoing evaluation in those who recover to assess chronic liver disease are necessary. Ultrastructural evaluation may unmask the etiologic agent for hepatitis and direct therapy.
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PMID:Neonatal syncytial giant cell hepatitis with paramyxoviral-like inclusions. 1129 22

The Liver Dialysis Unit (the Unit) is a liver-assist device that employs hemodiabsorption (dialysis of blood against powdered sorbents) to selectively remove numerous small molecular weight toxins of hepatic failure. The Unit has been cleared by the Food and Drug Administration and is indicated and marketed for treatment of acute hepatic encephalopathy (AHE) due to decompensation of chronic liver disease (A-on-C) or fulminant hepatic failure (FHF). Controlled, prospective, and randomized studies of liver dialysis were conducted at several centers, enrolling 56 patients with AHE, grades II-IV with or without renal and respiratory insufficiency or failure. Liver dialysis treatments were for 6 h daily, 1-5 days with similar observation periods for control patients. Physiologic status, neurologic status, and outcome (recovery of hepatic function, improvement for transplant, or death) were measured, and results were compared for treated patients versus controls for patients with A-on-C and patients with FHF. Liver dialysis resulted in physiologic and neurologic improvement of patients with AHE, regardless of etiology. Liver dialysis significantly improved the incidence of positive outcomes (recovery of hepatic function or improvement for transplant) of A-on-C patients versus controls (71.5% treated, 35.7% control, p = 0.036), but had an insignificant improvement in the outcome of patients with FHF as compared with the control group. Among the overall 31 treated patients, 51.6% survived. Outcome was not negatively affected by the presence of kidney failure or respiratory failure. The plasmafilter unit (PF-Unit) combines hemodiabsorption with push-pull sorbent-based pheresis (the PF add-on module, with powdered sorbent surrounding plasmafilters). At blood flow rates of 200 ml/min, the system clears creatinine and aromatic amino acids at 120-160 ml/min, unconjugated bilirubin at 20-40 ml/min, and cytokines at 15-25 ml/min. The PF-Unit has been tested in a few patients with hepatic failure with Grades III and IV encephalopathy, and respiratory, and kidney insufficiency. Treatment appeared to be safe, and there were no significant hematologic changes. Physiologic changes included improved blood pressure, and encephalopathy, and stable urine output. Chemical changes included a decrease in the plasma levels of bilirubin, aromatic amino acids, ammonium, creatinine, and IL-1beta. The PF add-on module adds the capability to the Unit to remove bilirubin and other strongly protein-bound toxins from treated patients and may be of clinical benefit in the management of patients with the most severe hepatic failure and encephalopathy, including patients with FHF or concomitant sepsis.
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PMID:Powdered sorbent liver dialysis and pheresis in treatment of hepatic failure. 1177 27

The vast majority of patients that are referred to a specialist hepatological centre suffer from acute deterioration of their chronic liver disease. Yet, this entity of acute-on-chronic liver failure remains poorly defined. With the emergence of newer liver support strategies, it has become necessary to define this entity, its pathophysiology and the short- and long-term prognosis. This review focusses upon how a precipitant such as an episode of gastrointestinal bleeding or sepsis may start a cascade of events that culminate in end-organ dysfunction and liver failure. We briefly review the pathophysiological basis of the therapeutic modalities that are available. Our current strategy for the management of liver failure involves supportive therapy for the end-organs with the hope that liver function would recover if sufficient time for such a recovery is allowed. Because liver failure, whether of the acute or acute-on-chronic variety, is potentially reversible, the stage is set for the application of newer liver-support strategies to enhance the recovery process.
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PMID:Acute-on-chronic liver failure: pathophysiological basis of therapeutic options. 1186 72

Extracorporeal blood detoxification by sorbent therapy long has been applied in treatment of hepatic failure and encephalopathy, starting with hemoperfusion columns and more recently with the currently marketed Liver Dialysis Unit. Liver Dialysis employs hemodiabsorption (dialysis of blood against powdered sorbents including charcoal and cation exchanger) to remove selectively numerous small-molecular-weight toxins of hepatic failure. Liver Dialysis is used in treatment of acute hepatic encephalopathy (AHE) because of decompensation of chronic liver disease (A-on-C) or fulminant hepatic failure (FHF). Controlled, prospective and randomized studies of daily 6-hour Liver Dialysis have shown physiologic and neurologic improvement of patients with AHE, regardless of etiology. Liver dialysis significantly improved the incidence of positive outcomes (recovery of hepatic function or improvement for transplant) of A-on-C patients versus controls (71.5% treated, and 35.7% control, P =.036), but had an insignificant improvement in outcome of patients with FHF as compared with the control group. Other extracorporeal sorbent devices are now in clinical testing phase. The molecular adsorbent regenerating system (MARS) device employs a polysulfone high-permeability dialyzer with albumin on the dialysate side to aid transfer of protein-bound toxins such as bilirubin and bile acids across the membranes. Sorbent columns of charcoal and an anion exchanger remove hepatic toxins from the albumin dialysate, and a second dialyzer removes water-soluble toxins, such as ammonium. Clinical results of daily MARS treatments of patients with hepatic failure are similar to that of Liver Dialysis, with neurologic and physical improvement occurs in most patients with AHE, and improved outcome for patients with A-on-C. The system extends the life of patients with hepatorenal syndrome. PF-Liver Dialysis is an experimental device combining hemodiabsorption with push-pull sorbent-based pheresis with powdered sorbent surrounding plasmafilters. PF-Liver Dialysis (Hemocleanse, Inc, W. Lafayette, IN) has been tested in a few patients with hepatic failure, grade 3-4 encephalopathy, and respiratory and kidney insufficiency. Treatments appeared to be safe and resulted in marked decreases in plasma levels of bilirubin, aromatic amino acids, ammonium, creatinine, and interleukin-1beta (IL-1beta). The PF add-on module adds the capability to Liver Dialysis to remove bilirubin, bile acids, and other strongly protein-bound toxins from treated patients and may be of clinical benefit in management of patients with the most severe hepatic failure and encephalopathy, including patients with FHF or concomitant sepsis.
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PMID:Extracorporeal blood detoxification by sorbents in treatment of hepatic encephalopathy. 1192 2

The vast majority of patients that are referred to a specialist hepatological centre suffer from acute deterioration of their chronic liver disease. Yet, this entity of acute-on-chronic liver failure remains poorly defined. With the emergence of newer liver support strategies, it has become necessary to define this entity, its pathophysiology and the short and long-term prognosis. This review focuses upon how a precipitant such as an episode of gastrointestinal bleeding or sepsis may start a cascade of events that culminate in end-organ dysfunction and liver failure. We briefly review the pathophysiological basis of the therapeutic modalities that are available. Our current strategy for the management of liver failure involves supportive therapy for the end-organs with the hope that the liver function would recover if sufficient time for such a recovery is allowed. Because liver failure, whether of the acute or acute-on-chronic variety, is potentially reversible, the stage is set for the application of newer liver support strategies to enhance the recovery process.
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PMID:The pathophysiological basis of acute-on-chronic liver failure. 1222 Feb 96

To understand recent temporal trends in acquired immunodeficiency syndrome (AIDS) mortality in the era of highly active antiretroviral therapy (HAART), trends in causes of death among persons with AIDS in San Francisco who died between 1994 and 1998 were analyzed. Among 5234 deaths, the mortality rate for human immunodeficiency virus (HIV)-related or AIDS-related deaths declined after 1995 (P<.01), whereas the mortality rate for non-HIV- or non-AIDS-related deaths remained stable. The proportion of deaths of persons with AIDS associated with septicemia, non-AIDS-defining malignancy, chronic liver disease, viral hepatitis, overdose, obstructive lung disease, coronary artery disease, and pancreatitis increased (P<.05). The standardized mortality ratio was high for these causes in both pre- and post-HAART periods, except for pancreatitis, a possible complication of HAART, which demonstrated an increasing standardized mortality ratio trend after 1996. With increasing AIDS survival, prevention of chronic diseases, assessment of long-term toxicity from HAART, and surveillance for additional causes of mortality will become increasingly important.
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PMID:Trends in causes of death among persons with acquired immunodeficiency syndrome in the era of highly active antiretroviral therapy, San Francisco, 1994-1998. 1223 45

We describe the remarkable case of a patient with septicemia caused by Non 0-1 Vibrio Cholerae associated with skin lesion of the lower and upper extremities. This patient suffered from chronic liver disease and a cervix carcinoma in IIIB stage, she had been admitted to the hospital the day before for dicompensated ascites. She received intravenous cefotaxime and had a satisfactory recovery and was completely free of signs and symptoms. We report its epidemiological discovery in inland freshwater and this is the first announced case in Spain with this confirmed environmental isolation and a rare report case in the literature.
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PMID:[Septicemia caused by Vibrio cholerae non-01 in immunocompromised patient]. 1469 85

Abnormal LCTs after surgery are common, and consultants are frequently called on to evaluate critically ill patients with abnormal tests. All patients undergoing consideration for elective surgery and a history of either acute or chronic liver disease require careful presurgical evaluation. A thorough history and physical examination, complete blood count, routine electrolytes, LCTs, and a coagulation profile should be ordered. For patients with marginal hepatic reserve, it is important that patient well-being be maximized before any elective operation. The type of surgery to be performed should also be reviewed. All patients with postoperative jaundice should be evaluated for a history of liver disease. The consultant should also review the surgical procedure performed, anesthetic agents administered, other medications used, and whether blood products were given during the perioperative and postoperative periods. The pattern and timing of LCT abnormalities may also give a clue to the underlying disorder. As in the preoperative assessment, a routine complete blood count,electrolyte panel, LCTs, and coagulation profile should be ordered. Unconjugated hyperbilirubinemia can develop as a consequence of blood transfusions, underlying hemolytic disorders, resorbing hematomas, drug effects, or Gilbert's syndrome. A haptoglobin, reticulocyte count, LDH, and Coomb's test should be considered in patients with unconjugated hyperbilirubinemia. Treatment is directed toward the underlying condition. Conjugated hyperbilirubinemia can occur as a result of either intrahepatic or extrahepatic disorders. Markedly abnormal aminotransferases and LDH in conjunction with a normal abdominal ultrasound scan suggest ischemic liver injury, drug-induced hepatitis, or viral infections of the liver. Treatment entails restoration of hepatic perfusion, removal of offending medications, and supportive care or antiviral agents, respectively. Extrahepatic biliary obstruction must be considered in all patients with conjugated hyperbilirubinemia. Abdominal sonography is the best screening test to assess for obstruction. Patients with common bile duct stones usually require ERCP with sphincterotomy and stone removal. Biliary strictures or leaks may require ERCP with balloon dilation of strictures or stent placement for strictures and leaks; percutaneous drainage of bilomas in combination with broad-spectrum antibiotic agents is recommended for patients with bile leaks and large intra-abdominal fluid collections. Surgery may be required for patients with strictures or leaks not amenable to either endoscopic or percutaneous intervention or for patients who have transected bile ducts after laparoscopic cholecystectomy. Medication effects, benign postoperative jaundice, sepsis, TPN, and acalculous cholecystitis are responsible for intrahepatic cholestasis and conjugated hyperbilirubinemia. Treatment includes removal of offending drugs, supportive care, broad-spectrum antibiotic agents with drainage of infected fluid collections, adjustment of TPN, and either cholecystectomy or cholecystostomy, respectively.
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PMID:Postoperative jaundice. 1506 98

Streptococcus bovis is one of the nonenterococcal species included among the streptococci group D. It is part of the normal bowel flora in humans and animals, but it is also responsible for infectious diseases (10-15% of all cases of bacterial endocarditis). Many cases of bacteremia and metastatic abscesses (spleen, liver, soft tissues, bone, meninges, endocardium) caused by S. bovis were reported as associated with digestive tract diseases, mainly colonic disease, and, in particular colonic neoplasms, or chronic liver diseases. A role in carcinogenesis has been suggested for this microorganism. The authors report two cases of S. bovis sepsis, one associated with colonic neoplasm and the other with liver cirrhosis and gastric carcinoma. Discussion is focused on probable mechanisms that favor gastric colonization and systemic diffusion of S. bovis from the gut in patients with gastrointestinal neoplasms or chronic liver disease and provides clinical recommendations for patients with S. bovis infections.
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PMID:Non-life-threatening sepsis: report of two cases. 1516 50

Transjugular intrahepatic portosystemic shunt (TIPS) has been the therapeutic option for severe decompensation of chronic liver disease and as a bridge to liver transplantation. The aim of this study was to analyze the complications of this procedure. The records of 47 patients (39 men) of mean age 48 years underwent TIPS procedures from 1998 to 2003 were reviewed. Forty-one patients received 45 successful TIPS; it failed in six patients. Improvement was observed in 20 of 28 patients with upper gastrointestinal bleeding (71%); 9 of 11 with ascites (82%); and 5 of 8 with impaired renal function (62%). The Child-Pugh scores improved in 6 of the 47 patients (13%). Transplantation was performed in 11 patients (23%). The complications were: encephalopathy (49%); infection (19%); renal failure (17%); TIPS migration to the portal vein (4%) and to the right atrium (4%). Mortality was 32% (15/47) over 3 months. Eight patients developed active bleeding during TIPS installation requiring mechanical ventilation and intensive care, and died within the first week. Other causes of death were sepsis (n = 2), liver failure (n = 1), accidental puncture of the Glisson's capsule leading to intra-abdominal bleeding (n = 1) and refractory upper gastrointestinal bleeding (n = 3). The latter four patients had TIPS placement failure. In conclusion, TIPS produced clinical improvement among 51% of patients with complications in 49%. The main complications were encephalopathy (49%), infection (19%), and renal failure (17%). The 3-month mortality rate after TIPS placement was 32%.
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PMID:Complications following transjugular intrahepatic portosystemic shunt: a retrospective analysis. 1519 19


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