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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four children with portal hypertension and ascites developed hematemesis, abdominal pain, and fever as the acute manifestations of bacterial peritonitis. Initial management in the emergency department was directed toward controlling the upper gastrointestinal hemorrhage, and antibiotic therapy was delayed in four of six episodes until ascitic fluid cultures grew Streptococcus pneumoniae. Gastrointestinal bleeding has not been previously reported as a presenting symptom of peritoneal infection. Our clinical experience emphasizes the need for antibiotic therapy during the initial management of children with ascites and hematemesis.
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PMID:Bacterial peritonitis and sepsis presenting as acute gastrointestinal bleeding in patients with portal hypertension. 848 39

Ascites is a common complication of chronic liver disease. Treatment of the underlying liver disease with modalities such as abstinence from alcohol in Laennec's cirrhosis, phlebotomy in hemochromatosis, copper removal in Wilson's disease, and steroids in autoimmune liver disease, can improve survival in many patients. In addition, therapy of ascites alleviates the symptoms and improves the quality of life of the patients, and probably decreases the incidence of life-threatening conditions including spontaneous bacterial peritonitis and hepatorenal syndrome. The mean survival rate at 2 years is approximately 50%. Precipitating factors such as gastrointestinal bleeding, nonsteroidal anti-inflammatory drugs and infections, should be identified, since most of them can be corrected. Most cirrhotics with ascites can be managed with a 'step-by-step' approach, including dietary salt restrictions, aldosterone antagonists, and loop diuretics. When tense or refractory ascites is present, large-volume paracentesis is safe and effective. Peritoneovenous shunting (i.e. Denver, LeVeen) is less frequently used because of perioperative morbidity and mortality, and thrombotic complications with occlusion of the stent. Reinfusion of concentrated ascites is of potential benefit and has been used in Europe. Transjugular intrahepatic portosystemic shunt (TIPS) is an alternative procedure performed by interventional radiologists that allows decompression of portal hypertension. In many cases, ascites is improved after TIPS, but long-term randomized trials for tense or refractory ascites comparing TIPS with standard therapy are not conclusive. Liver transplantation is the ultimate step for the treatment of ascites, providing the cure for the underlying liver disease as well. Transplantation is indicated when quality of life of the patient is impaired due to recurrent episodes of ascites, or in the presence of spontaneous bacterial peritonitis and hepatorenal syndrome.
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PMID:Treatment of ascites: old and new remedies. 886 22

The serum-ascites albumin (SAA) gradient has been defined as the serum albumin concentration minus the ascitic fluid albumin concentration. The SAA gradient is superior to the exudate-transudate concept to classify ascites, being a exact portal hypertension (PH) marker. An elevated SAA gradient (1.1 g/L or greater) correlates with PH, whereas a low gradient indicates no PH. The SAA gradient correlates well with PH in cirrhotic patients. It is also of particular utility to differentiate between congestive heart failure and malignant ascites without liver metastases (both of them with elevated ascites fluid proteins -AFP-). However, a low SAA gradient do not differentiate between tuberculous and malignant ascites. Consequently, there are still need for tests a cytology, culture for mycobacteria or ascites fluid polymorphonuclear cell count in some cases. The level of AFP, apart from the exudate-transudate concept, has some value for certain cases (a low level of AFP implicates a high risk of spontaneous bacterial peritonitis). The SAA gradient should replace the AFP concentration as the initial test to classify ascites.
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PMID:[Sero-ascitic gradient of albumin: usefulness and diagnostic limitations]. 892 34

Ascites formation in cirrhosis results from the interaction of "local" and "systemic" pathogenetic factors. Among local factors, post-sinusoidal portal hypertension plays the most important role, while the main systemic event is renal sodium retention. The latter precedes ascites formation and leads to plasma volume expansion. Many factors are responsible for renal sodium retention, but secondary hyperaldosteronism and reduced renal perfusion prevail. The events promoting the onset of sodium retention are far from being clarified. However, there is evidence that the main afferent mechanism is represented by the "effective" hypovolemia secondary to splanchnic venous vasodilation, due to portal hypertension, and reduced peripheral vascular resistance, which becomes evident in the advanced stage of the disease. Systemic hemodynamic abnormalities are responsible for the progressive reduction of renal perfusion, which ends in the hepatorenal syndrome. The appearance of ascites is a crucial event in the natural history of cirrhosis and has a negative prognostic meaning. In fact, ascites appears when pathogenetic factors, such as liver function abnormalities, portal and systemic hemodynamics, and renal function, have reached a critical threshold severity. Second, ascites itself induces additional complications, closely linked to its presence, such as spontaneous bacterial peritonitis, restrictive respiratory failure, or rupture of abdominal hernias. Finally, ascites implies pharmacological or invasive treatment which can lead to further morbidity or even to death.
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PMID:[Natural course and physiopathology of ascites in the cirrhotic patient]. 900 18

Ultrasonography detects ascites easily even in trace amounts. 80% of the cases are caused by hepatic disease, in the remaining 20% cancer, inflammation, pancreatic, renal, or cardiac disease can be found. The underlying disease should be investigated by few inexpensive laboratory test from serum, urine and ascites and by abdominal sonography. Hepatic ascites is caused by portal hypertension and disturbances of humoral factors. Sodium retention, peripheral, vasodilation, hyperdynamic circulation and progressive renal vasoconstriction lead to a stepwise deterioration of patients condition. Treatment with diuretics (furosemide, torsemide, or xipamide and spironolactone) and sodium-restriction (< 60 mval per day) control 85-90% of the cases with hepatic ascites. If this regimen fails, non-compliance, spontaneous bacterial peritonitis, hyponatremia or additional complications such as renal failure, Budd-Chiari syndrome or tumor should be considered. Ten to 15% of the patients develop refractory ascites and finally hepatorenal syndrome and have a poor prognosis. Early liver transplantation should be considered. Large volume paracentesis with albumin substitution is a therapeutic option in these patients. The transjugular intrahepatic portosystemic stent-shunt (TIPS) may be superior for patients with concurrent esophageal varices or hepatorenal syndrome. If TIPS is considered the patient should be referred to an experienced center. The peritoneo-venous shunt is restricted to rare indications. In the future, new drugs such as antagonists of endothelins or of the antidiuretic hormone may offer new therapeutic options.
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PMID:[Current ascites therapy]. 906 26

The reintroduction of paracentesis has modified the way in which patients with ascites are treated. Transjugular intrahepatic portosystemic shunt can be an alternative treatment for patients with refractory ascites and for those patients with hepatorenal syndrome, although more studies are needed to clarify its usefulness and safety. The use of more potent and less nephrotoxic antibiotics together with an earlier diagnosis have improved the outcome of patients with spontaneous bacterial peritonitis (SBP). Oral antibiotics can be used in patients with SBP and good clinical conditions with an efficacy similar to that obtained with intravenous antibiotics. Prophylactic antibiotics in SBP should be restricted to cirrhotic patients at high risk, including bleeding cirrhotic patients, those with a past history of SBP, and those with low protein content in ascitic fluid. This chapter describes the management of ascites in patients with portal hypertension.
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PMID:Management of ascites in the patient with portal hypertension with emphasis on spontaneous bacterial peritonitis. 936 Feb 84

Cirrhotic patients (23 with alcoholic cirrhosis, 5 with posthepatitic cirrhosis and 2 with cryptogenic cirrhosis) with ascites and portal hypertension were studied and divided into two groups corresponding to high or low risk to develop spontaneous bacterial peritonitis (SBP) related to the concentration of total protein in the ascitic fluid (A-TP): group I (high risk): A-TP < or = 1.5 g/dl and group II (low risk): A-TP > 1.5 g/dl. Fibronectin (FN), C3 and C4 concentrations were measured by radial immunodiffusion while total protein was measured by the biuret method. The mean values (group I vs group II) of C3 (12.59 +/- 4.72 vs 24.53 +/- 15.58 mg/dl), C4 (4.26 +/- 3.87 vs 7.26 +/- 4.14 mg/dl) and FN (50.47 +/- 12.49 vs 75.89 +/- 24.70 mg/dl) in the ascitic fluid were significantly lower (P < 0.05) in the group considered to be at high risk for SBP. No significant difference was observed in the plasma/ascites fibronectin ratio (3.91 +/- 1.21 vs 3.80 +/- 1.26) or gradient (131.46 +/- 64.01 vs 196.96 +/- 57.38) between groups. Fibronectin in ascites was significantly correlated to C3 (r = 0.76), C4 (r = 0.58), total protein (r = 0.73) and plasma FN (r = 0.58) (P < 0.05). The data suggest that the FN concentration in ascites is related to the opsonic capacity of this fluid, and that its concentration in the ascitic fluid may be a biochemical risk factor indicator for the development of spontaneous bacterial peritonitis.
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PMID:Fibronectin in the ascitic fluid of cirrhotic patients: correlation with biochemical risk factors for the development of spontaneous bacterial peritonitis. 936 7

This report summarizes a recent meeting cosponsored by the American Society of Transplant Physicians and the American Association for the Study of Liver Diseases to formulate minimal criteria by which patients with severe liver disease will be placed on the waiting list for liver transplantation. The participants agreed that only patients in immediate need of liver transplantation should be placed on the waiting list. Patients should not be placed in anticipation of some future need for such therapy. It was agreed that minimal criteria could assist but not replace the clinical judgment of the transplant professionals at individual centers. The criteria will be summarized below for adult patients with acute or chronic liver disease. The most important non-disease-specific criterion for placement on the transplant waiting list was an estimated 90% chance of surviving 1 year. This translated into a Child-Pugh score of > or = 7 for patients with cirrhosis which places the patient in Child-Pugh class B or C. Cirrhotic patients who have experienced gastrointestinal bleeding caused by portal hypertension or a single episode of spontaneous bacterial peritonitis would meet the minimal criteria irrespective of their Child-Pugh score. There were disease-specific criteria also. These include a sole minimal criterion for patients with fulminant hepatic failure regardless of etiology of the onset of stage 2 hepatic encephalopathy. A requirement for 6 months abstinence from alcohol before placement on the transplant waiting list was considered appropriate for most patients with alcoholic liver disease. Exceptional cases could get access to the waiting list through a regional review process. Chronic cholestatic diseases present difficulties because of a different natural history than that of chronic hepatocellular diseases. The use of specific risk scores for primary biliary cirrhosis and primary sclerosing cholangitis will likely replace Childs-Pugh classification as the scoring systems become refined. Minimal criteria for any patient with a primary hepatocellular cancer would admit any patient with a tumor confined to the liver irrespective of size or number of tumors, after careful investigation had failed to show spread to lymph nodes, the portal vein, or distant organs. Unusual or rare indications for liver transplantation, including Budd-Chiari syndrome, Wilson's disease, and other hereditary disorders, were also discussed. Finally, it was agreed that there should be no absolute contraindications to placement of patients on the liver transplant waiting list. These criteria should be open to regular review to accommodate advances in the field.
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PMID:Minimal criteria for placement of adults on the liver transplant waiting list: a report of a national conference organized by the American Society of Transplant Physicians and the American Association for the Study of Liver Diseases. 940 77

The pathophysiology of circulatory and renal dysfunction in cirrhosis and the treatment of ascites and related conditions (hepatorenal syndrome and spontaneous bacterial peritonitis) have been research topics of major interest during the last two decades. However, many aspects of these problem remain unclear and will constitute major areas of investigation in the next millennium. The pathogenesis of sodium retention, the most prevalent renal function abnormality of cirrhosis, is only partially known. In approximately one third of patients with ascites, sodium retention occurs despite normal activity of the renin-aldosterone and sympathetic nervous systems and increased circulating plasma levels of natriuretic peptides and activity of the so-called natriuretic hormone. These patients present an impairment in circulatory function which, although less intense, is similar to that of patients with increased activity of the renin-aldosterone and sympathetic nervous systems, suggesting that antinatriuretic factors more sensitive to changes in circulatory function that these systems may be important in the pathogenesis of sodium retention in cirrhosis. The development of drugs that inhibit the tubular effect of antidiuretic hormone and increase renal water excretion without affecting urine solute excretion has opened a field of great interest for the management of water retention and dilutional hyponatremia in cirrhosis. Two families of drugs, the V2 vasopressin receptor antagonists and the kappa-opioid agonists, have been shown to improve free water clearance and correct dilutional hyponatremia in human and experimental cirrhosis with ascites. The first type of drugs blocks the tubular effect of antidiuretic hormone and the second inhibits antidiuretic hormone secretion by the neurohypophysis. On the other hand, two new treatments have also been proved to reverse hepatorenal syndrome in cirrhosis. The most interesting one is that based on the simultaneous administration of plasma volume expansion and vasoconstrictors. The second is transjugular intrahepatic porto-systemic shunt. The long-term administration (1-3 weeks) of analogs of vasopressin (ornipressin or terlipressin) or other vasoconstrictors together with plasma volume expansion with albumin is associated with a dramatic improvement in circulatory function and normalization of serum creatinine concentration in patients with severe hepatorenal syndrome. Of interest is the observation that in many of these patients, hepatorenal syndrome does not recur following discontinuation of the treatment, thus raising important questions about the mechanism by which hepatorenal syndrome follows a progressive course in most untreated cases. The pathogenesis of circulatory dysfunction in cirrhosis and the role of local mechanisms in the development of the splanchnic arteriolar vasodilation associated with portal hypertension will continue as important topics in clinical and basic research in Hepatology. Of special interest is the study of the mechanism by which circulatory function further deteriorates following complications such as severe bacterial infection or therapeutic interventions such as therapeutic paracentesis, and the adverse consequences of the impairment in circulatory function on renal and hepatic hemodynamics. Finally, although major advances have been made concerning the treatment and secondary prophylaxis of spontaneous bacterial peritonitis in cirrhosis, many aspects of the pathogenesis of this infection remain unclear. The mechanism of bacterial translocation and of the colonization of bacteria in the ascitic fluid are particularly important to design adequate measures for primary prophylaxis of this severe bacterial infection.
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PMID:Complications of cirrhosis. II. Renal and circulatory dysfunction. Lights and shadows in an important clinical problem. 1072 2

The gut and the liver are the key organs in nutrient absorption and metabolism. Bile acids, drugs, and toxins undergo extensive enterohepatic circulation. Bile acids play a major role in several hepatic and intestinal diseases. Endotoxins deriving from intestinal Gram-negative bacteria are important in the pathogenesis of liver and systemic diseases. Chronic liver diseases can influence gastrointestinal motility, which together with other factors may contribute to bacterial overgrowth and in patients with ascites to an increased risk of spontaneous bacterial peritonitis. Patients with end-stage liver disease frequently develop portal hypertension leading to varices, gastric vascular ectasia, and portal hypertensive gastroenteropathy. Several liver and biliary abnormalities are observed in patients with inflammatory bowel disease (primary sclerosing cholangitis, autoimmune hepatitis, cholelithiasis). The primary defect in hemochromatosis is located in the intestine, causing an inappropriate increase in iron absorption, and the liver is the site of earliest and heaviest iron deposition. Elevated transaminases are observed in many patients with celiac disease, and steatohepatitis frequently develops in patients with jejunoileal bypass and short bowel syndrome. Furthermore, the liver is the primary organ for metastasis of intestinal cancer. Many viral, bacterial, fungal, and parasitic diseases affect the intestine as well as the liver and the biliary tract.
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PMID:Gut-liver axis. 1085 47


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