Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of hepatitis C virus (HCV) infection in patients with chronic liver disease (CLD) in Israel has not yet been reported. A retrospective analysis was performed on the first 92 consecutive patients referred to our Liver Unit with serologically confirmed antibodies to hepatitis C virus (anti-HCV) who had evidence for chronic hepatitis, cirrhosis, and hepatocellular carcinoma. We compared 31 patients who were anti-HCV positive with 61 patients who had evidence for both previous or present infection with hepatitis B virus (HBV) as well as HCV. Dual infection was significantly more prevalent in Jewish patients of non-Ashkenazi origin, who were also characterized by higher rates of portal hypertension manifested by ascites, bleeding esophageal varices as well as hepatic encephalopathy and spontaneous bacterial peritonitis. We conclude that dual infection of HBV and HCV was found in 66% of patients with anti-HCV positive liver disease in Jerusalem, and that these patients develop more serious complications than CLD patients with anti-HCV alone.
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PMID:Chronic hepatitis C virus infection with exposure to hepatitis B virus. 817 25

To define patients with an ascitic fluid polymorphonuclear cell count > or = 250 cells/mm3 or > or = 500 cells/mm3 but without spontaneous bacterial peritonitis, 166 patients with sterile cirrhotic ascites, 46 patients with spontaneous bacterial peritonitis, 123 patients with hepatocellular carcinoma, 67 patients with peritoneal carcinomatosis or massive liver metastasis and 12 patients with other miscellaneous diseases were studied. The sensitivity, specificity and accuracy of the diagnosis of spontaneous bacterial peritonitis were 100, 86 and 88% with the cut-off value of an ascitic fluid polymorphonuclear cell count > or = 250 cells/mm3; and were 93, 91 and 92% with that value > or = 500 cells/mm3, respectively. With the cut-off value > or = 250 cells/mm3 or > or = 500 cells/mm3, the prevalence was 18% or 14% in hepatocellular carcinoma; and 30% or 19% in peritoneal carcinomatosis or massive liver metastasis. The ascitic fluid lactate concentration was insensitive and nonspecific. Among the patients with an ascitic fluid polymorphonuclear cell count greater than the cut-off values, an ascitic fluid erythrocyte count > or = 10,000 cells/mm3, a ratio of ascitic fluid erythrocyte to total leukocyte count > or = 100, and the ratio of ascitic fluid polymorphonuclear cell to total leukocyte count < or = 75% indicated hepatocellular carcinoma, while serum to ascites albumin gradient < or = 1.1 g/dl and a ratio of ascitic fluid polymorphonuclear cell to total leukocyte count < or = 75% indicated peritoneal carcinomatosis or massive liver metastasis.
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PMID:Malignancy-related ascites: a diagnostic pitfall of spontaneous bacterial peritonitis by ascitic fluid polymorphonuclear cell count. 820 Dec 26

In a two-year period, ascitic fluid concentrations of complement 3c and complement 4 were measured in 110 patients with sterile cirrhotic ascites, 31 patients with spontaneous bacterial peritonitis, 65 patients with hepatocellular carcinoma, 36 patients with peritoneal carcinomatosis and 12 patients with miscellaneous diseases (nephrotic syndrome 4, systemic lupus erythematosus 3, secondary peritonitis 2, cardiac ascites 1, eosinophilic peritonitis 1 and tuberculosis peritonitis 1) to assess the clinical utility of ascitic fluid complements. The ascitic fluid level of complements 3c or C4 was significantly higher in patients with peritoneal carcinomatosis (32.8 +/- 10.2, 13.4 +/- 7.4 mg/dL) than in patients with sterile cirrhotic ascites (9.2 +/- 5.2, 4.5 +/- 3.9 mg/dL, p < 0.001), spontaneous bacterial peritonitis (8.2 +/- 4.1, 3.8 +/- 2.4 mg/dL, p < 0.001) or hepatocellular carcinoma (12.8 +/- 8.3, 5.6 +/- 4.4 mg/dL, p < 0.001). However, it was not significantly different from the miscellaneous disease group. To verify that ascites formation is not related to liver disease origin, diagnostic sensitivity, specificity and accuracy were 83.3%, 92.7% and 90.9%, respectively, by the ascitic fluid level of complement 3c higher than the cut-off value (20 mg/dl); or 60.4%, 89.8% and 84.3%, respectively, by the ascitic fluid level of complement 4 higher than the cut-off value (10 mg/dL). A direct correlation was found between the ascitic fluid protein level and the ascitic fluid complement 3c (r = 0.70) or complement 4 (r = 0.57) level. Based on results in this study, we can conclude that measuring ascitic fluid complements is clinically useful in disapproving the liver disease origin of ascites formation. However, it is of little value in diagnosing spontaneous bacterial peritonitis or hepatocellular carcinoma.
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PMID:Clinical significance of complements in ascitic diseases: elevated complement levels disapproving the liver disease origin. 893 44

We present a 68 year old male with alcoholic cirrhosis that was admitted with abdominal pain and fever. Hepatocarcinoma and spontaneous bacterial peritonitis by Listeria monocytogenes was diagnosed. The patient was treated with ampicillin and tobramycin during 25 days following a favorable course although ascitic fluid remained abnormal during 21 days. It is noted the rarity of Listeria as a cause of bacterial peritonitis in cirrhotic patients although they are immunodeficient. It is also important to establish the etiological origin because standard treatment of spontaneous bacterial peritonitis is cefotaxime and Listeria is resistant to this antibiotic. The 66% of spontaneous bacterial peritonitis secondary to Listeria monocytogenes infection in cirrhotic patients has been reported in Spain and this might be due to a higher incidence of human listeriosis in this country.
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PMID:[Spontaneous bacterial peritonitis caused by Listeria monocytogenes]. 992 95

Mannose-binding lectin (MBL) plays an important role in immune defense. We examined the MBL gene mutations and MBL levels in Chinese hepatitis B and hepatitis C patients with and without symptomatic cirrhosis. We recruited 190 hepatitis B and C patients, and 117 normal Chinese as controls. Serum MBL levels were measured by enzyme-linked immunosorbent assay. MBL gene mutation at codons 52, 54, and 57 was detected by polymerase chain reaction (PCR) assay. In asymptomatic hepatitis B and C patients, there was no increase in codons 52, 54, and 57 mutation, but the MBL levels were significantly lower than those in the controls. Codon 54 mutation rate was increased to 44.4% (P =.007) in symptomatic hepatitis B cirrhosis and 64.3% (P =.0026) in patients with spontaneous bacterial peritonitis (SBP). There was no increase in codon 54 mutation rate in hepatitis B-related hepatocellular carcinoma (HCC). In chronic hepatitis B infection, the odds ratio for an individual with codon 54 mutation to develop cirrhosis was 1.84 (95% CI: 1.21-2. 81) and to develop SBP was 4.58 (95% CI: 1.73-12.16). Chronic hepatitis B and hepatitis C infection lowered the MBL levels, probably by suppressing MBL production. Codon 54 mutation of MBL was associated with progression of disease in chronic hepatitis B infection.
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PMID:Mannose binding lectin gene mutations are associated with progression of liver disease in chronic hepatitis B infection. 1009 71

Chronic liver diseases are potentially evolving clinical situations which, independently by the etiology, could proceed towards progressive liver structural and functional impairments. The only efficient treatment is orthotopic liver transplantation. Chronic liver diseases, and up to 40% of liver cirrhosis, are initially asymptomatic, but cirrhosis is the most frequent cause of death among non-neoplastic digestive diseases. Important elements complicating a decompensated liver cirrhosis are ascites, hepatic encephalopathy, digestive bleeding and jaundice. Acute liver failure (ALF) is the expression of a clinical state, that is common to many conditions sharing severe liver structural and functional impairments. In patients affected by decompensated liver cirrhosis, ALF could be triggered by several factors, while the death is caused by bleeding episodes, hepato-renal syndrome, spontaneous bacterial peritonitis or hepatocarcinoma. In patients affected by chronic liver diseases, the diagnosis of ALF is based on progressively increasing jaundice, encephalopathy and coagulopathy. Recent clinical trials have evaluated the efficacy of extrahepatic liver support systems, either artificial or bio-artificial, in treating episodes of ALF in chronic liver patients. The preliminary results indicate a potential use of such systems in blood detoxification, but they also showed limits in increasing patient survival.
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PMID:[Acute liver failure in chronic hepatic disease. Clinico-therapeutic evaluation]. 1101 9

Chronic liver diseases often lead to cirrhosis of that organ. As this progresses, hepatic function decreases, and the risk of life-threatening complications increases. Common complications are variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome and hepatocellular carcinoma. The only therapeutic option that offers a chance of a cure is transplantation which, however, owing to strict selection criteria and the limited number of donor organs, can be applied only in a minority of patients. For most of the cases, the therapeutic strategy comprises treatment of the underlying disease, prevention and symptomatic treatment of typical complications.
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PMID:[Therapy of liver cirrhosis. Managing complications with fingertip control]. 1148 13

Several age-related changes occur in the structure and functions of the liver. The volume of the liver decreases, despite an increase in the size of hepatocytes, suggesting loss of liver cells. There are decreases in hepatic blood flow, the synthesis of urea and cholesterol, and the metabolism of drugs. Moreover, the regenerative capacity of liver becomes less efficient. Certain caveats are important when treating older patients with liver disease. Strict dietary restrictions, such as a low protein diet, should be avoided in the elderly (unless the patient is encephalopathic) because these patients are often undernourished to start with. Similarly, strict salt restriction should be enforced with caution, since it makes food less palatable and may take away what little desire such patients have to eat. Diuretic doses should be adjusted carefully because of greater risks of azotaemia and electrolyte disturbances in the elderly. Extra vigilance should be exercised in the early detection of infections that are more likely to occur in patients with cirrhosis. For example, spontaneous bacterial peritonitis can be missed in the elderly because of poor systemic (fever, abdominal tenderness) and laboratory responses (leucocytosis). In patients presenting with acute variceal bleeding, it is better to err on the side of underhydration than overhydration because of the risk of congestive heart failure. Vasopressin should be avoided in the elderly, since this drug has a high probability of precipitating an ischaemic event. Older patients do not tolerate beta-blockers as well as younger individuals and may require other treatment strategies for the prevention of variceal rebleeding episodes. Hepatic encephalopathy, especially the milder form, needs careful assessment because it can be easily confused with senile dementia syndromes. Cirrhosis is a premalignant condition and patients are at increased risk of developing hepatocellular carcinoma (HCC), a tumour seen predominantly in the elderly. All patients with cirrhosis should be maintained on a lifelong screening programme consisting of a 6-monthly assessment of alpha-fetoprotein and an imaging study, since early detection provides the only hope for cure of HCC. The only definitive treatment of cirrhosis is liver transplantation. Advanced age is not a contraindication to transplantation, and survival in older patients (aged >60 years) is comparable to that in younger individuals.
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PMID:Drug treatment of the complications of cirrhosis in the older adult. 1158 44

Liver cirrhosis is the end-stage of chronic liver disease with a prevalence of 0.5-0.8 percent in the German population. The main causes are chronic viral hepatitis B and C and alcohol abuse. Liver cirrhosis is often oligosymptomatic and frequently only diagnosed when complications occur (laboratory tests, ultrasound, computertomography or nuclear resonance imaging and histology). Complications include portal hypertension, gastrointestinal bleeding, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatopulmonary syndrome, hepatic encephalopathy and hepatocellular carcinoma. Therapeutic management should mainly focus on the treatment of the underlying chronic liver disease in a precirrhotic stage. In the case of cirrhosis, prevention and treatment of complications are clinically most important.
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PMID:[Clinical aspects of liver cirrhoses and its complications and diagnostic problems]. 1171 75

Hepatocellular carcinoma is a primary tumor complicating liver disease, associated with cirrhosis in 80-90% of the cases. A kidney transplant recipient with chronic B and C viral hepatitis was admitted because of general malaise, renal function impairment and positive AST, ALT and alkaline phosphatase tests, and very high alpha-fetoprotein levels. Ascites, spontaneous bacterial peritonitis and renal failure developed. A CT showed multiple liver masses. Renal failure required hemodialysis. The patient died 17 days after the initial symptoms with hepatic encephalopathy. A postmortem liver biopsy confirmed the diagnosis of cirrhosis and hepatocellular carcinoma (HCC). This report, as well as a few others, shows the accelerated evolution of chronic viral hepatitis in kidney transplant patients and questions the convenience of kidney transplantation and the adequate follow up in chronic viral hepatitis.
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PMID:[Fatal acute hepatic failure with hepatocarcinoma presentation in a patient with renal transplant with asymptomatic chronic B and C hepatitis]. 1172 27


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