Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatolithiasis, or the presence of intrahepatic stones, is prevalent in East Asia and is characterized by the finding of stones within the intrahepatic bile ducts proximal to the confluence of the right and left hepatic ducts. Bile stasis and bacterial infection have been incriminated as the major aetiopathogenic factors. Clinical features include recurrent pyogenic cholangitis, multiple liver abscesses, secondary biliary cirrhosis and cholangiocarcinoma. The goals of management include accurate localization of pathologies, control of biliary sepsis and the elimination of stones and stasis. Ultrasonography, computed tomography and direct cholangiography complement each other in defining the stones, strictures and degree of liver damage. Non-operative biliary decompression by endoscopy and interventional radiology is effective in controlling the infection, but surgery remains the mainstay for the treatment of stones and strictures. Intra-operative ultrasound and flexible choledochoscopy, combined with percutaneous transhepatic cholangioscopy and intraductal lithotripsy, facilitate stone removal. Balloon dilatation and biliary stenting serve to open the bile duct strictures. The creation of a hepaticocutaneous jejunostomy after conventional surgery allows atraumatic access to the biliary system for the removal of recurrent stones. The management of biliary parasites begins with conservative measures, including analgesics and anti-helminthic therapy. In refractory cases or patients with acute cholangitis, endoscopic biliary drainage and the extraction of worms may be necessary. Improvement in sanitation plays a crucial role in the epidemiological control of these biliary diseases.
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PMID:Hepatolithiasis and biliary parasites. 951 5

Parenteral nutrition associated cholestasis in preterm infants and newborn children is a frequent and serious disease with an incidence of 23% depended on duration of parenteral nutrition and birthweight. The incidence of liver cirrhosis is 40% when parenteral nutrition is given 74-242 days. The pathogenesis remains unclear. Several predisposing factors are discussed like immaturity, lack of hormonal stimulation by oral feeding, bacterial infection, liver toxicity of aminoacids and their products of photooxidation, lack of taurine, lack of antioxidation substances, hypermanganesaemia and pollution of infusion solutions. Furthermore sepsis during parenteral nutrition seems to multiply the risk of cholestasis. For prevention controlled studies recommend: 1. Early enteral nutrition. 2. The reduction of parenteral amino acids to less than 3 g/kg/d. 3. Light protection for parenteral solutions. 4. Cyclic infusion of parenteral nutrition. 5. The application of antibiotics (metronidazole, gentamicin) during parenteral nutrition. The most important therapeutic intervention is the beginning of oral feeding. Most of the time this leads to a decrease of icterus within two weeks. An icterus persisting longer than 3 weeks should be treated because of the risk of liver cirrhosis. Further therapeutic interventions are: 1. Cholecystokinin, good results in case studies which still has to be verified by a controlled study. 2. Ursodeoxycholic acid, its choleretic effectiveness is verified in several liver diseases by controlled studies, but it is not proven in parenteral nutrition associated cholestasis. 3. Laparoscopic biliary irrigation, successful in several case studies.
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PMID:[Parenteral nutrition associated cholestasis in the newborn]. 987 92

Variceal bleeding is a life-threatening complication of cirrhosis. Potential risk factors include clinical, endoscopic, and haemodynamic factors, but why bleeding occurs unpredictably in individual patients is not known. We postulate that bacterial infections in patients with variceal haemorrhage may be the critical factor that triggers bleeding. In patients with large varices and a high wall tension, the release of endotoxin into the systemic circulation during episodes of bacterial infection results in a further increase in portal pressure through the induction of endothelin and possibly vasoconstrictive cyclo-oxygenase products. The subsequent contraction of hepatic stellate cells causes a rise in intrahepatic vascular resistance. Furthermore, endotoxin-induced nitric oxide and prostacyclin, and prostacyclin induced by endothelin could inhibit platelet aggregation, which may result in a further deterioration of primary haemostasis at the level of varix. We propose that the combination of these two effects leads to the onset of variceal haemorrhage.
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PMID:Bacterial infection in the pathogenesis of variceal bleeding. 1019 80

Plasma fibronectin was determined in 29 patients with decompensated cirrhosis (7 patients had bacterial infection) and 23 patients with malignant liver disease. The obtained values were compared with the fibronectin values in 20 healthy subjects belonging to the control group in order to determine the possible diagnostic value of this dimer glycoprotein of high molecular weight whose role in the organism has not been completely explained. Fibronectin was determined on nephelometer with the use of specific antiserum by Behringwerke. The results expressed as mean values and SD were compared with monofactorial variance analysis (method One-way ANOVA). Fibronectin values in patients with liver cirrhosis were statistically significantly lower than in the control group (p < 0.01), which is also the case with correlation with malignant liver disease (p < 0.01). The fibronectin values in patients with malignant diseases were almost the same as the control group values (p < 0.01). In 7 patients with liver cirrhosis and bacterial infection the fibronectin values were statistically significantly higher in relation to those in the remaining 22 patients with cirrhosis but without bacterial infection (p < 0.001). The investigation in this study indicated that the decrease of mean fibronectin values is related to hepatic failure which is of diagnostic value, while normal values in malignant diseases do not favor the opinion on fibronectin as a tumor marker. Higher fibronectin values in infection in patients with liver cirrhosis are not clear, which indicated the total complexity of the relation between fibronectin as a dimer glycoprotein and chronic liver diseases including malignant.
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PMID:[Diagnostic importance of fibronectin in chronic liver diseases]. 1035 2

The incidence of bacterial infections in cirrhotic patients admitted to hospital is very high. In several studies, 30% to 50% of cirrhotics presented bacterial infections at admission, or developed this type of complication during hospitalization. Most bacterial infections in cirrhotic patients are hospital-acquired. Between 15% to 35% of cirrhotics admitted to hospital develop nosocomial infections; these figures contrast sharply with the hospital-acquired infection rate in the general hospital population (5% to 7%). Urinary tract infections (12% to 29%), spontaneous bacterial peritonitis (7% to 23%), respiratory tract infections (6% to 10%) and bacteraemia (4% to 9%) are the most frequent bacterial infectious complications seen in cirrhotic patients. However, since spontaneous bacterial peritonitis is the most characteristic bacterial infection in cirrhosis, this report will focus (mainly) on this infectious complication.
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PMID:Bacterial infections in liver cirrhosis. 1060 6

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

To delineate the clinical roles of plasma cytokine or endotoxin levels in the natural course of infection in patients with decompensated cirrhosis, 66 cirrhotic patients were studied within a 1.5-year period. Plasma levels of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), IL-6, IL-8 and endotoxin were determined on days 1, 4 and 7 after admission when hospital infection was suspected and 4 months later. A total of 24 patients (36.4%) were proven to be infected during hospitalization (group A), while 42 others were not infected (group B). Fever occurred in a very high proportion (22/24) of group A patients. Baseline levels of TNF-alpha (37.7+/-15.2 compared with 8.7+/-1.2 pg/ml; P<0.01) and IL-6 (180.5+/-20.5 compared with 24.6+/-7.5 pg/ml; P<0.0001) were higher in group A patients, while IL-1beta, IL-8 and endotoxin levels were not significantly different between the two groups. For patients with hospital infection, IL-6 levels determined during the episode were significantly higher than baseline levels. Using IL-6 >80 pg/ml as a baseline cut-off level to diagnose bacterial infection, the sensitivity, specificity and accuracy were 87.5, 100 and 95.5% respectively. The one-year cumulative probability of mortality (61.1% compared with 23.7%; P<0.001) and of bacterial re-infection (72.2% compared with 18.4%; P<0.0001) was higher in group A than in group B. Plasma TNF-alpha and IL-6 levels determined at 4 months were not different between the two groups. In conclusion, fever or elevated plasma IL-6 levels in patients with decompensated cirrhosis calls for early antibiotic treatment to prevent life-threatening bacterial infection. Bacterial infection is likely to recur in those patients with increased IL-6 levels, while severe episodes of infection occur in patients with increased TNF-alpha levels.
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PMID:Sequential changes in plasma cytokine and endotoxin levels in cirrhotic patients with bacterial infection. 1073 75

Liver disease is a frequent cause of haemostatic abnormalities, which may lead to overt or occult bleeding. Clinical manifestations of hepatic coagulopathy include upper and lower gastrointestinal haemorrhage, easy bruising and bleeding from gums, nose or the female genital tract. The most significant bleeding problem among patients with chronic liver disease is blood loss due to portal hypertension. About 30% of subjects with oesophageal or gastric varices resulting from cirrhosis have an episode of gastrointestinal bleeding in their lifetime. Risk factors for the first episode of variceal bleeding include the severity of liver dysfunction, large varices, and the presence of endoscopic red colour signs. Bacterial infection in patients with variceal haemorrhage may be critical in triggering bleeding. Nongastrointestinal bleeding events, either spontaneous or induced by minor trauma, are also a common complication of advanced cirrhosis. In women, for instance, dysfunctional uterine bleeding may become so severe that hysterectomy is required. In addition, invasive diagnostic tests (mostly solid tissue biopsies) and surgical procedures have a high risk of haemorrhage and are sometimes withheld in cirrhotic patients for fear of complications. In patients with portal hypertension, surgical procedures aggravate the injury of the hepatic parenchyma and may worsen the condition.
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PMID:Clinical aspects of bleeding complications in cirrhotic patients. 1085 May 69

This is a report of a post-mortem histological, histochemical, and immunohistochemical examination of a rare case of sclerosing encapsulating peritonitis (SEP) and non-occlusive mesenteric infarction (NOMI), two serious complications of continuous ambulatory peritoneal dialysis (CAPD), with which a man suffering hepatitis C virus (HCV)-induced liver cirrhosis for 7 years and trauma-induced paraplegia for 50 years had been treated for 1 year. The direct cause of death was encephalopathy caused by extreme hyperammonemia (11 250 microg/dL in serum). The autopsy revealed that the SEP had drastically reduced the length of the small intestine to 210 cm, 180 cm of which presented acute ischemic enteritis with Gram-negative bacterial infection. Histological examination of the SEP revealed that the exterior was composed of normal serosal elastic lamina, but with a cocoon-like appearance remarkably thickened by fibrosis to 3-8 times that of the normal subserosal layer and consisting of spindle cells and blood vessels, with some infiltration of mast cells and lymphocytes. The immunohistochemical examination of the spindle cells revealed few AE1/AE3(+) cells, HHF35(+) cells, and CD34(+) cells, many CD117(+) cells with slight proliferative activity based on MIB-1 positivity (proliferation index <1%), but no CD44(+) cells. It was concluded that either the few CD34(+) and/or the many CD117(+) cells were mesenteric stem cells that had originated from the serosa, proliferated, then differentiated into myofibroblasts or fibroblasts, producing collagen and hyaluronic acid in the matrix, leading to the gradual formation of the SEP, which was induced by the continual irritation of CAPD.
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PMID:Sclerosing encapsulating peritonitis and non-occlusive mesenteric infarction found at autopsy in a man who had undergone continuous ambulatory peritoneal dialysis: a histochemical and immunohistochemical study. 1097 66

Phlegmonous colitis (PC) is an acute infectious entity caused by bacteria. In this study, we reviewed 8,822 autopsy cases and found 13 cases of PC (0.15%). PC affected 2.43% of patients with hepatic cirrhosis or subacute liver atrophy, both of which were considered to be due to hepatitis viral infection. Before autopsy, none of the cases studied was suspected to involve PC, irrespective of the immediate cause of patient death. Thirteen autopsy cases showed some or all of the following pathohistologic characteristics: (1) involvement of the cecum (9 cases, 76.9%), (2) phlegmonous inflammatory changes and edema in the submucosa (100%), (3) bacterial infection (100%), (4) no microscopically detectable mucosal injuries (12 cases, 92.3%), and (5) acute serositis (peritonitis) (2 cases, 15.4%). These results suggest that PC is an unrecognized, but fatal complication of patients with some hepatic diseases and that PC has pathohistologic characteristics in common with previously reported spontaneous bacterial peritonitis in animal models. PC probably arises due to spontaneous infection in patients with hepatic cirrhosis.
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PMID:Phlegmonous colitis: a specific and severe complication of chronic hepatic disease. 1119 78


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