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)

Systemic endotoxaemia without evidence of gram-negative bacterial infection occurs in liver diseases in man. The endotoxaemia is probably due to impaired hepatic clearance of endotoxin absorbed from the gastrointestinal tract, but portal venous endotoxaemia has never been reported in man. By means of the limulus gelation test, portal venous blood from 21 patients without parenchymal liver disease and arterial blood from 21 patients without parenchymal liver disease and 31 patients with cirrhosis was examined for endotoxin. Portal venous endotoxaemia was found in 9 of 21 samples and systemic endotoxaemia was found in 2 of 21 samples from patients without liver disease. Systemic endotoxaemia in cirrhosis occurred with a frequency of 15/31. No relationship to gram-negative bacteraemia was found. Leucocytosis was only seen in endotoxin-positive patients with cirrhosis. In cirrhosis higher levels of E. coli O antibodies were found in endotoxin-positive than in endotoxin-negative patients, supporting the view that the limulus gelation test specifically detects endotoxin (i.e. E. coli O antigen). The study suggests that endotoxin is a normal constituent of portal venous blood in man. The normal human liver clears endotoxin from the portal venous blood. This effect is diminished in cirrhosis, most probably owing to decreased phagocytic function of the liver. The increased humoral immune response in cirrhosis may be related to spillover of endotoxin from the liver.
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PMID:Portal venous and systemic endotoxaemia in patients without liver disease and systemic endotoxaemia in patients with cirrhosis. 79 99

Spontaneous bacterial peritonitis is one of the most common complications of ascitic fluid in patients with liver cirrhosis. The aim of this study was to investigate the role of total protein, albumin, globulin and complement ascitic fluid concentrations in development of spontaneous bacterial peritonitis in patients with liver cirrhosis. In patients with liver cirrhosis and spontaneous bacterial peritonitis (n = 8) the ascitic fluid total protein, albumin and globulin concentrations were significantly lower than in patients with sterile ascites (n = 11) (p < 0.01). The ascitic fluid complement C3 and C4 concentrations were significantly lower in patients with spontaneous bacterial peritonitis than in patients with sterile ascites (9.1 +/- 3.1 mg/dL to 22.9 +/- 17.4 mg/dL, p < 0.01; 3.8 +/- 5.9 mg/dL to 8.2 +/- 5.9 mg/dL, p < 0.01, respectively). The ascites total protein, albumin, globulin and complement concentrations in cirrhotic patients with spontaneous bacterial peritonitis were significantly lower than in patients with sterile ascites demonstrating the importance of those factors in ascitic fluid defense against secondary bacterial infection.
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PMID:[The significance of low levels of total proteins, albumins, globulins and complement factors in ascitic fluid and the development of spontaneous bacterial peritonitis in patients with liver cirrhosis]. 134 19

A 33-year-old male patient with hepatitis B surface antigen positive cirrhosis, received 2 courses of endoscopic injection sclerotherapy for bleeding esophageal varices. A Streptococcus viridans brain abscess developed 2 weeks after the first sclerotherapy (or 1 week after the second sclerotherapy). In cirrhotic patients, an increase in pulmonary vasodilatation and pulmonary arteriovenous shunting has been well recognized. Sclerosant as well as bacteria may pass through a pulmonary arteriovenous shunt and reach the brain, directly after an infection of esophageal varices. Brain ischemia and a bacterial infection may occur at the same time, this can accelerate the development of a pyogenic brain abscess. Careful observation for the early detection and treatment of infection following endoscopic sclerotherapy is essential.
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PMID:Brain abscess following endoscopic injection sclerotherapy: report of a case. 168 87

Medical emergencies involving the liver and biliary tract are common clinical problems. If it is already known that the patient has cirrhosis it may be an easy matter to identify the cause of complications such as gastro-intestinal bleeding or coma, but it must be borne in mind that oesophageal varices are not the only cause of such bleeding in cirrhotics and that hepatic encephalopathy is not the only cause of coma. Bacterial infection should always be considered as a possible cause of deterioration in the clinical picture; it may be a complication of pre-existing acute or chronic liver or biliary tract disease or a cause of hepatobiliary disease; prompt administration of appropriate antibiotics may save the patient's life. If there is any suspicion of biliary obstruction in a patient with signs of bacteraemia the biliary tree should be drained without delay. The key to the management of hepatobiliary emergencies lies in prompt and appropriate supportive therapy, and then in a correct diagnosis which may allow specific treatment to be administered. However, it is often difficult to establish the cause, and the resources of a specialist centre may be needed. Prompt referral is indicated when a patient is clearly very ill and shows no signs of rapid improvement.
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PMID:Hepatobiliary disease: medical emergencies. 176 20

In a retrospective study of 100 patients with pleural effusion the final diagnosis was tuberculosis in 49, malignancy in 43, malignancy with tuberculosis, bacterial infection, hydrothorax with cirrhosis, reaction to pneumothorax in one each, and unknown in 4. Most of the effusions analysed were exudates (94%). Pleural biopsy was diagnostic in 46% of tuberculous effusions (13/28) and 67% of malignant effusions (20/30). Tuberculosis accounted for 87% of cases in patients aged 40 years and under. In this age group, patients with exudative pleural effusion and a positive tuberculin test are likely to have tuberculosis and early therapeutic trial is justified.
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PMID:Pleural effusion in 100 Malaysian patients. 184 Apr 36

To clarify the morphology and pathogenesis of intrahepatic calculi in the incipient stage, we examined biliary sludge and microcalculi in intrahepatic bile ducts by morphologic and X-ray microanalytical methods in 18 (1.5%) among 1,179 autopsied livers. The hepatobiliary conditions of these 18 livers were intra- and extrahepatic biliary obstruction in 14 cases, hepatic fibrosis in three cases, and cirrhosis with hepatocellular carcinoma in the remaining one. Grossly, brown-pigmented microcalculi were observed floating in biliary sludge. Microscopically, the biliary sludge was composed of mucin, fibrinous materials, desquamated epithelial cells and a few bilirubin granules. The microcalculi were embedded in the sludge and consisted of mucin and precipitates of bilirubin with a granular, lamellar or amorphous appearance. Bacterial colonies were recognized in both the sludge and microcalculi in all but three cases. Intrahepatic bile ducts harboring sludge and microcalculi showed a minimal to moderate degree of glandular proliferation with mucin production. X-ray microanalysis disclosed that the sludge contained little calcium ion, whereas microcalculi were calcium-rich. These findings suggest that biliary obstruction, bacterial infection and mucin hypersecretion play an important role in the formation of intrahepatic biliary sludge and microcalculi, and that sludge is causally related to the formation of intrahepatic microcalculi. Intrahepatic microcalculi and biliary sludge may represent a pathogenetic sequence in the early stage of calcium bilirubinate hepatolithiasis.
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PMID:Biliary sludge and microcalculi in intrahepatic bile ducts. Morphologic and X-ray microanalytical observations in 18 among 1,179 consecutively autopsied livers. 209 92

Alpha-interferon has emerged as the most effective agent for the treatment of chronic hepatitis when active replication of virus B, C, or D is present. Exogenous administration of human alpha-interferon, now possible through modern large-scale production methods, is associated with suppression of virus in blood. Amelioration of liver disease occurs in 35% of patients with hepatitis B virus and in 50% with hepatitis C virus with interferon doses of 30 and 10 MU per week, respectively, for 16-26 weeks; after therapy, persistent normalization of serum alanine aminotransferase is observed in 35% and 27%, respectively. Similar results have now also been reported for chronic hepatitis D. Enhanced response rates (greater than 50%) may be obtained by prolonged intermittent interferon therapy. Combination of interferon with another 'antiviral' agent (vidarabine, acyclovir, prednisone) has not increased therapeutic efficacy. Alpha-interferon induces side effects such as fatigue, flu-like syndrome, myalgia, and changes in mood and granulocytes. Patients with decompensated cirrhosis are particularly prone to bacterial infection and disease exacerbation and should receive lower doses. Interferon, when applied skillfully, induces the highly beneficial transition of active viral replication into viral latency, thereby greatly reducing infectivity, symptoms, and activity of the liver disease. Prevention of death from liver failure or hepatocellular carcinoma is to be expected.
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PMID:Treatment of chronic viral hepatitis anno 1990. 212 46

Bacterial infection is a serious and often fatal complication of patients with liver disease and can prove fatal either directly or by precipitation of gastrointestinal bleeding, renal failure, or hepatic encephalopathy. At greatest risk are patients with alcoholic cirrhosis or decompensated chronic liver disease, or cases of acute liver disease who progress to fulminant hepatic failure or subacute hepatic necrosis. Infection appears to be unusual in patients with primary biliary cirrhosis. The site and type of infection is unrelated to the aetiology of the liver disease. Bacteraemia, pneumonia, urinary tract infection and spontaneous bacterial peritonitis are most common but infective endocarditis and meningitis, especially with pneumococci, are easily overlooked. Clinical suspicion of infection must be high as the only indication may be a general deterioration in the patients' clinical state, increasing encephalopathy or renal impairment. In the case of patients with fulminant hepatic failure, infection may precipitate the initial or recurrent encephalopathy and contributes to death in 10% of fatal cases. Spontaneous bacterial peritonitis is now recognized to occur in the absence of clinical features of peritonitis. The PMN content of the ascitic fluid may provide the only indication of infection and is the most readily available screening test. The most common types of organism responsible for all types of infection are Gram-negative enteric and streptococci, especially pneumococci, while infection with anaerobes is rare. Risk factors for infection include decompensated alcoholic liver disease, fulminant hepatic failure, gastrointestinal bleeding, invasive practical procedures and impaired host defence mechanisms against infection. Of the host defence mechanisms, impaired function of the reticuloendothelial system, complement, and PMNs represent the most common and serious defects. Defects of humoral immunity are present in ascitic fluid from patients with cirrhosis and are probably a major reason for development of spontaneous bacterial peritonitis. Diuresis improves these functions and reduces the risk of peritonitis. Treatment of infections even with the appropriate antibiotic is still associated with a high mortality but the use of adjuvant gut sterilization is promising, particularly in cases infected with Gram-negative enteric organisms. Infusions of fresh frozen plasma, blood and cryoprecipitate improve some systemic host defences and may be beneficial in the treatment and reduction of risk of infection.
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PMID:Bacterial infections complicating liver disease. 265 49

Serum inhibition of complement-derived leukocyte chemotaxis was examined in alcoholic liver disease with or without cirrhosis. Chemotactic inhibitory activity (CIA) was detected with higher frequency and degree in alcoholic liver disease, especially with liver cirrhosis compared with normal subjects and non-alcoholic liver cirrhosis. CIA was found in anti-IgA adsorbed fractions in the sera of patients with alcoholic liver cirrhosis. Serum concentrations of IgA1 and IgA2 in alcoholic liver disease were statistically higher than in non-alcoholic liver cirrhosis. However, no correlation between CIA and the concentrations of IgA subclasses was demonstrated in alcoholic liver disease. This serum inhibitor may partly explain the high susceptibility to bacterial infection in alcoholic liver disease.
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PMID:Serum inhibition of complement derived leukocyte chemotaxis and levels of immunoglobulin A subclass in alcoholic liver disease. 274 44

The case is reported of a 66-year old man who developed Streptococcus bovis endocarditis on a fairly loose aortic stenosis and who also presented with alcoholic cirrhosis complicated by an ultimately lethal hepatoma. On this occasion, comments are made on the following points: -Str. bovis is increasingly responsible for bacterial endocarditis. This micro-organism is now rapidly and reliably identified. -Str. bovis endocarditis has some clinical features of its own. -Patients in whom the usual portals of entry of bacterial infection (i.e. benign or malignant tumours of the colon or rectum) cannot be identified should be investigated systematically for hepatic cirrhosis. -Drug sterilization of the gut is useful to prevent bacteremia of intestinal origin in cirrhotic patients.
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PMID:[Infectious endocarditis caused by Streptococcus bovis and alcoholic cirrhosis complicated by hepatoma]. 282 37


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