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)

The pathogenesis of ascites can be divided into (1) factors that favor efflux of fluid from the vascular into the peritoneal space (sinusoidal hypertension, hypoalbuminemia), (2) factors that favor accumulation of fluid in the peritoneal cavity (thoracic duct insufficiency), and (3) factors responsible for repletion of the intravascular volume, and thereby continuous formation of ascites (sodium and water retention). Ascites is perhaps the one complication of cirrhosis with the lowest therapeutic priority. Current therapy of ascites is mainly directed at attaining a negative sodium balance (sodium restriction, diuretics) or at removing intraperitoneal fluid and returning it or its components back to the systemic circulation (large volume paracentesis accompanied by plasma volume expanders, peritoneovenous shunt, ascites "recycling" procedures). Future studies of ascites should investigate the usefulness of peripheral vasoconstrictors and nonsurgical side-to-side portosystemic shunting to relieve sinusoidal hypertension (transjugular intrahepatic portosystemic shunt). More than 90% of patients respond to diuretics and salt restriction. Other therapeutic measures should be directed at the 10% of patients with ascites refractory to diuretics. Prognosis in these patients is poor, and liver transplantation should be contemplated.
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PMID:Cirrhotic ascites: pathogenesis and management. 774 21

This study investigated the relationship between urinary sodium excretion and liver function, as assessed by the aminopyrine breath test (ABT) and conventional parameters, in 62 patients with cirrhosis kept on a constant salt diet. Urinary sodium excretion was related non-linearly to the ABT (r = 0.76). Less significant correlations were observed to the Child-Pugh score (r = -0.65), cholinesterase (r = 0.58), bilirubin (r = -0.56), albumin (r = 0.51) and prothrombin time (r = 0.49). When patients were arbitrarily divided into 6 groups according to the ABT, sodium excretion balanced the sodium intake up to a 50% reduction in ABT. In groups with more than a 50% reduction sodium retention occurred. When patients were grouped according to the Child-Pugh score, urinary salt output was balanced in patients with scores of 5 and 6 and decreased in patients with scores greater six. However, the change in sodium output from normal salt excretion to sodium retention was less pronounced in patients grouped according to the Child-Pugh score than in patients grouped according to the ABT. The results suggest a non-linear relationship between the impairment in hepatic and renal function in cirrhosis. They are compatible with the concept of a threshold of hepatic function necessary to maintain normal renal function.
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PMID:Relationship of the aminopyrine breath test and the Child-Pugh score to urinary sodium retention in patients with liver cirrhosis. 775 46

The most frequent cause of ascites in the Czech Republic is cirrhosis of the liver. Treatment of ascites in cirrhotic patients must be very careful as the use of strong diuretics is associated with some adverse complications. The latter are reviewed. The basic therapeutic provision is restriction of water and salt intake. Aldosterone antagonists are diuretics of first choice. A commonly used diuretic is also furosemide and thiazides. The author outlines the algorithm of treatment of ascites, in particular from the aspect of the general practitioner.
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PMID:[Modern therapy of ascites in liver cirrhosis]. 776 78

We investigated whether the oral administration of SAMe influences the hepatic availability of sulphur amino acids and the extent of bile salt amidation with taurine in liver cirrhosis. Ten patients with cirrhosis (eight Child-Pugh A and 2 B, aged 48-65 years), were studied before and 2 months after oral SAMe administration (800 mg per day). Bile was obtained using a string-test device (Entero-test), after gall-bladder contraction with caerulein. No significant changes were found in the per cent composition of biliary amino acids, except for an increase in glutamic acid (from 3.7 +/- 0.6% before to 6.1 +/- 1.1% after SAMe, p = 0.003) and taurine from 2.2 +/- 2.3% (range 0.4-6.8) to 7.2 +/- 9.2% (range 0.5-28.1), (NS). HPLC analysis showed a trend towards increased per cent tauroconjugation of all individual bile salts, with a significant rise in taurochenodeoxycholic acid (from 15.0 +/- 9.4% to 25.3 +/- 9.7%, p = 0.05) and a drop in glycocholic acid (from 39.1 +/- 15.3% to 25.3 +/- 9.8%, p = 0.05). These data suggest that in the cirrhotic liver exogenous SAMe is partially metabolized to taurine, which is used for bile salt amidation.
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PMID:Oral S-adenosyl-L-methionine (SAMe) administration enhances bile salt conjugation with taurine in patients with liver cirrhosis. 780 79

This study investigated the relationship between changes in renal sympathetic activity as assessed by renal norepinephrine spill-over and the onset of renal sodium retention in the phenobarbital/carbon tetrachloride model of experimental cirrhosis in rats. In this model, sodium retention occurs when hepatic function, assessed by the aminopyrine breath test (ABT), falls below a critical threshold. Three groups of rats, studied on a constant salt diet, included a group with cirrhosis and sodium retention, a group with cirrhosis of similar duration and no sodium retention and a time-control phenobarbitaltreated group. ABT, renal plasma flow (RPF), glomerular filtration rate (GFR) and mean arterial pressure (MAP) were measured at the time of catecholamine sampling in anesthetized rats. Cirrhosis was associated with reductions in MAP, no change in RPF and GFR, and an ABT below the threshold in rats with sodium retention. In contrast, rats without sodium retention had liver function above the threshold. Renal norepinephrine spill-over increased continuously from controls to non-sodium retaining and sodium retaining animals. The difference between sodium retaining animals and controls was significant. Norepinephrine spill-over correlated to ABT and MAP but not urinary salt excretion. The data suggest that, under these experimental conditions, increased sympathetic activity may contribute to the onset of sodium retention. A plausible explanation for the continuous increase is that catecholamines are released as a compensatory mechanism in response to a primary yet undefined vasodilator.
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PMID:Relationship between oxidative hepatic metabolism, urinary sodium excretion and sympathetic nerve activity in experimental cirrhosis in the rat. 788 79

This review concerns studies of the comparative efficacy and safety of torasemide and furosemide in patients with cirrhosis of the liver complicated by ascites and oedema. The short-term trials reviewed indicated that in patients who had failed to respond with adequate diuresis and loss of body weight and ascites to bed rest, restricted salt and water intake and spironolactone, torasemide had a longer duration of action than furosemide and resulted in a greater urinary excretion of salt and water and greater loss of body weight. Torasemide also had less effect than furosemide on urinary potassium excretion and unlike furosemide did not increase the fractional excretion of magnesium or phosphate or the blood ammonia concentration. Two longer term trials in similar patients with decompensated hepatic cirrhosis confirm the results of the shorter term studies. These studies, albeit each in relatively small numbers of patients, confirm the ability of torasemide to enhance diuresis, free water clearance and fractional excretion of sodium and chloride, resulting in loss of body weight and mobilization of ascites in patients with decompensated hepatic cirrhosis. In these patients, the relatively small increase in urinary excretion of potassium, induced by torasemide without any marked effect on renal function or on the plasma neurohormonal profile, enhances its potential safety.
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PMID:Comparative analysis of torasemide and furosemide in liver cirrhosis. 795 49

Cocaine was the first drug to be used as a local anaesthetic. It was introduced into medicine in 1884 by Koller. Other drugs soon followed, for example, ethyl chloride spray, tropocaine, eugenol (oil of cloves) and Nupercaine. A wide range of uses for local anaesthetics soon developed and the term 'regional anaesthesia' was first used by Cushing in 1901 to describe pain relief by nerve blockade. Local anaesthetic drugs are water soluble salts of lipid soluble alkaloids. Each molecule is composed of an aromatic portion, intermediate chain and an amide portion. The portions are joined by either amide or ester linkages. Ester-linked drugs are hydrolysed in the plasma by plasma cholinesterase and their half-life varies from one to eight minutes. Amide-linked drugs are degraded by oxidative dealkylation in the liver. The half-life of these drugs varies from 1.5 to more than three hours. The addition of a vasoconstrictor, such as adrenaline, will prolong the duration of action of both the amide- and ester-linked drugs. Degradation of the amide-linked drugs depends on factors such as hepatic blood flow and liver conditions, such as cirrhosis, and congestive cardiac failure. Anaphylactic reactions are more common with ester-linked drugs than amide-linked drugs. The drugs are usually available for injection as hydrochlorides in a salt solution with small amounts of fungicides or preservatives added to give stability.
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PMID:Local anaesthesia in the operating theatre. 799 96

Primary biliary cirrhosis (PBC) is a chronic, progressive disorder characterized by destruction of small and medium-sized bile ducts within the liver. Current evidence suggests that liver damage in this condition may occur via immunological and nonimmunological mechanisms. The immunological element is mediated by activated T lymphocytes, which are directed toward biliary epithelial cells. Destruction of biliary epithelium may lead to impaired secretion and subsequently increased concentrations of hydrophobic, toxic bile acids in the microenvironment of the hepatic lobule. These bile acids may in turn damage hepatocyte membranes and may also exacerbate secondary reactive immune-mediated destruction of both bile ducts and hepatic parenchyma. Long-standing inflammation may lead to hepatic fibrosis and, ultimately, cirrhosis. Although a variety of agents have been used to treat PBC with variable efficacy, the most promising treatment regimens appear to be those that combine an immunomodulatory agent, such as methotrexate, with a water-soluble bile salt, such as ursodeoxycholic acid. Colchicine, which may modulate cytokine activity and decrease fibrosis, may also have a role in treatment. Because PBC is a chronic, slowly progressive disease, long-term treatment trials, such as those currently under way, will be needed to assess the real benefit of such regimens. Meanwhile, liver transplantation has an excellent success rate in patients with advanced PBC, and should be used in patients with decompensated liver disease.
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PMID:Treatment of primary biliary cirrhosis. 804 96

Fasting serum conjugated bile salt concentrations were measured in a group of 20 patients with moderate post-hepatitis cirrhosis. Twenty healthy volunteers were used as controls. The individual conjugated bile acids were analyzed by a specific and sensitive method which couples reversed-phase high-performance liquid chromatography with mass spectrometry. Significantly elevated levels of the total and individual conjugated bile acids were found in cirrhotic patients. The predominant serum bile acids were conjugates of chenodeoxycholic acid. The conjugates of lithocholic acid were also increased; in subjects with normal liver function, on the contrary, they were found only in traces.
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PMID:Serum bile acid concentrations in mild liver cirrhosis. 814 35

In this study we investigated whether the retention of compounds which are excreted into the bile could contribute to portal hypertension in secondary biliary cirrhosis. Choledochovenous fistulas were grown in rats for 4 weeks. 6/13 of the animals had biochemical evidence of partial obstruction. Microsomal function, as measured by the aminopyrine breath test, was decreased in all animals with biliary retention while microsomal cytochrome P-450 content was decreased only in rats with evidence of obstruction. All animals with biliary retention with or without partial obstruction had portal hypertension. Animals with biliary retention and partial obstruction had hypercholeresis but decreased bile salt excretion. All animals with a chronic catheter in the biliary tree had a loss of the negative permselectivity of the sinusoidal-canalicular barrier and decreased maximal bile secretory pressure. Only animals with biochemical evidence of obstruction had moderate fibrosis and ductular proliferation as determined by stereological techniques. Unexpectedly, morphometric analysis also revealed an increase in hepatocyte mass induced by biliary retention. We conclude that bile contains a compound(s) which induces portal hypertension. This putative substance is neither bilirubin nor a bile acid since portal hypertension was also observed in animals with biliary retention without obstructive signs.
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PMID:Biliary retention in a chronic choledocho-venous fistula in the rat: induction of portal hypertension but not of biliary cirrhosis. 830 Oct 31


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