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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The potential for hepatic injury associated with the therapeutic use of salicylates and acetaminophen has recently attracted considerable attention. About 300 cases have been reported in which elevated transaminase levels or other evidence of hepatic injury developed following treatment with salicylates. Review of the spectrum of abnormalities reveals a group of patients (4 percent) with symptomatic liver damage in whom progressive or chronic liver disease is a possibility with continued use of the drug. In a few patients in this group, jaundice developed; several had abnormal prothrombin times; 11 (70 percent) had transaminase values in excess of 500 units; and five patients (30 percent) had encephalopathy and/or Reye's syndrome. In several reports liver damage has also been associated with the use of acetaminophen in therapeutic or near-therapeutic dosages. Of 18 patients, nine appeared to have ingested acetaminophen in amounts approaching overdose. Of the remaining nine patients, six were alcoholics. In the entire group, only five patients did not have a history of alcohol abuse; in three, glutathione depletion was suggested as a possible explanation for hepatotoxicity. The association with alcoholism or glutathione depletion suggests that host susceptibility may play a critical role. In two patients, long-term use of acetaminophen resulted in liver injury suggestive of chronic active hepatitis, possibly on the basis of an idiosyncratic reaction. In a study of chronic liver disease, acetaminophen half-life was prolonged (168 percent) without accumulation at 4 g a day over five days. In a double-blind, two-week, cross-over study, no clinical or laboratory evidence of adverse effects was found. There is, therefore, no evidence that chronic liver disease increases the risk of hepatotoxicity following the administration of acetaminophen in therapeutic doses. Thus, acetaminophen is the preferred antipyretic analgesic in patients with liver disease. Salicylates should be avoided since many of the adverse effects associated with these drugs are similar to the complications of chronic liver disease.
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PMID:Hepatotoxicity following the therapeutic use of antipyretic analgesics. 635 71

Portal systemic encephalopathy is a neuropsychiatric disorder that occurs secondary to chronic liver disease. It is a chronic and disabling disorder that must be treated concurrently with liver disease. In chronic liver disease, the regenerative capacity of the liver to produce new cells is eventually hampered and scar tissue develops. Scarring reduces blood flow through the liver. The vein most affected is the portal vein which contributes 75 percent of the blood to the liver as it evolves from tributaries off the abdominal organs. To eliminate the high pressure in the portal vein caused by the reduced blood flow, the portal vein develops collateral vessels that bypass the liver and drain directly into the inferior vena cava. When blood is not cleared, or when hepatic functioning fails, toxins accumulate in the circulation and affect the central nervous system. The neuropsychiatric manifestations that occur represent the symptoms seen in portal systemic encephalopathy. With renewed understanding of the disease and its neuropsychiatric manifestations, both clinicians and patients are able to minimize its untoward effects. This article reviews the pathogenesis, stages, diagnosis and treatment of the disease and aims at giving nurse practitioners a thorough review so they can better teach patients how to help themselves.
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PMID:Portal systemic encephalopathy. 646 41

The spontaneous development of chylous ascites in patients with cirrhosis is documented, but its clinical features are not well defined. The incidence of this complication of chronic liver disease was 0.5% in ascitic patients in our liver unit. These patients were older than a control group with nonchylous cirrhotic ascites and, despite better liver tests, appeared to have a higher diuretic requirement. Several had disabling, recurrent spontaneous encephalopathy. The mechanism of chylous ascites in cirrhosis is probably portal hypertension causing lymphatic rupture; however, the fact that serum-to-ascites albumin gradients were similar in the two groups, indicating similar degrees of portal hypertension, suggests that other factors also play a role. Spontaneous transformation of previously clear ascites appeared to be associated with a poor prognosis. In contrast, the appearance of chylous ascites de novo in a cirrhotic patient appeared to have a more favorable outcome. Conservative management is recommended for most patients, as the degree of their liver disease appears to be the most important factor determining prognosis.
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PMID:Spontaneous chylous ascites of cirrhosis. 648 Nov 22

In 26 patients with chronic liver disease, the serum viscosity was studied. In 42% of subjects, the serum viscosity was found increased, almost always associated with clinical findings of central nervous system involvement. The remission of central nervous system symptoms occurs with fall into normal range of serum viscosity levels. Therefore, the serum hyperviscosity should be included among various causes of cirrhosis encephalopathy. When serum viscosity is increased, relates rather to immunoglobulins (IgG, IgA, IgM) increases then to increased amounts of total globulins.
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PMID:[Serum viscosity and chronic hepatopathies]. 667 48

Forty one patients with chronic liver disease and intractable ascites were treated by a portal-systemic shunt. Operative mortality was 4.8 p. 100. Ascites was definitely cleared in 97 p. 100 of the 39 survivors. Fourteen patients later developed encephalopathy which was severe in 6 (15.3 p. 100). One-year survival rate was 72 p. 100. Late deaths were mainly due to complications of liver disease. These results suggest that portal diversion is an efficient and permanent treatment of intractable ascites in cirrhotic patients. Operative mortality and overall survival rates are similar to those observed after peritoneo-venous shunting. The peritoneo-venous shunt is preferable as the first-choice treatment of intractable ascites in cirrhotics because of the risk of encephalopathy. Portal diversion should be proposed for patients with previous variceal hemorrhage and for those in whom peritoneo-venous shunt has failed.
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PMID:[Treatment of intractable ascites in cirrhotic patients by portal shunt]. 687 67

This study examined the effect of large spontaneous portosystemic shunts on the incidence of variceal hemorrhage and hepatic encephalopathy. Twenty cases of chronic liver disease with large spontaneous shunts were compared with a group of patients with liver disease and with Cruveilhier-Baumgarten (C-B) murmurs and with a control group having liver disease and absence of large shunts on angiography. Gastrointestinal hemorrhage was present in similar proportions of patients in the three groups. Hepatic encephalopathy occurred more frequently in the spontaneous shunt group and C-B murmur group. The encephalopathy was spontaneous in 12 of 14 patients with large natural shunts whereas it was precipitated by events such as gastrointestinal bleeding, diuretics, or infection in 14 of 15 of the patients with C-B murmur and five of the seven controls. Therefore, spontaneous portosystemic shunts do not protect against gastrointestinal hemorrhage and are associated with an increased risk of spontaneous hepatic encephalopathy.
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PMID:Spontaneous portosystemic shunt: relationship to spontaneous encephalopathy and gastrointestinal hemorrhage. 697 95

Plasma amino-acid concentrations were measured in 167 patients with liver disease of varying aetiology and severity, all free of encephalopathy, and the results compared with those in 57 control subjects matched for age and sex. In the four groups of patients with chronic liver disease (26 patients with chronic active hepatitis, 23 with primary biliary cirrhosis, 11 with cryptogenic cirrhosis, and 48 with alcoholic hepatitis +/- cirrhosis) plasma concentrations of methionine were significantly increased, while concentrations of the three branched chain amino-acids were significantly reduced. In the first three groups of patients plasma concentrations of aspartate, serine, and one or both of the aromatic amino-acids tyrosine and phenylalanine were also significantly increased, while in the patients with alcoholic hepatitis +/- cirrhosis plasma concentrations of glycine, alanine, and phenylalanine were significantly reduced. In the three groups of patients with minimal, potentially reversible liver disease (31 patients with alcoholic fatty liver, 10 with viral hepatitis, and 18 with biliary disease) plasma concentrations of proline and the three branched chain amino-acids were significantly reduced. Patients with alcoholic fatty liver also showed significantly reduced plasma phenylalanine values. Most changes in plasma amino-acid concentrations in patients with chronic liver disease may be explained on the basis of impaired hepatic function, portal-systemic shunting of blood, and hyperinsulinaemia and hyperglucagonaemia. The changes in patients with minimal liver disease are less easily explained.
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PMID:Plasma amino-acid patterns in liver disease. 707 13

The accumulation of false neurotransmitters such as octopamine and depletion of true neurotransmitters such as dopamine have been purported to play a pathogenetic role in portal systemic encephalopathy (PSE). Therefore, we measured plasma prolactin, a known sensitive indicator of functional dopamine activity in man, in an attempt to evaluate dopaminergic function in 21 patients with alcoholic liver disease and PSE and several control groups. Subjects with PSE had markedly elevated prolactin levels (P less than 0.01) when compared to all control groups. Moreover, patients with PSE were divisible into two groups, 12 having mildly increased prolactin levels and 9 having markedly elevated levels. Although the degree of PSE was similar in both groups, those PSE patients with the higher prolactin values had significantly greater derangement of serum albumin, bilirubin, prothrombin time, and also had a higher mortality (100%). These data: (1) provide evidence consistent with the hypothesis of altered neurotransmitter function in individuals with chronic alcoholic liver disease, particularly those manifesting evidence of PSE; (2) suggest that altered dopamine function in chronic liver disease may have pathophysiologic significance as judged by altered hormone release; (3) demonstrate that a markedly elevated plasma prolactin level in individuals with PSE carries an ominous prognosis; and (4) suggest a possible role for the plasma prolactin in the selection and monitoring of PSE patients who are to be treated with agents aimed at correcting neurotransmitter abnormalities.
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PMID:Hyperprolactinemia in portal systemic encephalopathy. 723 64

Forty patients with chronic liver disease and portal hypertension but without clinical signs of portasystemic encephalopathy (15 patients with nonalcoholic cirrhosis, 15 patients with alcoholic cirrhosis, and 10 patients with minimal EEG changes) and a control group of 12 patients with chronic alcohol pancreatitis were studied using an extensive psychometric program, which, in the same form, is used for expert reports on driving capacity. Of the cirrhotic patients, 60% were considered unfit to drive; in 25% driving capacity was questionable, 15% (only nonalcoholic cirrhotics) were considered fit to drive. In contrast 75% of the patients with alcoholic pancreatitis were considered fit to drive. Major defects were found only in three heavy alcoholics. Patients with alcoholic cirrhosis scored lower than patients with nonalcoholic cirrhosis. This was due to differences in liver function rather than to the effect of alcohol consumption. Patients with minimal EEG changes were practically all considered unfit to drive.
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PMID:Latent portasystemic encephalopathy. I. Nature of cerebral functional defects and their effect on fitness to drive. 724 98

Hyperammonemia and changes in brain monoamine metabolism have been proposed to contribute to the pathogenesis of the neuropsychiatric symptoms characteristic of human portal-systemic encephalopathy (PSE) resulting from chronic liver disease. Portacaval anastomosis (PCA) in the rat leads to sustained hyperammonemia and mild encephalopathy. In order to evaluate the role of dopamine (DA) metabolism in PSE, levels of DA and its metabolites were measured by HPLC with electrochemical detection in brain regions of rats with PCA at various stages of encephalopathy precipitated by ammonium acetate administration. Following ammonium acetate administration, rats with PCA rapidly develop severe neurological signs of encephalopathy progressing through loss of righting reflex to coma; sham-operated control animals administered ammonium acetate showed no such neurological deterioration. Concentrations of the DA metabolites DOPAC and HVA as well as [DA metabolites]/[DA] ratios, an indirect measure of DA turnover in brain, were increased in caudate-putamen, in cingulate and pyriform entorhinal cortices as well as in raphe nucleus and locus coeruleus. Increased DA metabolites, however, did not worsen at coma stages of PSE. Increased DA turnover thus appears to relate to early neuropsychiatric and extrapyramidal symptoms of PSE.
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PMID:Regional alterations of dopamine and its metabolites in rat brain following portacaval anastomosis. 773 63


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