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

Sixty-four patients admitted with acute alcoholic hepatitis, with or without underlying cirrhosis, were randomized regardless of encephalopathy to receive a controlled diet either alone, or supplemented orally, nasogastrically, or intravenously as necessary, with 2000 kCal and 10 g nitrogen daily. Whether this came from a conventional protein source or a branched chain amino acid enriched formulation was also randomly determined. In the absence of renal failure, nitrogen intakes of 10 g or more daily were invariably associated with positive nitrogen balance, but complications of liver dysfunction prevented the attainment of significantly more positive balance in the supplemented groups than in controls. Neither in the series as a whole, nor in any identifiable subgroup of patients, was mortality affected by treatment. Changes in prothrombin time and in measured nutritional parameters during the study did not differ between supplemented and control groups, and the observed changes in midarm muscle circumference appeared to reflect changes in degree of fluid retention. Neither enteral nor parenteral branched chain amino acids showed any consistent effect upon encephalopathy.
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PMID:Controlled trial of nutritional supplementation, with and without branched chain amino acid enrichment, in treatment of acute alcoholic hepatitis. 393 9

Peritoneovenous shunts (PVSs) have provided salutary effects on medically recalcitrant ascites, functional renal impairment, nutritional derangements, ventilatory embarrassment, and locomotion potential in patients with cirrhosis. While the LeVeen (LPVS) and Denver (DPVS) PVSs are most frequently implanted in such patients, postoperative complications of bleeding gastroesophageal varices, sepsis, and shunt occlusion occur with notable frequency. Addressing primarily the complication of PVS occlusion, a randomized prospective trial of LPVSs and DPVSs was conducted in cirrhotic patients with refractory ascites. From July 1, 1982 to July 1, 1984, 26 initial PVSs were implanted for hepatic-related intractable ascites. Twenty-two patients were eligible for randomization (cirrhosis, sterile ascites, initial PVS, total bilirubin level less than or equal to 6.0 mg/dL, prothrombin time less than or equal to 5-s prolongation, serum creatinine level less than or equal to 2.0 mg/dL [creatinine clearance rate greater than or equal to 20 mL/min], absence of recent [less than 30 days] bleeding gastroesophageal varices, or absent spontaneous encephalopathy). Twelve LPVSs and ten DPVSs were implanted; however, one patient with a DPVS was found to have hepatic polycystic disease and was excluded from analysis. All patients were followed up until death or Jan 1, 1985. The PVS patency determinations included contrast shuntography, technetium Tc 99m albumin scintigraphy, sequential manual compression (DPVS), and operative or autopsy observation. Using the Kaplan-Meier actuarial analysis, the LPVS patency proved to be highly superior to that of the DPVS, while survival was not significantly different. As LPVS and DPVS complications other than patency are comparable, the LPVS is preferred for its superior patency in cirrhotic patients with intractable ascites.
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PMID:LeVeen vs Denver peritoneovenous shunts for intractable ascites of cirrhosis. A randomized, prospective trial. 394 33

Hornet's venom is known to possess a variety of toxic effects. A 19-mo-old girl who developed a Reye-like syndrome following multiple stings by the Oriental hornet (Vespa orientalis) is described. She presented with encephalopathy associated with hepatomegaly, elevated transaminase levels, low prothrombin time, and hyperammonemia. Liver biopsy demonstrated microvesicular fatty infiltration and diffuse mitochondrial changes. Additional features were acute renal tubular necrosis and massive hemolysis.
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PMID:Multiple hornet stings with features of Reye's syndrome. 405 32

The aim of this study was to assess the prognostic value of total serum bilirubin (TSB), gamma-glutamyl transpeptidase (GGT) and the TSB/GGT ratio in 129 consecutive cirrhotic patients, and to determine how seven other clinical and biochemical variables affect the prognostic value of these measurements. The Cox model and log rank test were used to compare survival rates at 1 year. Considered alone, encephalopathy, ascites, TSB, prothrombin time, serum albumin, GGT and the TSB/GGT ratio (TSB expressed in mumoles per liter and GGT in IU per liter were associated to the 1-year survival (p less than 0.10). The estimated per cent surviving at the end of 1 year was 20% for those with encephalopathy and 59% for those without, 46% and 62% for those with and without ascites, 28% for those with TSB greater than 3.0 mg per dl, 68% for those with TSB less than or equal to 3.0 mg per dl, 44% for those with GGT less than or equal to 100 IU per liter, 60% for those with GGT greater than 100 IU per liter, and 12% for those with TSB/GGT greater than 1, 66% for those with TSB/GGT less than or equal to 1. With the Cox model, which was used to assess the combined effect of several prognostic variables, GGT was the only biochemical variable which added significant prognostic value to TSB. The combination of TSB and GGT added significant prognostic value to encephalopathy and ascites.
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PMID:Prognostic value of total serum bilirubin/gamma-glutamyl transpeptidase ratio in cirrhotic patients. 614 56

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

It has been proposed that hepatic encephalopathy and malnutrition in cirrhosis can be reversed by infusion of a protein formula (F080) enriched with branched-chain amino acids (valine, leucine, isoleucine) and containing decreased amounts of aromatic amino acids (phenylalanine, tyrosine, tryptophan). This hypothesis was tested by measuring changes in encephalopathy status, plasma ammonia, amino acid profile, and liver function during seven metabolic balance studies in three patients with cirrhosis and subclinical encephalopathy given increasing amounts (20-100 g/d) of F080. The results showed the following: 1) positive nitrogen balance was achieved only with 80 and 100 g F080/day; 2) plasma ammonia fell during negative, but increased during positive nitrogen balance; 3) plasma tyrosine and cystine fell significantly (p less than 0.05) with all intakes of F080; 4) the abnormal branched-chain to aromatic amino acid ratio was reversed; 5) extracellular volume was expanded in all patients; 6) albumin, bilirubin, prothrombin time became abnormal; and 7) encephalopathy did not significantly change from baseline. It is concluded that, in this population, F080 is an inadequate nutritional formula when given as the sole protein source because it produces hypotyrosinemia and hypocystinemia. The marked changes in the ratio of branched-chain to aromatic amino acids are not accompanied by improvement in encephalopathy.
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PMID:Total parenteral nutrition with F080 in cirrhotics with subclinical encephalopathy. 640 94

In 73 patients with fulminant viral hepatitis, non-A non-B hepatitis (NANB) was most common (43.8%), with hepatitis type A (HAV) diagnosed in 31.5% and hepatitis type B (HBV) in 24.7%. The non-A non-B group had a significantly longer duration from the onset of symptoms to the appearance of encephalopathy (median 21 days) compared with the HAV and HBV groups (medians 10 and seven days, p less than 0.01 and p less than 0.005 respectively). In the HAV group the severity of liver damage, judged by the maximum prolongation of the prothrombin time, was significantly less than in the HBV group (58 and 150 seconds prolonged respectively, p less than 0.005), and cerebral oedema was significantly less frequent (39% and 72% respectively, p less than 0.05). Consistent with this, the survival rate was higher in the HAV group (43.4%) compared with the HBV group (16.6%) and NANB group (9.3%) (p less than 0.005). These variations in presentation and clinical course may be a consequence of differences in the pathogenesis of the hepatic necrosis.
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PMID:Clinical and prognostic differences in fulminant hepatitis type A, B and non-A non-B. 641 35

Death or uncorrectable shunt malfunction occurred within 4 months in a majority (23) of 39 consecutive alcoholics who had peritoneovenous shunts. Clinical, biochemical, and operative variables in these patients were reviewed to detect factors that might predict early failure. Hepatorenal disease, expressed as the sum of total bilirubin and creatinine greater than 4 mg/dl, characterized 15 of 18 early deaths and was a reliable preoperative criterion of clinical outcome (p less than 0.001). Except for prothrombin elevation, abnormal coagulation indices did not predict early failure. Encephalopathy was more prevalent in patients who died (p less than 0.05). Among operative variables, failure to drain ascites was associated with more hospital deaths (p less than 0.05) and documentation of venous catheter placement in a central location reduced likelihood of early shunt malfunction (p less than 0.001). Preference for the LeVeen or Denver shunt did not affect the rate of early shunt malfunction. The overriding predictive factor was hepatorenal disease, both obvious and occult, by which judicious patient selection may avoid early death in surgical palliation for intractable alcoholic ascites.
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PMID:Peritoneovenous shunts: predictive factors of early treatment failure. 646 13

The prognostic significance of a battery of clinical, laboratory, and histological indicators was assessed in relation to mortality risk in a 1-year study of 253 patients with alcoholic liver disease, of whom 51 died within such time. The relative risk associated with each abnormality was calculated. A number of abnormalities was found to be statistically associated with a higher risk of death. Among the clinical abnormalities, these were: collateral circulation, edema, ascites, encephalopathy, spider nevi, anorexia, and weakness. Among the laboratory tests, these were: albumin, bilirubin, hemoglobin, abnormal prothrombin time, and alkaline phosphatase. Two hundred and sixteen of these patients had liver biopsies in which the quantifiable abnormalities were scored. Among the histological findings, the alterations significantly related to mortality were necrosis, Mallory, and inflammation, while the presence of cirrhosis per se did not influence the mortality risk. The relative risk factors for mortality associated with the histological alterations were lower than those derived from clinical or laboratory measurements. The advantage of using only clinical and laboratory items to derive a global, quantitative expression of severity is discussed. The relative mortality risks provided a means of calculating a "unit of severity" for each clinical and laboratory abnormality. A combined clinical and laboratory index (CCLI) results when these mortality-risk units are added. Such a combined index had a quasi-linear relationship with the risk of mortality for the complete population. This method compared well with severity scores derived from computerized, linear step-wise discriminant function (SDF) analysis and from a logistic regression (LR) analysis. The factors chosen to have independent prognostic significance by the SDF analysis were: encephalopathy, albumin, prothrombin time, and hemoglobin, while only encephalopathy, albumin, and hemoglobin were chosen by the LR analysis. Within a range of values, LR can provide a good discrimination in relation to mortality, similar to that observed for the CCLI in its complete range. However, there are some advantages to the CCLI method vs. the LR or SDF analyses. The CCLI is less susceptible to being unduly influenced by a nonspecific effect of treatment on the items chosen than the SDF and LR analyses, as the CCLI contains a large number of factors. Obtaining a single-severity score such as the CCLI is of value in: (a) assessing the effectiveness of treatment modalities; (b) analyzing the success of randomization; (c) separating cohorts of different severity, and (d) comparing new liver tests, histological abnormalities, or specific biological events with the severity of alcoholic liver disease.
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PMID:Assessment of prognostic factors in alcoholic liver disease: toward a global quantitative expression of severity. 662 18

The prevalence of impaired renal acidification in alcoholic liver disease and its relationship to clinical and biochemical features were evaluated during a one-year period in a 60-bed liver unit. No cases of overt renal tubular acidosis (RTA) were found; all of 12 patients with low serum bicarbonate values and normal anion gap proved to have chronic respiratory alkalosis. However, there was a 57% prevalence of incomplete distal RTA in 42 patients who were tested with an acid load. Subjects with RTA had higher serum bilirubin levels (5.3 +/- 6.1 v 2.1 +/- 2.7 mg/dL) and lower prothrombin times (45% +/- 22% v 64% +/- 20%). Urinary pH correlated directly with serum bilirubin levels (r = +.38) and inversely with prothrombin times (r = -.46). The frequency of ascites and encephalopathy did not differ notably between the two groups of patients. No pathogenetic relation was observed with avid sodium retention, decreased excretion of nonreabsorbable anions, and elevated urinary excretion of bile acids. Therefore, we conclude that impaired renal acidification in alcoholic liver disease may be a sign of liver cell failure since it is more frequently observed in patients with a greater degree of liver dysfunction.
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PMID:Impaired renal acidification in alcoholic liver disease. 671 10


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