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

In order to define further the therapeutic role of hemodialytic procedures in acute hepatic failure, 20 pigs with ischemic hepatic necrosis underwent randomized hemodialysis against an electrolyte solution (n = 6), hemofiltration with re-infusion of an electrolyte solution (n = 5), control hemofiltration with re-infusion of autologous ultrafiltrate (n = 4) or no extracorporeal procedure at all (n = 5). Pigs on hemodialytic procedures survived significantly longer (51 +/- 11 hrs) than controls (36 +/- 8 hrs). There were no differences in the duration of survival between hemodialysis and hemofiltration, nor between controls undergoing and those not undergoing an extracorporeal procedure. Electroencephalograms showed more rapid (p less than 0.05) deterioration in control animals than in the treatment group. Putative toxins such as ammonia, glutamine, tyrosine, tryptophan, and methionine all decreased transiently in the treatment group; in the control group a continuous increase in the levels of the putative toxins was observed. Comparison of all pigs surviving 35 hrs or less (n = 6) and animals surviving more than 45 hrs (n = 7) showed that long-term survival was significantly associated with lower plasma ammonia and methionine concentrations and fewer abnormalities on the electroencephalogram 10 hrs after the start of extracorporeal procedures; moreover six of the 7 long-term survivors underwent hemodialysis or hemofiltration procedures. We conclude that hemodialytic procedures prolong survival in pigs with ischemic hepatic necrosis by slowing the development of encephalopathy; this effect of hemodialytic procedures may be mediated by the lowering of plasma ammonia and methionine levels.
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PMID:Large-pore hemodialytic procedures in pigs with ischemic hepatic necrosis; a randomized study. 651 36

In an attempt to investigate the role of the lipidic emulsion Intralipid in the development of metabolic encephalopathy in a patient showing high free tryptophan levels, the relationship between lipidic emulsion and free tryptophan was examined in in vitro experiments. The addition of intralipid to normal serum produces an immediate increase in non-esterified fatty acids and a parallel rise in free tryptophan. Moreover, when serum with intralipid is incubated at 37 degrees C, the lipases release new non-esterified fatty acids and the free tryptophan increases proportionally. The non-esterified fatty acid content of intralipid was found to be 12 +/- 2 mEq X 1(-1). An inverse correlation was seen between free tryptophan and different serum albumin concentrations. It is concluded that intralipid causes an increase in free tryptophan levels. It is known that in vivo free tryptophan modulates 5-hydroxytryptamine synthesis and thus may be considered a possible causal agent for encephalopathy.
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PMID:Intralipid and free plasmatic tryptophan in vitro. 686 41

The influx of phenylalanine, tryptophan, leucine, and lysine across the blood-brain barrier of individual brain structures was studied in rats 7--8 weeks after a portacaval shunt or sham operation. The method involved a brief infusion of labeled amino acid in tracer quantity and quantitative autoradiography. The clearance rates of phenylalanine, tryptophan, and leucine were increased in proportion to each other in every region examined, but not by the same factor. Tryptophan clearance increased the most (about 200%) and leucine the least (about 30%), compared with phenylalanine (about 80%). This was unexpected, as all three amino acids are believed to be transported by the same mechanism. The changes were most marked in several limbic structures and the reticular formation, whereas the hypothalamus was least affected. Plasma clearance of lysine was decreased in all areas by about 70%. Since the circulating lysine concentration was decreased by 13%, the actual rate of lysine influx was even more reduced. The results demonstrate specific alterations in two different amino acid transport systems. The resulting excess brain neutral amino acids, some of which are neurotransmitter precursors, as well as reduced basic amino acid availability, may be of etiological significance in heptic encephalopathy.
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PMID:Regional blood-brain barrier permeability to amino acids after portacaval anastomosis. 705 89

The pathogenesis of neuropathy and encephalopathy in patients with renal failure remains unknown. Possible factors include particularly aluminium intoxication, accumulation of certain middle molecular substances (MMS) and disturbances of tryptophan metabolism. Serum and CSF taken post-mortem from 8 uremic subjects who had been treated conservatively and from 4 patients on a chronic intermittent hemodialysis program who had dialysis dementia were subjected to MMS fractionation. Although MMS could not be detected in the CSF of normal controls, these substances were found in the CSF of uremic subjects in a pattern similar to that found in serum, although their concentrations were clearly lower than in serum. Their appearance could be due to impairment of the blood-CSF barrier. Uremic patients who had been treated conservatively had significantly increased CSF tryptophan concentrations when compared to the control subjects, but the CSF tryptophan concentrations of patients with dialysis dementia were in the normal range. Thus the pathogenesis of dialysis dementia cannot be related to the accumulation of MMS or to disturbances of tryptophan metabolism in the CSF.
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PMID:Middle molecular weight substances in the cerebrospinal fluid of uremic patients. 710 4

Acute hepatic ischaemia was induced in pigs by means of a portacaval shunt with hepatic artery ligation after 24 hours. Despite significant elevation in blood ammonia, fatty acids, aspartate aminotransferase, cerebrospinal fluid glutamine and ammonia, and brain tissue glutamine, ammonia and tryptophan, the experimental animals remained awake and alert and indistinguishable from sham-operated controls. The molar ratio of branched-chain to aromatic amino acids fell sharply in the arterial blood, but showed a terminal attempt at compensation in muscle venous samples. Portal and muscle venous insulin levels were elevated, and glucagon values rose in all circulation segments in the experimental group. The failure to induce coma in these pigs, despite the presence of many of the classical biochemical features, suggests that the syndrome of encephalopathy comprises several stages, and that the pig may be an important model in which to define these.
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PMID:Acute hepatic ischaemia in the pig- the changes in plasma hormones, amino acids and brain biochemistry. 725 Aug 93

To determine the role of liver dysfunction in the plasma amino acid profile of cirrhotic patients, we correlated basal plasma amino acids and several biochemical and functional hepatic variables in 29 cirrhotics with normal mental state or mild encephalopathy. Increased levels of aromatic amino acids and free tryptophan correlated positively with the extent of portosystemic shunt, as assessed by the ammonia tolerance test (r = 0.758 and r = 0.589, respectively). There was a negative correlation between these amino acids and liver function, as evaluated by the galactose elimination capacity test (r = -0.657 and r = -0.551), thus suggesting that phenylalanine, tyrosine, and free tryptophan may be considered indexes of liver dysfunction in non-comatose cirrhotics.
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PMID:Plasma amino acids as markers of liver dysfunction in cirrhotics. 732 2

The pathogenesis of the uraemic polyneuro-encephalopathy is unclear. Among the many possible factors also accumulations of certain medium molecule fractions of peptides and disturbances of the tryptophan metabolism shall play a role. Of 8 deceased conservatively treated uraemics and 4 patients of the chronic haemodialysis programme with a dementia of dialysis serum and postmortally got cerebrospinal liquor underwent a medium molecule fractioning. While in the liquor of normal persons no medium molecules could be proved, these substances were found in the liquor of uraemics in a nearly serum-identical pattern with clearly reduced concentrations. First of all their provenience by a toxically injured blood liquor barrier is to be explained. In contrast to the control values only conservatively treated uraemics showed significantly increased tryptophan concentrations in the liquor. However, the tryptophan concentrations of the patients with dementia were within the normal area.
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PMID:[Analysis of middle molecules in the cerebrospinal fluid of uremic patients]. 734 20

Neuropsychological status, as assessed by trailmaking test; plasma amino acids, and ammonia, were studied in 54 cirrhotics without clinical evidence of encephalopathy to determine the prevalence of subclinical mental dysfunction and its relationship to metabolic abnormalities. Control values for psychometric performance were established in 54 normal subjects matched for age, sex, educational level, and employment status. Of these subjects, 16 were also used as controls for fasting ammonia and plasma amino acids. Eighteen cirrhotics (33%) showed impaired performances of the psychometric test; free tryptophan and the ratio free tryptophan to neutral amino acids were increased in 37% and 62% of cases and correlated with the psychometric scores (r = 0.45 and r = 0.70, respectively). In eight cirrhotics with mild encephalopathy, psychometric and metabolic evaluations were repeated several times during the infusion of amino acid solutions rich in branch-chain amino acids. Again significant correlations were observed between the psychometric scores and plasma amino acids. We conclude that a considerable proportion of clinically normal cirrhotics have neuropsychological deficits. The severity of impairment may be related to the plasma amino acid imbalance, namely to an increased passage of tryptophan across the blood-brain barrier.
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PMID:Prevalence of subclinical hepatic encephalopathy in cirrhotics and relationship to plasma amino acid imbalance. 742 85

Quinolinic acid is an excitatory, neurotoxic tryptophan metabolite proposed to play a role in the pathogenesis of hepatic encephalopathy. This involvement was investigated in rat and rabbit models of fulminant hepatic failure at different stages of hepatic encephalopathy. Although plasma and brain tryptophan levels were significantly increased in all stages of hepatic encephalopathy, quinolinic acid levels increased three-to sevenfold only in the plasma, CSF, and brain regions of animals in stage IV hepatic encephalopathy. Plasma-CSF and plasma-brain quinolinic acid levels in rats and rabbits with fulminant hepatic failure were strongly correlated, with CSF and brain concentrations approximately 10% those of plasma levels. Moreover, there was no significant regional difference in brain quinolinic acid concentrations in either model. Extrahepatic indoleamine-2,3-dioxygenase activity was not altered in rats in stage IV hepatic encephalopathy, but hepatic L-tryptophan-2,3-dioxygenase activity was increased. These results suggest that quinolinic acid synthesized in the liver enters the plasma and then accumulates in the CNS after crossing a permeabilized blood-brain barrier in the end stages of liver failure. Furthermore, the observation of low brain concentrations of quinolinic acid only in stage IV encephalopathy suggests that the contribution of quinolinic acid to the pathogenesis of hepatic encephalopathy in these animal models is minor.
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PMID:The relationship between plasma and brain quinolinic acid levels and the severity of hepatic encephalopathy in animal models of fulminant hepatic failure. 776 40

Fourteen patients with Borrelia burgdorferi infection were investigated for possible abnormalities of tryptophan and neopterin metabolism. Four patients (2 were investigated before therapy, 2 when therapy had been already started) had acute Lyme neuroborreliosis, and 10 patients were investigated months to years after an acute infection. Increased concentrations of neopterin and of the tryptophan-degradation product, L-kynurenine, were detected in the cerebrospinal fluid of patients with acute Lyme neuroborreliosis; one patient presented with subnormal tryptophan. Similar but less marked changes were seen in the treated patients and in some of the patients with Lyme encephalopathy. No such abnormalities were seen in the serum of the patients. The data indicate a role of the immune system and particularly of endogenously formed cytokines, like interferon-gamma and tumour necrosis factor-alpha, effecting tryptophan and neopterin metabolism in patients with acute Lyme neuroborreliosis.
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PMID:Neopterin production and tryptophan degradation in acute Lyme neuroborreliosis versus late Lyme encephalopathy. 786 24


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