Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 59 patients with respiratory insufficiency due to chronic obstructive pulmonary disease (COPD) the relationship between the state of consciousness, the blood gases and blood ammonia were studied. Interindividually, a significant correlation was found between the encephalopathy and SaO2, PaCO2 or ammonia, and also between the blood gases and ammonia. On the other hand, an intraindividual study, performed on patients with minor cerebral dysfunction, showed that only PaCO2 was significantly correlated with the stage of consciousness. Ammonia did not appear to have a neurotoxic influence. The ammonia level seemed to be influenced primarily by other factors than the blood gases, although there was a borderline influence of SaO2 on aterial ammonia and a significant influence of PaCO2-HCO3 and pH on venous ammonia.
 ...
PMID:Respiratory failure: correlation between encephalopathy, blood gases and blood ammonia. 0 6

The cyclotron-produced radionuclide, 13N, was used to label ammonia and to study its metabolism in a group of 5 normal subjects and 17 patients with liver disease, including 5 with portacaval shunts and 11 with encephalopathy. Arterial ammonia levels were 52-264 micron. The rate of ammonia clearance from the vascular compartment (metabolism) was a linear function of its arterial concentration: mumol/min = 4.71 [NH3]a + 3.76, r = +0.85, P less than 0.005. Quantitative body scans showed that 7.4 +/- 0.3% of the isotope was metabolized by the brain. The brain ammonia utilization rate, calculated from brain and blood activities, was a function of the arterial ammonia concentration: mumol/min per whole brain = 0.375 [NH3]a - 3.6, r = +0.93, P less than 0.005. Assuming that cerebral blood flow and brain weights were normal, 47 +/- 3% of the ammonia was extracted from arterial blood during a single pass through the normal brains. Ammonia uptake was greatest in gray matter. The ammonia utilization reaction(s) appears to take place in a compartment, perhaps in astrocytes, that includes less than 20% of all brain ammonia. In the 11 nonencephalopathic subjects the [NH3]a was 100 +/- 8 micron and the brain ammonia utilization rate was 32 +/- 3 mumol/min per whole brain; in the 11 encephalopathic subjects these were respectively elevated to 149 +/- 18 micron (P less than 0.01), and 53 +/- 7 mumol/min per whole brain (P less than 0.01). In normal subjects, approximately equal to 50% of the arterial ammonia was metabolized by skeletal muscle. In patients with portal-systemic shunting, muscle may become the most important organ for ammonia detoxification. Muscle atrophy may thereby contribute to the development of hyperammonemic encephalopathy with an associated increase in the brain ammonia utilization rate.
 ...
PMID:The dynamics of ammonia metabolism in man. Effects of liver disease and hyperammonemia. 42 64

The method of Pattern Flash elicited P300 (PFP300) has been applied to evaluate the dynamic alterations in cognitive function of a 58 year old woman (H. C.) presenting with hepatic failure due to fulminant hepatitis Non-A-Non-B. At the time of the first investigation she complained about slight memory deficits and revealed signs of hepatic encephalopathy grade I according to Parson-Smith et al. (bilirubin 26.0 mg/dl, NH3 102 micrograms/dl, electrolytes and blood sugar normal). Psychometric tests: Number connection test (NCT): 54 s (28-53 s, greater than 2sd); Syndrom-Kurz-Test (SKT): total score = 9 (0-4), compatible with a slight "organic brain syndrome". PFP300: N250 latency 343.5 ms (276.4 +/- 14.7 ms, greater than 4sd); PFP300-latency: 442.5 ms (326.9 +/- 14.7, greater than 7sd); PFP300 amplitudes: 16.0 microV (14.4 +/- 8.4, +/- 1sd), indicating severe disturbance in visual discrimination without visual attention deficits. Due to progressive deterioration of liver function the patient had to undergo orthotopic liver transplantation. The patient was reinvestigated four weeks later. The clinical and laboratory status were normal and no signs of hepatic encephalopathy could be detected clinically or by means of the psychometric tests. The parameters of the PFP300 complex had also completely returned to normal: N250-latency: 273.0 ms (less than 1sd); PFP300-latency: 348.0 ms (less than 1sd). This observation suggests that the analysis of P300 can help to detect and follow minor cognitive deficits in cases of acute hepatic encephalopathy. It further underscores the hepatic etiology as well as the potential reversibility of this type of encephalopathy.
 ...
PMID:[Visual P300 in acute hepatic encephalopathy resulting from non-A-non-B fulminant hepatitis: analysis of the course before and after orthotopic liver transplantation]. 178 89

One year prospective study of 25 cirrhotic patients with portal systemic encephalopathy (PSE) admitted to the Emergency Care Centre in Belgrade was performed in order to investigate the significance of clinical, biochemical and electroencephalographic (EEG) parameters and blood ammonia in the diagnosis, differential diagnosis and prognosis of PSE. 15 cirrhotic patients without PSE (of comparable age, sex, duration and etiology of liver cirrhosis) constituted the control group. Ammonia levels were elevated in 84% of patients with PSE (112 +/- 72 mumol/l) and reached normal range within 3 +/- 0.44 days, but with no correlation to clinical improvement (p greater than 0.1). Ammonia levels correlated with the severity of PSE (p less than 0.05), but not with other biochemical parameters (prothrombin time, bilirubin, albumin, urea, creatinine, potassium). Overall mortality was 44% and was strongly correlated (p less than 0.01) to the severity of PSE. In addition, the mortality in patients with gastrointestinal bleeding and PSE was higher (p less than 0.05), than in PSE precipitated by other conditions. We concluded that the ammonia may be a primary diagnostic parameter for PSE in the absence of the most important diagnostical methods (EEG, psychometric tests). Secondly, ammonia are of great diagnostic importance in patients with coma of unknown origin and can help in deciding admission priorities. The ammonia levels do not appear to be a useful prognostic factor.
 ...
PMID:[Ammoniemia in portosystemic encephalopathy--diagnostic, differential diagnostic and prognostic significance]. 207 39

Nutritional support in patients with advanced cirrhosis is difficult due to protein, fluid and salt restrictions. Successful liver transplantation should improve nutrient tolerance. We randomly assigned 28 hypoalbuminemic cirrhotic patients to receive, immediately after liver transplantation, one of three regimens: group 1, no nutritional support (n = 10); group 2, total parenteral nutrition (TPN) (35 kcal/kg/day) with standard amino acids (1.5 g/kg/day) (n = 8); or group 3, isocaloric isonitrogenous TPN with added branched-chain amino acids (n = 10). Therapy was continued for 7 days posttransplant. Jaundice resolution was unaffected by nutritional support. Nitrogen balance favored both TPN groups. Branched-chain amino acid (BCAA) aromatic amino acid ratios were highest in group 3. Coma scores and serum ammonia levels were similar in all groups. Both TPN groups achieved respirator independence earlier; this difference was not statistically significant. Group 1 patients stayed longest in ICU; the difference was statistically significant. TPN with either standard or BCAA- enriched amino acids is tolerated well immediately after successful liver transplant. Positive nitrogen balance is achieved; large protein loads do not worsen encephalopathy. Nutritional support may improve respiratory muscle function, allowing earlier weaning from ventilatory support. A shortened length of ICU stay justifies the expense of TPN.
 ...
PMID:Nutritional support after liver transplantation: a randomized prospective study. 179 69

Cerebral blood flow (CBF), measured by the non-invasive 133-Xenon inhalation method, plasma levels of ammonia (NH3) and free tryptophan (fTRP) were determined in 30 cirrhotic patients without overt encephalopathy. Psychometric evaluation detected subclinical hepatic encephalopathy (SHE) in 20 of them, and was normal in the other 10. A significant CBF difference (p less than 0.05) was found between the SHE and the non-SHE patients. fTRP levels were significantly (p less than 0.05) higher in patients with SHE than in those without SHE, and a significant negative correlation (p = 0.003) was found between CBF values and fTRP in the whole group of patients. NH3 did not differ in the two subgroups and did not correlate with CBF values. It is concluded that CBF could have some implications in SHE, although its relevance is still unclear. The negative correlation between CBF and fTRP prompts further investigation concerning the relationships between plasma fTRP, brain serotonin, cerebral metabolism and blood flow in the development of brain derangement during cirrhosis.
 ...
PMID:Cerebral blood flow and plasma free tryptophan in cirrhotics with and without hepatic encephalopathy. 279 14

Ammonia intoxication allegedly plays a significant role in the pathophysiology of hepatic encephalopathy. In order to understand the pathogenesis of this encephalopathy it is necessary to know the effects of ammonia on the mechanisms by which neurons communicate, i.e., excitatory and inhibitory synaptic transmissions. NH4+ decreases excitatory synaptic transmission mediated by glutamate. Possibly, this effect is related to a depletion of glutamate in presynaptic terminals. NH4+ decreases inhibitory synaptic transmission mediated by hyperpolarizing Cl(-)-dependent inhibitory postsynaptic potentials. This effect is related to the inactivation of the extrusion of Cl- from neurons by NH4+. By the very same action, NH4+ also decreases the hyperpolarizing action of Ca2+- and voltage-dependent Cl- currents. These currents may modify the efficacy of the synaptic input to neurons and increase neuronal excitability. Estimates derived from experimental observations suggest that an increase of CNS tissue NH4+ to 0.5 mumol/g is sufficient to disturb excitatory and inhibitory synaptic transmission and to initiate the encephalopathy related to acute ammonia intoxication. Chronic portasystemic shunting of blood, as in hepatic encephalopathy, significantly changes the relation between CNS NH4+ and function of synaptic transmission. A portacaval shunt increases the tissue NH4+ necessary to disturb synaptic transmission. However, after a portasystemic shunt, synaptic transmission becomes extremely sensitive to any acute increase of NH4+ in the CNS.
 ...
PMID:Synaptic transmission in ammonia intoxication. 281 92

To obtain a more precise pathophysiological evaluation of the role of ammonia in acute hepatic encephalopathy, we compared the plasma ammonia concentrations and electroencephalographic recordings (EEGs) of rabbits with surgically induced acute hepatic failure (AHF, n = 10) and normal rabbits administered an infusion of ammonium acetate (NH4-Ac, n = 7) over a 10-hr period. AHF was surgically induced by portocaval shunting followed by hepatic artery ligation 48 hr later. In the infusion group the dose of NH4-Ac, initially 0.78 mmol/kg/hr, was increased every 2 hr by 0.13 mmole/kg/hr during a 10-hour period to simulate the arterial NH3 concentrations observed in AHF. Ammonia levels in rabbits administered the NH4-Ac infusion were identical to those observed in AHF, with the exception of the higher initial value in the AHF group. Moreover, the mean rates of increase in grade of encephalopathy in the two groups were similar, although the EEG grades in the infusion group were significantly less at all time points. In conclusion, this study demonstrates that a more pathophysiological approach to identification of the putative toxins in hepatic encephalopathy is feasible. Some of the EEG abnormalities of acute hepatic encephalopathy in rabbits are presumably due to hyperammonemia; the encephalopathy observed in AHF at zero time is probably caused by the previously constructed portocaval shunt via an undefined, but possibly also ammonia-related, mechanism.
 ...
PMID:Continuous intravenous ammonia infusion as a model for the study of hepatic encephalopathy in rabbits. 292 62

There is substantial clinical and experimental evidence to suggest that ammonia toxicity is a major factor in the pathogenesis of hepatic encephalopathy associated with subacute and chronic liver disease. Ammonia levels in patients with severe liver disease are frequently found to be elevated both in blood and cerebrospinal fluid (csf). Hepatic encephalopathy results in neuropathological damage of a similar nature (Alzheimer type II astrocytosis) to that found in patients with congenital hyperammonemia resulting from inherited defects of urea cycle enzymes. Following portocaval anastomosis in the rat, blood ammonia concentration is increased 2-fold, and brain ammonia is found to be increased 2-3-fold. Administration of ammonia salts or resins to rats with a portocaval anastomosis results in coma and in Alzheimer type II astrocytosis. Since the CNS is devoid of effective urea cycle activity, ammonia removal by brain relies on glutamine formation. Cerebrospinal fluid and brain glutamine are found to be significantly elevated in cirrhotic patients with encephalopathy and in rats following portocaval anastomosis. In both cases, glutamine is found to be elevated in a region-dependent manner. Several mechanisms have been proposed to explain the neurotoxic action of ammonia. Such mechanisms include: Modification of blood-brain barrier transport; alterations of cerebral energy metabolism; direct actions on the neuronal membrane; and decreased synthesis of releasable glutamate, resulting in impaired glutamatergic neurotransmission.
 ...
PMID:Ammonia: key factor in the pathogenesis of hepatic encephalopathy. 330 79

To assess side effects of propranolol in the treatment of portal hypertension, we measured blood ammonia in 14 cirrhotics before and after administration of propranolol, and in six cirrhotics before and after placebo. We evaluated ammonia blood levels obtained from three sites: venous, arterial, and arterialized-venous, obtained by warming the forearm. Ammonia concentration of arterial and arterialized-venous blood were abnormal for all cirrhotics studied and significantly greater than the ammonia concentration of venous blood (p less than 0.01). When propranolol was administered to patients with alcoholic cirrhosis and marginal liver function, as reflected by ammonia levels above 60 microM, it caused a significant increase in ammonia levels in arterialized-venous and arterial, but not in venous, blood (p less than 0.05). Propranolol caused a significant increase in the time required to perform sensitive psychometric tests (p less than 0.05). Encephalopathy usually became clinically apparent when the mean of the arterial and arterialized-venous blood ammonia levels rose above 122 microM.
 ...
PMID:Venous, arterial, and arterialized-venous blood ammonia levels and their relationship to hepatic encephalopathy after propranolol. 334 27


1 2 3 4 5 6 7 8 Next >>