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)

Helicobacter pylori infection is being correlated to a number of human diseases, among which also those of the liver. From a clinical point of view, 4 "areas of interest" for the suggested correlation can be identified: 1. Helicobacter pylori and portal hypertension-related congestive gastropathy in cirrhotics. There are, in the literature, at least 7 studies confirming that the microorganism has no role in causing or worsening the disease. 2. Helicobacter pylori and duodenal ulcer in cirrhotic patients. Apparently, in the cirrhotic patient, the microorganism has no role in causing duodenal ulcer. 3. Helicobacter pylori, ammonia production and hepatic encephalopathy. In this case, there are at least three studies showing that Helicobacter pylori infection increases the risk of developing encephalopathy in the cirrhotic patient, this being a somewhat expected finding. 4. Helicobacter pylori infection in chronic liver disease and its diagnosis. Evidence in the literature suggests: a) that hypertensive gastropathy might not represent a favourable environment for Helicobacter pylori thus making the diagnostic sensitivity of the biopsy lower than expected, and b) that even serological diagnosis might provide data of difficult interpretation, as shown in non alcoholic cirrhosis and, by our own group, in primary biliary cirrhosis. More intriguing are the data generated with respect to the potential capacity of Helicobacter pylori and Helicobacter pylori-like bacteria such as, in particular, Helicobacter hepaticus to damage the liver by producing toxins with a granulating effect on liver cell lines which, in vivo, through the portal tract, might reach the liver, thus causing hepatocellular damage. The point has been addressed by a number of investigators and autoimmune mechanisms have also been suggested. In summary, from the clinical point of view, some evidence suggests that Helicobacter pylori infection might be relevant in the pathogenesis of hepatic encephalopathy in cirrhosis. The data being generated with respect to a direct hepatotoxicity are, at present, stimulating but only speculative.
 ...
PMID:Helicobacter pylori and the liver: any relationship? 961 80

Increased plasma and CSF concentrations of substances which bind to brain benzodiazepine receptors have previously been reported in cirrhotic patients with hepatic encephalopathy (HE). However, their relationship to previous intake of pharmaceutical benzodiazepines has not been clearly established. In the present study, plasma levels of benzodiazepine receptor ligands (BZRLs) were measured using a sensitive radioreceptor assay in 12 control subjects with no evidence of hepatic, neurological or psychiatric illness, 11 cirrhotic patients without HE, 24 cirrhotic patients with moderate (grade I-II) HE and in 45 cirrhotic patients with severe (grade II-IV) HE. In addition, CSF concentrations of BZRLs were measured in 8 cirrhotic patients with HE and an equal number of age-matched controls. Recent intake (within 10 days) of pharmaceutical benzodiazepines was assessed by detailed review of medical files, and interviews with the patient, at least one family member as well as the pharmacist. Significantly increased plasma concentrations of BZRLs were observed in cirrhotic patients with severe encephalopathy (p < 0.02) compared to controls and to cirrhotic patients without (or with mild) neurological impairment. Increased plasma BZRLs could be accounted for by prior exposure to benzodiazepine medication in all cases. CSF concentrations of BZRLs in cirrhotic patients were not significantly different from control values. These findings do not support a role for "endogenous" benzodiazepines in the pathogenesis of HE in chronic liver disease but suggest that pharmaceutic benzodiazepines administered to cirrhotic patients as sedatives or as part of endoscopic work-up could have contributed to the neurological impairment in some patients.
 ...
PMID:Plasma and CSF benzodiazepine receptor ligand concentrations in cirrhotic patients with hepatic encephalopathy: relationship to severity of encephalopathy and to pharmaceutical benzodiazepine intake. 980 65

Cirrhosis of the liver results from a variety of mechanisms that cause progressive hepatic injury. It is the sixth leading cause of death in all patients between the ages of 35 and 55. This study attempts to correlate the morbidity and mortality of spontaneous bacterial peritonitis in liver failure patients to numerous etiologic and clinical variables. A retrospective review of 26 patients with spontaneous bacterial peritonitis associated with chronic liver disease was performed in a university hospital. Demographics (age and gender), clinical variables (etiology of liver failure, Child's classification, prior history of ascites, fever, abdominal pain, encephalopathy, and upper gastrointestinal hemorrhage), and laboratory variables (ascitic polymorphonuclearcyte count and cultures, serum albumin, bilirubin, creatinine, and prothrombin time) were studied. All of the patients had Child's C liver disease. Mortality rate was 46 per cent. Alcohol (46%) and hepatitis (30%) were the most common etiologies. Escherichia coli and Klebsiella pneumoniae were the most common culture isolates. All of the infections were monomicrobial. The only significant predictor of mortality (P < 0.05) in this study was the peritoneal fluid polymorphonuclear (PMN) cell count. PMN count >1000 PMN/mm3 was associated with a mortality of 88 per cent. Few patients with spontaneous bacterial peritonitis are ultimately transplanted.
 ...
PMID:Spontaneous bacterial peritonitis in liver failure. 984 34

Scintigraphy with 99mTc-diethylenetriaminepentaacetate with galactosyl human serum albumin (99mTc-GSA) and per-rectal portal scintigraphy are useful for evaluating hepatic functional reserve and portal circulation, respectively. We did the procedures simultaneously in some patients to examine the relationship between hepatic functional reserve and portal circulation in chronic liver disease. Scintigraphy with 99mTc-GSA was done in 10 healthy subjects, 45 patients with chronic hepatitis, and 165 patients with cirrhosis. Fifty-seven patients (13 with hepatitis and 44 with cirrhosis) also underwent per-rectal portal scintigraphy with 99mTc-pertechnetate within two weeks. A receptor index was calculated by dividing the radioactivity of the liver region of interest (ROI) by that of the liver-plus-heart ROI at 15 min after the injection of 99mTc-GSA. The index of blood clearance was calculated by dividing the radioactivity of the heart ROI at 15 min by that of the heart ROI at 3 min. A solution containing 99mTc-pertechnetate was instilled into the rectum, and serial scintigrams were taken while radioactivity curves for the liver and heart were recorded sequentially. A per-rectal portal shunt index was determined by calculating the ratio of counts for the liver to counts for the heart integrated for 24 seconds immediately after the appearance of the liver time-activity curve. The median receptor index was lower for more severe liver disorders, increasing in the order of chronic hepatitis, compensated cirrhosis and decompensated cirrhosis, and the median index of blood clearance was higher. The median receptor index was significantly lower when a complication (varices, ascites, or encephalopathy) was present, and the median index of blood clearance was higher. The shunt index was correlated significantly with the two other indices, but these values for some one-third of the patients disagreed in either indices. Scintigraphy with 99mTc-GSA and per-rectal portal scintigraphy with 99mTc-pertechnetate are both needed for accurate assessment of the severity of chronic liver disease before treatment-making decisions, because in some patients, results are not correlated.
 ...
PMID:Clinical need for both scintigraphy with technetium-99m GSA and per-rectal portal scintigraphy in some patients with chronic liver disease. 1051 Aug 80

The autoregulation of cerebral blood flow (CBF) is impaired in patients with end-stage liver disease and encephalopathy. These patients are vulnerable to sudden deterioration of cerebral perfusion and oxygenation during liver transplantation. We compared CBF and metabolism during liver transplantation without venovenous bypass and 24 hours postoperatively in 9 patients with acute liver failure (ALF) and 16 patients with chronic liver disease. A fiberoptic catheter was inserted cranially through the left internal jugular vein for determination of jugular venous oxygen saturation, cerebral oxygen extraction ratio (COER), lactate level, and neuron-specific enolase (NSE) level. Arterial concentrations of lactate were also measured. Flow velocity in the middle cerebral arteries was monitored bilaterally using transcranial Doppler sonography. Mean flow velocity and pulsatility index (PI) were regarded as indicators of intracranial pressure. Core body temperatures were recorded. Mild hyperventilation, perioperative hemofiltration, and N-acetylcysteine infusion were used according to our clinical practice. NSE level was greater in acute patients at the end of surgery (P <.05), but not 24 hours later. Lactate concentrations were greater in patients with ALF (P <.001) preoperatively and intraoperatively but were similar in both groups 24 hours postoperatively. There was no difference between arterial and jugular venous concentrations of lactate. Changes in blood flow velocity, PI, and COER were parallel and without statistical significance between the groups. The patients' core temperature did not correlate with CBF, NSE level, or clinical outcome. Caval clamping was well tolerated in both patient groups.
 ...
PMID:Cerebral blood flow and oxygenation in liver transplantation for acute or chronic hepatic disease without venovenous bypass. 1091 71

Lidocaine (LID) is an aminoethylamide used in hepatology to perform the monoethylglycinexylidide (MEGX) test for the evaluation of liver function in patients with cirrhosis (CIR) or chronic hepatitis (CH). The authors evaluated whether the MEGX test changes psychometric performance in patients with chronic liver disease and, in particular, whether it might trigger subclinical portosystemic encephalopathy in patients with CIR. Thirty patients with CIR and 20 patients with CH were studied. They underwent a standard-dose MEGX test, before and after which a psychometric test was administered and blood pressure, heart rate, and adverse effects were recorded. The MEGX test did not modify psychometric performance. Mean arterial blood pressure and heart rate did not change at the end of the MEGX test in either patients with CH or CIR. Adverse effects were present in 66% of all patients during lidocaine injection and lasted up to 3 minutes afterwards. They were more frequent in patients with CH than in patients with CIR (85% vs 53%). No relationship was found between adverse effects and lidocaine dosage, nor between adverse effects and MEGX or lidocaine concentration at 15 minutes. Standard-dose MEGX test does not worsen or trigger portosystemic encephalopathy in CIR. Adverse effects were frequent but mild.
 ...
PMID:The monoethylglycinexylidide test does not impair psychometric performance in patients with chronic hepatitis or cirrhosis. 1094 73

Most of the care of liver disease in alpha(1)-antitrypsin (alpha(1)-AT) deficiency involves supportive management for complications of chronic liver disease including gastrointestinal bleeding, ascites, edema, encephalopathy, coagulation disturbances, spontaneous bacterial peritonitis, and hepatorenal syndrome. Some of these patients will have manifestations of cholestatic injury, including pruritus, hypercholesterolemia, and steatorrhea with fat-soluble vitamin deficiencies. The major challenge for the clinician taking care of these patients is the timing of referral for liver transplantation therapy. Timing of such referral is a relatively straightforward decision in alpha(1)-AT-deficient patients with progressive liver dysfunction. Some patients have nonprogressive or slowly progressing liver disease even after the development of cirrhosis or portal hypertension. Timing of liver transplantation in these patients should not be based simply on the presence of cirrhosis, portal hypertension or mild liver synthetic dysfunction, but rather on the basis of a subjective judgment by the hepatologist, patient, and family that manifestations of liver disease are interfering with overall life functioning.
 ...
PMID:Alpha(1)-Antitrypsin Deficiency. 1109 5

The purpose of this study was to determine the intracellular pH of the whole head and in voxels localized to the basal ganglia in patients with chronic liver disease using phosphorus-31 magnetic resonance spectroscopy (31P MRS). The study group compromised 82 patients with biopsy-proven cirrhosis (43 Child's grade A, 25 Child's grade B and 14 Child's grade C). Eleven subjects showed no evidence of neuropsychiatric impairment on clinical, psychometric and electrophysiological testing, 37 showed evidence of minimal hepatic encephalopathy and 34 had overt hepatic encephalopathy. Unlocalized 31P MRS of the whole head was performed in 48 patients and 10 healthy volunteers. Localized 31P MRS of the basal ganglia was performed in the 34 patients and in 20 healthy volunteers. The intracellular pH values were calculated from the chemical shift difference between the inorganic phosphate (P) and phosphocreatine (PCr) resonances. The percentage inorganic phosphate (%Pi), phosphocreatine (%PCr) and betaNTP signals, relative to the total 31P signal, and peak area ratios of inorganic phosphate and phosphocreatine, relative to betaNTP were also measured. There were no differences between patients and volunteers in intracellular pH in 31P MR spectra measured from the whole head or the basal ganglia. There was no correlation between the severity of encephalopathy (West Haven criteria) or liver dysfunction (Child score) and intracellular pH values. There was also no significant change in the inorganic phosphate, phosphocreatine or betaNTP resonances in spectra acquired from the whole head. However, in spectra localized to the basal ganglia, there was a significant increase in mean P/NTP (p=0.02) and PCr/NTP (p=0.009). The mean %Pi and mean %PCr were also increased (p=0.06; p=0.05, respectively), but there was no significant change in mean %betaNTP. When the patient population was classified according to the severity of encephalopathy, those with overt disease had a higher mean P/NTP and %Pi (p=0.03; p=0.01), compared to the reference population. Our results suggest that there are detectable bioenergetic abnormalities in patients with minimal hepatic encephalopathy or stable, overt chronic hepatic encephalopathy, but any associated intracellular pH change is probably a secondary, rather than a primary phenomenon.
 ...
PMID:Intracellular pH measurements of the whole head and the basal ganglia in chronic liver disease: a phosphorus-31 MR spectroscopy study. 1120 91

Portal hypertension is a common clinical syndrome with chronic liver diseases and is characterised by a pathological increase in portal pressure. Moreover, portal hypertension is associated with increased portal blood flow. Increased vascular resistance in portal hypertension is because of an increase in both intrahepatic and portosystemic collateral resistance. Chronic elevations in systemic and splanchnic blood flow have been documented as key elements of hyperdynamic circulatory state of hypertensive animals and humans. Peripheral vasodilatation initiates the development of the classic profile of decreased systemic elevated splanchnic blood flow and elevated cardia index that characterises this state. Portosystemic collaterals develop as a result of portal hypertension. This is the central pathophysiological event that leads to bleeding from oesophagogastric varices and portosystemic encephalopathy. Collateral vessels respond to various vasoconstrictors and vasodilators.--Varices in the distal 5 cm of the distal oesophagus are easily identified by endoscopy because of their superficial location in the lamina propria and therefore are must apt to bleed and why the current practise of endoscopic therapy is likely to be successful in obliterating the varices. In patients with oesophageal varices the dilated deep intrinsic veins displace the superficial venous plexus, assume a supepitheal position and are endoscopically visible as teleangiectasia, cherry red spots, red colour signs, hemocystic spots, red wale markings or varices on varices. As alternative endoscopic way of treatment the paravariceal injection has been propagated by our group thus preserving the pathophysiologic collaterals and preventing early new formation of collaterals and rebleeding. Pathophysiologically the concept of erosion has been abandoned and replaced by the explosion theory: bleeding probably occurs when the expanding force by pressure and flow can no longer be counter-balanced by the variceal wall tension; at this point the varices rupture and bleed. When the varix distension has increased, the radius has increased and the wall thickness decreased. Thus early diagnosis of patients with a high tendency to bleed can easily be made by endoscopy, measuring portal and/or oesophageal-variceal pressure and characteristising the chronic liver disease according to the Child-Pugh-classification.
 ...
PMID:Causes and pathomechanisms of oesophageal varices development. 1120 32

Portal-systemic encephalopathy may be seen with hyperammonemia that complicates chronic liver disease. We report an unusual case of reversible parkinsonism associated with hyperammonemia and portal vein thrombosis. An active 90-year-old male developed motor slowing and resting hand tremor over 6 months. Examination showed asterixis, bradykinesia, cogwheel rigidity, rest tremor, and a parkinsonian gait. Serum venous ammonia was elevated at 145 microM. The next day, the patient became comatose and serum ammonia was 178 microM. With lactulose therapy, serum ammonia level normalized and examination showed only minimal parkinsonism after 1 week. An abdominal CT scan identified portal vein thrombosis with porto-systemic shunting that reversed after 7 months of treatment. Examination 2 years later showed no signs of parkinsonism. Parkinsonism can dominate the clinical picture of patients with hyperammonemia before the onset of encephalopathy.
 ...
PMID:Reversible parkinsonism and hyperammonemia associated with portal vein thrombosis. 1124 May 69


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>