Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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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

Twenty-eight patients with suspected Reye's syndrome (RS) were seen in our Department from 1974 through 1987. Liver biopsy confirmed the diagnoses of RS and non-icteric fulminant hepatitis (NIFH) in 7 and 5 cases, respectively. NIFH was the most common RS mimicker. Total bilirubin, LDH and serum ammonia levels showed no significant differences between RS and NIFH. However, the levels of serum GOT and GPT were significantly higher in the NIFH group. Serum and urinary carnitine levels were measured in both groups, but the results were inconclusive. Amino acid analysis in one RS and two NIFH patients showed no significant differences in the ratio of branched chain to aromatic amino acids. However, one RS patient showed a high level of lysine. Histological findings in the liver of two NIFH patients showed minor mitochondrial swelling and microvesicular fat, but the major finding was hepatic necrosis. Our experience indicates that NIFH and RS cannot be differentiated by routine laboratory tests. Liver biopsy is essential for the accurate diagnosis of RS.
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PMID:Non-icteric fulminant hepatitis and Reye's syndrome: comparison of laboratory data. 228 22

Spontaneous regression of oesophageal varices in liver cirrhotics without sclerotherapy or shunt operation has only been known in alcoholic cirrhosis after alcohol abstinence. Therefore, 20 liver cirrhotics of different aetiologies were controlled over 13 years (six alcohol, nine hepatitis, five haemochromatosis). Under strict alcohol abstinence, all underwent treatment with lactulose and ammonia-reducing amino acids to improve the urea synthesis in the liver. Since gastrointestinal bleeding was not observed, neither sclerotherapy nor shunt operation were performed. Initially, all patients had oesophageal varices (nine stage III, three stage II-III, eight stage II). Following conservative therapy, eight cirrhotics showed total regression and twelve showed stage I-II. Their Child-Pugh index, and urea synthesis rate improved significantly. Possible causes for the spontaneous regression of oesophageal varices are strict abstinence from alcohol, spontaneous seroconversion in six posthepatic B-cirrhoses and consequent phlebotomy in haemochromatosis.
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PMID:Spontaneous regression of oesophageal varices after long-term conservative treatment. Retrospective study in 20 patients with alcoholic liver cirrhosis, posthepatitic cirrhosis and haemochromatosis with cirrhosis. 205 Oct 8

A 2-month-old boy was admitted to our hospital because of poor sucking and jaundice. There were no abnormalities during the whole period of pregnancy and at birth. His mother was a HBeAb positive HBsAg carrier, but prophylactic maneuver such as anti-HB immunoglobulin and HB vaccine was not performed on him at birth. Physical examination on admission revealed mild disturbance of consciousness. The laboratory findings showed marked increments of serum bilirubin, GOT, GPT, and NH3, and prolongation of prothrombin time, activated partial thromboplastin time and hepaplastin test. Thus, he was diagnosed as fulminant hepatitis and treated with exchange transfusion once or twice a day. Biochemical data improved gradually, but hypocoagulable states remained unchanged. At that time we decided to use Factor VII concentrate, because we found that, among several coagulation factors, factor VII activity decreased most rapidly after exchange transfusion. The alternate therapy of exchange transfusion and Factor VII concentrate improved his coagulation abnormality without any side effects. Our experience suggests that the combination therapy of exchange transfusion and Factor VII concentrate may be useful for management of fulminant hepatitis, particularly for uncontrollable coagulopathy.
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PMID:[Successful treatment of an infant with fulminant hepatitis by factor VII concentrate]. 260 16

Changes in biochemical and electroencephalographic parameters were followed over time during the development of acute hepatic encephalopathy (HE) in two different experimental models. In the rat, (sub)acute liver failure was obtained either by ligation of the hepatic artery in previously portacaval-shunted animals or by intraperitoneal injection of a high dose of galactosamine (GALN). The EEG changes were characterized in both models by a significant increase in low-frequency activity of the EEG power density spectra: the so-called 'left shift'. This 'left shift' was significant in liver ischemia after 4-5 h and in GALN hepatitis after about 30 h. The changes in plasma biochemical indices also showed a great similarity in both models. The concentration of all measured plasma amino acids (except histidine and arginine in GALN hepatitis and arginine in liver ischemia), NH3 and ALAT were significantly increased during the development of (sub)acute HE. Correlation of the combined data of electroencephalographic and biochemical indices showed a significant (P less than 0.01) correlation between the 'left shift' and NH3, taurine, threonine, proline, alanine, methionine, cystathionine, phenylalanine, tryptophan, ornithine and histidine. It is concluded that EEG spectral analysis is a useful parameter for following the development of (sub)acute hepatic encephalopathy in relation to biochemical parameters.
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PMID:Correlation between electroencephalographic and biochemical indices in acute hepatic encephalopathy in rats. 359 63

Alcohol, hepatitis B, and Non A Non B hepatitis were the main aetiologies of 124 patients with hepatic encephalopathy (HE) due to histologically proven liver cirrhosis. All had severe portal hypertension (PH) and usually increased inflammatory activity of the liver. In stage I (n = 27) 7.4% died, in stage II (n = 28) 14.3%, in stage III (n = 32) 50% and in stage IV (n = 37) 94.6%. Even in cirrhotics without PH, serum albumin, cholinesterase activity and prothrombin time (PT) were significantly decreased. But only in the case of PT did the magnitude of the decrease parallel the stage of HE. Hyperammonaemia and serum creatinine were increased in parallel with the stage of HE. Therefore, in liver cirrhosis a quotient derived from decreased PT and increased serum creatinine has a good prognostic value. Early diagnosis of HE is possible on the basis of writing tests and the determination of free or toxic ammonia.
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PMID:The role of protein metabolism in 204 liver cirrhotics with and without hepatic encephalopathy. I. Clinical and general biochemical findings. 372 88

We report the case of a 32 year old man who present two weeks after a typical varicella an alteration of consciousness with pleocytosis in the cerebrospinal fluid and abnormalities of EEG and CT Scan. An hepatic dysfunction with cytolysis and a high level of transaminases and ammonia was noted. About this case the author precise the encephalitic complication of varicella, and the different liver abnormalities, such as Reye's syndrome, hepatitis with parcellar necrosis, or hepatitis with hyperammonemia but without cytolysis or necrosis, as in our own.
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PMID:[Encephalitis and hepatitis after varicella. Relations with Reye's syndrome]. 383 44

We have carried out several basic experiments on artificial liver support and found that the plasma free amino acid balance was lost after treatment according to this procedure. Application of fluid therapy--Using conventional amino acid preparations available on the market--Is not adequate during and after the treatment with artificial liver. Fluid therapy using mainly special amino acid preparations should have been established; preparations, named Todai Hospital fluid (THF), are intended to correct the deranged aminogram, supply nutrition and promote the improvement in symptoms. Furthermore, experimental animals with acute hepatic insufficiency of diverse severity were prepared and basic experiments were performed which these animals to see how the efficacy of THF developed. In the basic experiments, psychoneurotic symptoms and the electroencephalogram were improved with the lowering of the blood ammonia level. Clinically, THF was not only used as a therapeutic agent after treatment by artificial liver support in patients with fulminant hepatitis, but is also served as a further indication in hepatic encephalopathy accompanying chronic liver diseases in late stages. Improvement in encephalopathy was observed immediately after the administration of THF and persisted while the aminogram pattern returned to the premedication representation. There was more improvement in patients in whom ammonemia was complicated, and the blood ammonia level was reduced markedly.
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PMID:[Effect of amino acid solutions on the blood ammonia level]. 408 43

Plasma levels of tyrosine were assayed in the fasting state and after oral administration of either tyrosine (tyrosine tolerance test) or phenylalanine (phenlyalanine conversion test) in normal subjects and in patients with hepatitis, biliary obstruction, or cirrhosis. Fasting tyrosine levels tended to be slightly increased in patients with hepatitis and biliary obstruction and markedly increased in patients with cirrhosis. Tyrosine tolerance tests in patients with cirrhosis were characterized by larger than normal increments in tyrosine levels and by delayed returns toward fasting levels. The results of phenylalanine conversion tests were abnormal in approximately one-half of patients with either hepatitis or biliary obstruction and four-fifths of patients with cirrhosis. Abnormalities were characterized by elevated fasting plasma tyrosine levels, or small and delayed increments in tyrosine levels, or both. Abnormal phenylalanine conversion test results in patients with cirrhosis did not correlate closely with any clinical feature of cirrhosis or with the results of any standard liver function test; there was positive correlation only with abnormal ammonia tolerance, a test of portalsystemic shunting. Tests of tyrosine metabolism do not appear to be useful for routine clinical assessment of liver function. Tyrosine tolerance tests and phenylalanine conversion tests done for purposes of diagnosis of other diseases may yield misleading results in patients with liver disease.
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PMID:Tyrosine metabolism in patients with liver disease. 607 4

Significant elevation of glutamic acid and glutamine concentrations in CSF was observed in hepatic encephalopathic patients with fulminant hepatitis and liver cirrhosis. However, the ratios of CSF glutamic acid to CSF glutamine levels and of CSF to serum glutamic acid and glutamine levels were significantly higher only in cirrhotic patients with hepatic encephalopathy. CSF glutamine levels were positively correlated with blood ammonia and CSF tyrosine levels in cirrhotic patients. The results indicate that CSF glutamic acid and glutamine levels are important tools in diagnosing hepatic encephalopathy in severe liver disease.
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PMID:Glutamic acid and glutamine levels in serum and cerebrospinal fluid in hepatic encephalopathy. 615 Jul 6


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