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 authors studied the content of nucleic acids in the tissues (the skeletal muscle and myocardium, the liver) in albino rats with toxic affection of the liver caused by ccl4, in protein deficiency and parental administration of amino acid mixture of moriamin S-2 and "improved" caseine hydrolysate. Protein deficiency in albino rats with toxic hepatitis was accompanied by a considerable increase of RNA and DNA in the skeletal muscle and the myocardium with a simultaneous reduction of their level in the liver. The RNA/DNA ratio changed. The RNA content in the hepatocytes diminished on account of reduction of the nuclear RNA fraction closely bound with chromatin. Parenteral administration of nitrogen preparations led to normalization of the nucleic acid content in all the tissues under study.
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PMID:[Nucleic acids in the tissues of white rats with toxic liver damage following protein starvation and parenteral nitrogen nutrition]. 9 93

The authors studied the assimilation of nitrogen preparations--moriamin S-2 and "improved" caseine hydrolysate in parenternal administration to 100 albino rats. Healthy animals and those with toxic affection of the liver induced with CCl4 were experimented upon. In healthy animals administration of nitrogen preparations led to the change of negative nitrogen balance into a positive one, normalized the content of blood and tissue amine nitrogen deranged in protein deficiency. Assimilation of nitrogen preparations fell considerably in toxic hepatitis. An 8-day parenteral nutrition failed to change the negative nitrogen balance into positive, and did not eliminate hypoproteinemia; however, it normalized the amine nitrogen concentration in the blood and tissues.
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PMID:[Anabolic effectiveness of nitrogenous preparations for parenteral nutrition in the presence of toxic liver damage]. 9 94

The nitrogen metabolism in rats with toxic affection of the liver caused by administration of CCl4 was studied as affected by the amino acid mixture moriamine S-2. It is established that with toxic hepatitis the nitrogen metabolism is sharply disturbed, especially during protein deficiency. The following evidences for this fact: a rise in the depth of the nitrogen negative balance, an increase in the intensity of amine nitrogen and ammonia excretion with urea as well as an increase in the amount of amine nitrogen in blood and tissues with a simultaneous decrease in the content of protein. The parenteral administration of the amino acid mixture for eight days to the animals with a toxic affection of the liver is more effective when nitrogen preparation is combined with the group B vitamin, vitamin C, insulin, nerobolyl and sirepar.
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PMID:[Correction of nitrogen metabolism in rats with toxic hepatitis by parenteral administration of an amino acid mixture]. 42 34

Severe, often fatal liver damage results from extreme overdosage with acetaminophen. In usual dosage, it is considered harmless. We describe three cases of toxic hepatitis associated with the chronic ingestion of excessive doses of acetaminophen. Each patient took approximately 5 to 8 g of acetaminophen per day during a period of several weeks. The transient elevations of serum hepatocellular enzyme concentrations and the histologic evidence of a toxic hepatitis suggest the liver damage was related to the use of acetaminophen. Alcohol abuse in one patient and negative nitrogen balance in another may have increased the susceptibility to acetaminophen toxicity. With the increasing popularity of acetaminophen for mild pain relief, hepatotoxicity from acute or chronic ingestion may be more common than previously recognized, especially in those patients with predisposing conditions.
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PMID:Chronic excessive acetaminophen use and liver damage. 90 Jun 73

Nitrate balance and N-nitrosodimethylamine (NDMA) excretion were studied in woodchucks chronically infected with woodchuck hepatitis virus (WHV). Twenty-four-h urinary recovery of a bolus dose of [15N]nitrate was 54 +/- 12% in woodchucks. WHV-infected animals formed 3-fold more nitrate endogenously than did control animals (P less than 0.01). Treatment of WHV-infected animals with Escherichia coli lipopolysaccharide increased nitrate excretion 15-fold, while uninfected animals increased nitrate excretion 4-fold. The endogenous formation of NDMA was higher in WHV-infected woodchucks than in uninfected controls. After administration of L-[15N2]arginine, [15N]nitrate, and [15N]NDMA were detected in urine indicating that arginine is a precursor of biosynthesized nitrate and the hepatocarcinogen NDMA. NDMA probably results from the formation of nitrosating agents during the oxidation of arginine to oxides of nitrogen and citrulline. Woodchucks chronically infected with WHV develop hepatocellular carcinomas with high frequency. Our observations suggest an additional mechanism that may be involved in the pathogenesis of hepatocellular carcinoma associated with chronic WHV infection.
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PMID:Elevated formation of nitrate and N-nitrosodimethylamine in woodchucks (Marmota monax) associated with chronic woodchuck hepatitis virus infection. 185 9

The outbreak of wasting disease of nude mice occurred in the laboratory colony of a Pharmaceutical Company. The viruses producing cytopathic effect with syncytium formation were isolated from the wasted nude mice by DBT cells, and were identified as mouse coronavirus by direct immunofluorescence. The nude mouse colony was closed and all the nude mice (about 500) were killed by the reason of disease control. At autopsy about 60% of nude mice showed necrotic hepatitis. By the virus isolation to see the source of contamination, viruses were isolated from the feces of apparently healthy mice of ICR, CDF1, DBA/2 and C3H, and from human cancer cell line stocked in liquid nitrogen. In experimental infection, the isolates produced only mild hepatitis in ICR mice treated with cortisone. By cross-neutralization test, the nude isolate reacted closely with the virus from C3H mice but not with the virus from cancer cell line. The isolates from nude and C3H mice produced experimentally wasting disease with necrotic hepatitis in nude mice. These findings suggest that wasting disease in nude mice might be caused by low-virulent mouse coronavirus shed in feces from C3H mice introduced before the outbreak of disease.
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PMID:Natural infection of nude mice with low-virulent mouse coronavirus. 196 24

The raw carp bile has both nephrotoxic and hepatotoxic effects which are not well known. Recently, we studied 13 patients who had toxic acute renal failure and toxic hepatitis after ingestion of raw bile of carp in 3, grass carp in 8 and silver carp in 2 cases. The purpose of this report is to alert physicians to this very rare cause of toxic acute renal failure and hepatitis. All patients presented initially with gastrointestinal upset after eating. These symptoms were followed by oliguria in 7 patients (54%), hematuria was noted in 10 (77%) and jaundice in 8 patients (62%). Elevation of blood urea nitrogen, creatinine and transaminases lasted for about 3 weeks. The severity of the symptoms depended on the amount of bile ingested. All the patients recovered with conservative therapy and hemodialysis. Biopsy of the kidney revealed findings compatible with acute tubular necrosis similar to that produced by other nephrotoxins. Biopsy of the liver revealed findings consistent with acute toxic hepatitis. Both suggest toxic effects of carp bile as a cause of toxic acute renal failure and hepatitis.
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PMID:Toxic acute renal failure and hepatitis after ingestion of raw carp bile. 224 75

We studied cell-mediated cytotoxicity to hepatitis A virus-infected cells in seven patients with acute type A hepatitis and two controls. Skin fibroblast cultures obtained from the skin biopsies of seven patients after acute hepatitis A virus infection and from two persons without history of current or past hepatitis A virus infection were inoculated with hepatitis A virus. Infection of fibroblast cultures always resulted in an inapparent, persistent infection with production and release of infectious hepatitis A virus. Peripheral blood lymphocytes were collected from the same patients at different times after onset of icterus and were stored in liquid nitrogen. Cytolytic activity of peripheral blood lymphocytes was determined by a microcytotoxicity assay using autologous 51Cr-labeled hepatitis A virus-infected and uninfected target cells. Cytotoxic peripheral blood lymphocytes capable of lysing autologous hepatitis A virus-infected skin fibroblasts were detected in all patients with hepatitis A but were not demonstrable in the controls without antibodies against hepatitis A virus. The clinical course of the hepatitis A virus infection was normal in five patients; and in these patients, cytolytic activity of peripheral blood lymphocytes against hepatitis A virus-infected autologous targets peaked 2 to 3 weeks after onset of icterus. A clinically protracted form of the disease with persistent elevation of aminotransferases for at least 5 months after onset was present in two patients. In these cases, the highest cytolytic activity was demonstrated in peripheral blood lymphocytes collected 8 to 12 weeks after onset of icterus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cell-mediated cytotoxicity in hepatitis A virus infection. 302 69

Soluble interleukin 2 receptors (sIL 2R) in the sera of patients with viral liver diseases were quantified with a solid-phase enzyme immunoassay using two monoclonal antibodies against the receptors. The sIL 2R levels in patients with acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma were significantly higher than those in control subjects. In acute hepatitis patients, the high levels of sIL 2R observed during the florid stage returned to normal during remission. Levels in patients with chronic active hepatitis were significantly higher than in those with chronic persistent and lobular hepatitis, and levels observed during the exacerbation phase of chronic hepatitis were higher than they were during remission. Thus, in chronic hepatitis, sIL 2R levels increased in proportion to the inflammatory activity, and correlated well with serum transaminase (glutamic oxaloacetic transaminase: SGOT, glutamic pyruvic transaminase: SGPT) activities, but not with blood urea nitrogen or creatinine concentrations. In patients with a high degree of focal and piecemeal necrosis, serum sIL 2R levels increased further during recombinant interleukin 2 therapy. In post-hepatitic liver cirrhosis and hepatocellular carcinoma, sIL 2R levels correlated with serum cholinesterase and creatinine concentrations, but not with transaminase activities. Measurement of serum sIL 2R levels in patients with liver disease but without renal injury, may help in the diagnosis of inflammation in hepatitis, a process in which interleukin 2 may participate.
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PMID:Increased serum soluble interleukin 2 receptor levels in patients with viral liver diseases. 306 11

Hospitalized patients with hepatic insufficiency often suffer from severe catabolic states and are in urgent need of nutritional support during their acute illness. Protein intolerence, however, remains a significant problem with respect to the provision of adequate nutrition, either enterally or parenterally. The following report is an anecdotal series of 63 consecutive patients in a large urban hospital treated prospectively with nutritional support using a prototype high branched-chain amino acid solution (FO80) given by technique of total parenteral nutrition by the subclavian or internal jugular route with hypertonic dextrose. Sixty-three patients, of which 42 had chronic liver disease (cirrhosis) with acute decompensation and 17 with acute hepatic injury as well as four with hepatorenal syndrome, are the subject of this report. All required intravenous nutritional support and were either intolerant to commercially available parenteral nutrition solutions or were in hepatic encephalopathy at the time they were initially seen. The cirrhotic patients had been hospitalized for a mean of 14.5 +/- 1.9 days before therapy, had a mean bilirubin of 13 mg/100 ml, and had been in coma for 4.8 +/- 0.7 days despite standard therapy. Patients with acute hepatitis had been in the hospital for 16.2 +/- 4.1 days before therapy, had a mean bilirubin of 25 mg/100 ml, and had been in coma 5.2 +/- 1.6 days before therapy. Routine tests of liver function, blood chemistries, amino acids, EEGs, and complex neurological testing including Reitan trailmaking tests were used in the evaluation of these patients. Up to 120 grams of synthetic amino acid solution with hypertonic dextrose was tolerated in these patients with improvement noted in encephalopathy of at least one grade in 87% of the patients with cirrhosis and 75% of the patients with hepatitis. Nitrogen balance was achieved when 75 to 80 grams of synthetic amino acids were administered. Survival was 45% in the cirrhotic group and 47% in the acute hepatitis group. Encephalopathy appeared to correlate with individual amino acids differentially in the various groups and with the ratio between the aromatic and the branched-chain amino acids. Ammonia did not correlate with either the degree of encephalopathy or improvement therefrom. In 24 Patients therapy for hepatic encephalopathy was limited to infusion of the branched-chain enriched amino acid solution only, with wake-up in 66% of this group. The results strongly suggest that in protein intolerant patients requiring nutritional support, infusion with branchedchain enriched amino acid solutions is well tolerated with either no worsening of or improvement in hepatic encephalopathy coincident with the achievement of nitrogen equilibrium and adequate nutritional support.
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PMID:Infusion of branched-chain enriched amino acid solution in patients with hepatic encephalopathy. 628 73


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