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)

Boatbuilding is a complex, chemically intensive industry which employs approximately 43,000 workers in the United States, 77% of them in shops with fewer than 20 workers. Boatbuilders and repairers are at high risk of occupational injury from falls, lacerations, low back trauma, repetitive motion, noise, burns, fires, and explosions. Also they are at risk of acute and chronic illness, including dermatitis, toxic hepatitis, peripheral neuropathy, and chronic encephalopathy as a result of their occupational exposures to such materials as styrene, resins, solvents, paints, welding fumes, and coating systems. Boatbuilders also are exposed to toxic woods and to lead. Hazard recognition is the first step toward reduction of injury and disease in boat building. Control of recognized hazards is achieved through engineering controls, ventilation in particular, and through medical surveillance. Strong programs for injury prevention and for health and safety education will produce significant health and economic benefit in the boatbuilding industry.
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PMID:Safety and health in boatbuilding and repair. 405 Aug

To evaluate the alterations of plasma catecholamines in chronic and acute liver diseases and their complications: hepatic encephalopathy (grade 1-4), ascites, deranged metabolism, and circulatory alterations, we measured the concentrations of norepinephrine, epinephrine, and dopamine in plasma in 49 patients with cirrhosis of the liver, in 2 patients with fulminant hepatitis B, in 2 patients with acute gestational fatty liver, and in 11 patients with fatty liver. We examined 21 healthy controls. The norepinephrine concentrations in patients with cirrhosis were raised and reached the highest values in hepatic coma grade 4. As well patients with fulminant hepatitis B had excessive high norepinephrine concentrations. The epinephrine concentrations were not significantly raised in patients with toxic cirrhosis and in patients with posthepatitic cirrhosis without encephalopathy. In hepatic coma grade 4 in patients with cirrhosis and fulminant hepatitis they reached again the highest values. Patients with acute gestational fatty liver had only slightly increased, and patients with fatty liver had normal catecholamine concentrations in plasma.
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PMID:[Plasma catecholamine levels in liver disease]. 406 Aug 3

Dengue hemorrhagic fever/dengue shock syndrome is a serious manifestation of dengue fever, which is observed predominantly in the tropical regions of the West Pacific and in Southeast Asia and is associated with secondary infections, mainly in children under age 15. A concomitant microangiopathic coagulopathy has been described; moreover, encephalopathy and even Reye's syndrome have been rarely reported. This report describes a 51-year-old man with secondary dengue infection who presented with clinical evidence of severe hepatitis, encephalopathy, cranial nerve palsy, and microangiopathic coagulopathy and who had a favorable outcome. A careful surveillance for the occurrence of secondary dengue in the Western Hemisphere is proposed, and dengue is suggested as a diagnostic possibility in obscure febrile illnesses presenting as either hepatitis, encephalopathy, or coagulopathy in places in which the mosquito vector, Aedes aegypti, is present.
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PMID:Dengue and hepatic failure. 406 82

A comparative study of two patients, one affected by haemorrhagic shock and encephalopathy (HSE) and the other by heatstroke is reported. Both presented shock, disseminated intravascular coagulation, neurological damage and hepatopathy. A lowered alpha 1-antitrypsin concentration as well as a slightly increased circulating immune complexes and complement consumption were observed in the HSE patient but not in the heatstroke one. In both, cultures for bacteria were negative, the viral serology was non-specific and hepatitis A and B studies were negative. HSE patient died. A possible relationship between HSE, heatstroke, malignant hyperthermia and halothane hepatitis is postulated. Fever, potentially hepatotoxic drugs or unknown agents (HSE) might trigger this clinical picture.
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PMID:[Hemorrhagic shock and encephalopathy. Its possible relation with heat stroke]. 407 88

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

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

Serum methionine levels increased to a greater extent in patients with severe liver diseases such as fulminant hepatitis and liver cirrhosis with and without hepatic encephalopathy. However, the concentrations remained unchanged in non-encephalopathic cirrhotic cases associated with hepatocellular carcinoma, and their serum methionine levels increased only moderately even at the time of encephalopathy. At least two different mechanisms of serum methionine elevations, possibly due to release from injured hepatocytes or diminished catabolisms of this amino acid in the damaged liver, could be differentiated; the former would be involved mainly in fulminant hepatitis and the latter in liver cirrhosis. A methionine-loading test performed in cirrhotic patients supported the validity of these considerations. No significant increase of serum methionine levels in cirrhotic patients with hepatocellular carcinoma was observed, possibly by remarkable consumption of this amino acid in hepatoma tissues. During the clinical course of several patients, serial determinations of serum methionine concentrations indicated that the levels varied depending upon alterations in the pathophysiological state of the damaged liver; much higher levels were observed concomitantly with decompensated signs such as ascites, jaundice and hepatic encephalopathy. These results suggest that monitoring of serum methionine levels would be very valuable, especially for judging prognosis and predicting hepatic encephalopathy in severe liver disease.
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PMID:Impaired metabolism of methionine in severe liver diseases. I. Clinical and pathophysiological significance of elevated serum methionine levels. 628

In 73 patients with fulminant viral hepatitis, non-A non-B hepatitis (NANB) was most common (43.8%), with hepatitis type A (HAV) diagnosed in 31.5% and hepatitis type B (HBV) in 24.7%. The non-A non-B group had a significantly longer duration from the onset of symptoms to the appearance of encephalopathy (median 21 days) compared with the HAV and HBV groups (medians 10 and seven days, p less than 0.01 and p less than 0.005 respectively). In the HAV group the severity of liver damage, judged by the maximum prolongation of the prothrombin time, was significantly less than in the HBV group (58 and 150 seconds prolonged respectively, p less than 0.005), and cerebral oedema was significantly less frequent (39% and 72% respectively, p less than 0.05). Consistent with this, the survival rate was higher in the HAV group (43.4%) compared with the HBV group (16.6%) and NANB group (9.3%) (p less than 0.005). These variations in presentation and clinical course may be a consequence of differences in the pathogenesis of the hepatic necrosis.
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PMID:Clinical and prognostic differences in fulminant hepatitis type A, B and non-A non-B. 641 35

The effect of a short course of prednisone therapy on serum IgM type antibody to the hepatitis B core antigen (anti-HBc IgM) was studied in 14 male patients with chronic active type B hepatitis. Eleven patients (78.5%) became positive for serum anti-HBc IgM either during or shortly after prednisone withdrawal. Detection of anti-HBc IgM correlated with an increase in hepatitis B virus specific DNA-polymerase activity and was followed by a rise in serum transaminase levels. Six patients with histologic evidence of cirrhosis developed anti-HBc IgM which lasted six or more months after prednisone therapy and had a rapid onset of hepatic decompensation manifested by encephalopathy with ascites and/or variceal bleeding. In 17 untreated chronic active type B hepatitis patients who served as controls, anti-HBc IgM was detected at low levels in only a single serum sample from each of two patients during the same observation period.
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PMID:Detection of anti-HBc IgM following prednisone treatment in patients with chronic active hepatitis B virus infection. 650 May 8

The medical records of 31 immunocompromised patients who experienced varicella infections from 1975 to 1982 were reviewed. Fifteen of these patients had visceral involvement. In these 15 patients, two clinical patterns of progression were noted: (1) Eleven patients with life-threatening involvement experienced hepatitis (n = 11), pneumonitis (n = 11), abdominal pain (n = 11), encephalopathy (n = 10), coagulopathy (n = 10), inappropriate antidiuretic hormone (ADH) syndrome (n = 10), back pain or myalgia (n = 5), and myocarditis (n = 1). Seven of these patients survived, all without sequelae. (2) Four patients with a milder course experienced subclinical hepatitis (n = 4), mild pneumonitis (n = 4), postinfectious encephalitis (n = 1), and septic arthritis associated with disseminated intravascular coagulopathy (n = 1). All four of these patients recovered completely. In patients with severe involvement, intense abdominal pain was frequently the first sign of dissemination. Abdominal pain and inappropriate ADH syndrome were unexplained and have not been previously described in progressive varicella. A predictable pattern of organ involvement enabled starting therapy early and resulted in the survival of 11 of 15 patients.
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PMID:Varicella in immunocompromised children. Incidence of abdominal pain and organ involvement. 661 54


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