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)

Marked activity of cobalt-activated acylase was found in the sera of 33 of 37 patients with acute toxic hepatitis due to poisoning with either amanita mushrooms or chemicals. The activity of the enzyme showed a positive correlation with that of serum transaminases, reached the highest levels on the patient's admission to hospital and within a few days fell rapidly to undetectable levels. Slight acylase activity was observed in the majority of patients intoxicated with drugs or carbon monoxide but was not seen in sera of those poisoned with non-amanita mushrooms who showed no signs of liver injury. Unlike acylase, the serum activity of gamma-glutamyl transpeptidase remained unchanged over the first days of acute toxic hepatitis. The determination of serum cobalt-activated acylase might be of value in the diagnosis of acute liver injury.
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PMID:Serum cobalt-activated acylase and gamma-glutamyl transpeptidase activities in toxic hepatitis. 24 82

Methacetin undergoes rapid O-dealkylation by hepatic microsomal enzyme systems, and the resultant CO2 is present in the expired air. The rate of O-dealkylation of methacetin was assessed by the [13C]methacetin breath test in seven healthy volunteers and 30 patients with histologically proven chronic liver diseases. The 30-min recovery of orally administered [13C]methacetin as 13CO2 in the exhaled air was significantly reduced in patients with chronic aggressive hepatitis and in those with liver cirrhosis but not in patients with chronic persistent hepatitis or healthy controls. Patients with either advanced cirrhosis or hepatocellular carcinoma showed significantly lower values than those with well-compensated cirrhosis. The levels in two patients with late primary biliary cirrhosis were reduced. These results show that the severity of liver damage can be effectively evaluated by [13C]methacetin breath test. In addition, this test is simple, safe, and time efficient.
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PMID:[13C]methacetin breath test for evaluation of liver damage. 303 Jun 79

16, 16 Dimethyl prostaglandin E2 (dmPGE2), a known cytoprotective agent, was examined for its ability to alter the course of fulminant hepatitis in an experimental model of fulminant viral hepatitis, murine hepatitis murine hepatitis type 3 (MHV-3). Fully susceptible BALB/cJ mice, infected with 100 50% lethal doses (LD50) of MHV-3 developed histologic and biochemical evidence of fulminant hepatitis, as evidenced by massive hepatic necrosis with hypoglycemia, metabolic acidosis, and a markedly elevated serum alanine aminotransferase (ALT) (mean, 1,402 +/- 619 IU/liter). In contrast, animals treated with dmPGE2 either before or after infection (up to 48 h) demonstrated a marked reduction in both histologic and biochemical evidence of liver damage as characterized by normal blood glucose, total CO2, and ALT determinations (mean ALT, 63 +/- 40 IU/liter). Treatment of infected mice with PGF2 alpha demonstrated no cytoprotective effects. High titers of infectious virus were recovered from the livers of both dmPGE2-treated and -untreated animals throughout the course of infection. In a parallel in vitro study, dmPGE2 (10(-4)-10(-8) M) demonstrated a similar cytoprotective effect on monolayers of isolated cultured hepatocytes from fully susceptible BALB/cJ mice infected at a multiplicity of infection of 0.1, 1.0, and 10.0. In addition, splenic macrophages recovered from infected and untreated BALB/cJ mice demonstrated a marked augmentation in procoagulant activity (PCA) from a basal 10 +/- 5 mU/10(6) splenic macrophages to a maximum of 615 +/- 102 mU/10(6) splenic macrophages, whereas no increase in macrophage PCA was detected in infected animals treated with dmPGE2. These results suggest that dmPGE2, without detectably altering viral replication or infectivity in vivo, confers a marked cytoprotective effect on hepatocytes both in vivo and in vitro, and prevents the induction of macrophage PCA in vivo in fully susceptible BALB/cJ mice after murine hepatitis virus type 3 infection.
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PMID:16, 16 Dimethyl prostaglandin E2 prevents the development of fulminant hepatitis and blocks the induction of monocyte/macrophage procoagulant activity after murine hepatitis virus strain 3 infection. 362 90

In 16 healthy volunteers and in 39 patients with liver diseases (fatty liver, chronic persistent and chronic active hepatitis, hepatic cirrhosis) a simplified aminopyrine breath test (ABT) was carried out using a "tracer" dose of 3 mg (111 kBq) 14C-aminopyrine. The exhaled 14CO2 measured 1 h after intake amounted to values between 771 and 1337 DPM/mmol CO2/70 kg body weight in healthy controls. The amount of exhaled 14CO2 decreased in the order: fatty liver greater than chronic, active hepatitis greater than active, compensated cirrhosis greater than active, decompensated cirrhosis. Between the values of ABT and various conventional laboratory liver tests (alanine-aminotransferase, alanine-aminopeptidase, aspartate-aminotransferase, gamma-glutamyltransferase, total serum bilirubin) significant correlations were found (r = 0.6019 to 0.7765, n = 55; p less than 0.001). The proposed modification of the breath test is of advantage in that it requires a very low dose of aminopyrine and is easily practicable.
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PMID:A simple method for routine determination of the metabolic liver capacity: the aminopyrine breath test. 392 2

The kinetics of plasma and breath elimination of aminopyrine after 14C-aminopyrine given orally were studied using an open one-compartment model and first order rates of elimination. The study comprised eight healthy volunteers and two groups with histologically verified chronic liver diseases (cirrhosis, n = 12, and chronic aggressive hepatitis, n = 12). Elimination rates from plasma and breath were significantly reduced in the group with cirrhosis, but only so in chronic aggressive hepatitis when they were expressed relative to each other. Monomethylaminopyrine was eliminated more rapidly compared to aminopyrine, and the rate of formaldehyde formation was positively correlated to the excretion rate of CO2 (r = 0.53, P less than 0.002). No correlation was found with clinical or other laboratory data in the groups of liver diseases studied. The test is a quantitative indicator of the drug metabolizing mixed function oxidases of the endoplasmatic reticulum of the liver, and may reflect the degree of damage to this system in chronic liver disease.
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PMID:The determination of aminopyrin elimination for control of the metabolic capacity of the liver in man. 680 87

Lack of knowledge of the exact contents of the materials and improper handling of the toxic chemicals lead to the occurrence of occupational illnesses in the developing countries. However, the incidence of occupational diseases was usually underestimated. This article presents the profile of occupational diseases in Taiwan from two sources, i.e. occupational disease benefit payments of labor insurance and the review of relevant literature. The primarily documented occupational diseases in Taiwan were pneumoconioses. The second most common occupational disease was carbon monoxide intoxication, followed by lead poisoning and noise-induced hearing loss. Less than five percent of occupational diseases were due to the other causes, including decompression syndrome, heat stroke, toxic hepatitis, neurological disorders and hematologic disorders. The number of occupational diseases recognized in Taiwan was considered to be seriously underestimated due to the shortage of occupational medical specialists. Priority in the development of occupational medicine in Taiwan is to educate industrial hygienists and physicians to recognize health hazards in the work environment and to diagnose occupational diseases. Recognition of occupational diseases could subsequently highlight the health hazards in the workplace and prevent workers from overexposure.
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PMID:Occupational disease profile in Taiwan, Republic of China. 769 1

The authors present the results of analysis of data on occupational diseases in Poland during the years 1984-1992. The statistical material covers 86,871 cases of various diseases. Among them hearing lesions, vocal organ diseases, contagious and invasive diseases, pneumoconioses, dermatoses, vibration syndrome, poisonings and chronic bronchitis proved to be most common. In Poland, among the etiological factors, noise, industrial dusts, hepatitis virus, chromium and its compounds, lead and its inorganic compounds, carbon disulphide and carbon monoxide pose the highest risk. Apart from the statistics concerning the number of cases of occupational diseases according to sex, age, exposure duration, national economy branches and regions (voivodeships), the article presents, for the first time, some consequences of occupational diseases, such as granting disability pensions and/or indemnity depending on the per cent of health impairment.
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PMID:Occupational diseases in Poland during the years 1984-1992. 814 74

A 17-year-old woman was admitted because of a liver tumor found incidentally by ultrasonography. Liver function was normal and there were no markers of hepatitis viruses or malignancy. Abdominal ultrasonography, computed tomography (CT), and magnetic resonance imaging revealed a mass (2 cm in diameter) in the lateral segment of the left lobe of the liver. The lesion was not detected by hepatic arteriography. However, dynamic CT with fast scanning and dynamic CO2-enhanced ultrasonography demonstrated initial central enhancement of the mass followed by centrifugal spread of enhancement to the periphery. Color Doppler flow imaging detected a central color spot, shown to be an artery by a pulsed Doppler spectrum analysis. Fine-needle biopsy confirmed a diagnosis of focal nodular hyperplasia. Dynamic CT with fast scanning, dynamic CO2-enhanced ultrasonography, and color Doppler flow imaging were useful in detecting the vascular pattern specific to focal nodular hyperplasia. Investigation of further cases with these novel imaging modalities should help to establish a comprehensive diagnostic procedure and thus avoid unnecessary surgery for focal nodular hyperplasia, which is a completely benign lesion.
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PMID:Usefulness of novel imaging modalities in diagnosis of focal nodular hyperplasia of the liver. 934 97

A case of disseminated extrahepatic hepatocellular carcinoma (HCC) occurring after ultrasound (US)-guided biopsy and percutaneous ethanol injection therapy is presented. A 72-year-old man with hepatitis-C-virus-related cirrhosis underwent percutanous ethanol injection therapy (PEIT) two times with complete remission: the first for moderately-differentiated HCC in segment six (S6), and the second for well-differentiated HCC in another part of S6. Imaging studies including carbon dioxide (CO(2))-US angiography, incremental computed tomography, and dynamic magnet resonance imaging showed that both HCCs were hypovascular. Twenty-one months after the first PEIT and 7 months after the second, a 5.5x4.5 cm extrahepatic mass interfaced with S6 of the liver was detected by imaging studies. The patient underwent surgery for extrahepatic HCC. Grossly, the main tumor was 5.5x4.5 cm with capsule and septum; the disseminated tumors were detected on the surface of the liver, including the right diaphragm and the falx ligamentosa. Histologically, it was moderately- to poorly-differentiated HCC, which, although not attributed to direct track seeding, was suspected of being induced by the percutaneous US-guided biopsy procedure or by PEIT, irrespective of a hypovascular tumor. Further studies may provide insight into the risk factor engendered by these procedures.
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PMID:A case of disseminated extrahepatic hepatocellular carcinoma after US-guided biopsy and percutaneous ethanol injection therapy. 1134 59

Compound A (2-fluoromethoxy-1,1,3,3,3-pentafluoro-1-propene) is produced by reaction of the inhalation anesthetic, sevoflurane, with CO2 absorbents. Compound A has been reported to directly react with protein. Since adduction of proteins can transform them into antigenic material, Compound A was assessed for its ability to produce a humoral immune response. Male outbred Hartley guinea pigs (500-600 g, N = 7) were exposed via inhalation for 4 h to a subtoxic level (100 ppm) of Compound A, 3 times, at 42 day intervals. Blood samples obtained at 2, 14, 28 and 40 days after each exposure were measured for ALT, creatinine, and urea nitrogen and for the presence of antibodies to trifluoroacetylated guinea pig albumin (TFA-GSA). All indicators of liver and kidney injury remained within normal range throughout the course of the study. A humoral immune response to TFA-GSA was observed following each exposure to Compound A with a titer appearing by day 14 after exposure, peaking near day 28, and resolving to normal levels by day 40. The titer levels were approximately equivalent after each exposure and about one-third that previously seen in guinea pigs after multiple exposures to halothane. Compound A would appear to have the ability to form antigenic adducts during inhalation exposure. These findings are similar to those observed for halogenated inhalation anesthetics that have been linked to cases of immune-medicated idiosyncratic hepatitis and indicate that Compound A exposure may pose the same hazard.
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PMID:Humoral immune response to a sevoflurane degradation product in the guinea pig following inhalation exposure. 1166 47


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