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)

Drugs and other chemicals are usually metabolized in the liver in the drug-metabolizing enzyme system. The metabolites sometimes bind with cellular macromolecules and injure the cell directly or serve as new antigens to create immunologic injury in a delayed fashion. The immediate or toxic injury is dose-dependent, predictable and zonal in the liver lobule, usually in the central region. Carbon tetrachloride intoxication and acetaminophen overdose are examples of injury resulting from microsomal metabolism. Other injuries related to microsomal metabolism are those produced by vinyl chloride in polymerization plant workers and by methotrexate in psoriatics or leukemic children. Most adverse drug reactions affecting the liver and producing jaundice are unpredictable, delayed in onset, and only hypothetically related to microsomal metabolism in some instances. The two main types are cholestasis and viral-hepatitis-like. The former may be in a pure form, in which case it may be partly dose-dependent, or in a form mixed with hepatitis. Many drugs produce cholestasis in a small percentage of persons, and because the reaction is benign, albeit prolonged at times, such drugs continue to be used. The viral-hepatitis-like reaction involves few drugs and affects few persons, but can be fatal. The recognition that chronic hepatitis can be caused by drugs such as oxyphenisatin, alpha-methyldopa, and isoniazid has added a new dimension to the clinical problem of adverse drug reactions, which may extend to widely used and commonly available agents like aspirin.
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PMID:Hepatic drug metabolism and adverse hepatic drug reactions. 17 22

Several agents have recently been implicated in the development of benign and malignant liver neoplasms. Recognition of their possible role by the primary care physician may prevent serious consequences to patients exposed to these agents, which include oral contraceptives, androgens, hepatitis virus, and vinyl chloride.
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PMID:Benign and malignant liver neoplasms: some new etiologic associations. 20 4

Di-2-ethylhexyl phthalate (DEHP), the most frequently occurring plasticiser in medical equipment manufactured from polymers of vinyl chloride, forms about 40% w/w of tubes and containers used for storing blood and for haemodialysis. The plasticiser leaches out into liquids with lipid contents, although it is very sparingly soluble in purely aqueous solutions. On infusion of 2-3 1 of stored blood, up to 200 mg DEHP may be transferred to the patient, while much higher quantities may be given during dialysis, which is moreover often repeated frequently over long periods. The acute toxicity of DEHP is very low (greater than 20 g/kg as LD50 in rats), and the ester is rapidly metabolised to products which are excreted in the urine and bile; chronic toxicity from the levels of dosage obtaining is thus very improbable. Carcenogenicity has never been demonstrable in animals, while teratological effects are of a very low order. Serious acute results observed after transfusion of neonates have not been proved to be caused by DEHP, and might be ascribable to accompanying foreign substances. Atheroma in chronic dialysis subjects is still unexplained, but hepatitis probably caused by diethylphthalate from plastic was resolved when apparatus plasticised by DEHP alone was substituted. The benefits of DEHP appear vastly to outweigh any risks. The status of DEHP as environmental contaminant is noted.
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PMID:Diethylhexyl phthalate as a factor in blood transfusion and haemodialysis. 35 59

Exposure of mice to 1000 ppm of vinyl chloride (VC), 6 hr/day, 5 days/week, caused some acute deaths with toxic hepatitis and marked tubular necrosis of the renal cortex. Starting the sixth month, mice exposed to 1000, 250, or 50 ppm of VC became lethargic, lost weight quickly, and died. Only a few mice exposed to 50 ppm survived for 12 months. Pulmonary macrophage count was elevated in some mice. There was a high incidence of bronchiolo-alveolar adenoma, mammary gland tumors including ductular adenocarcinoma, squamous and anaplastic cell carcinomas with metastasis to the lung, and hemangiosarcoma in the liver, and, to a lesser extent, in some other organs. The incidence of these tumors quickly increased, and the severity was in direct proportion to the levels of VC and the length of exposure. Malignant lymphoma involving various organs was observed in a few mice. Rats were more resistant to the toxic effects of VC. Exposure to 1000 ppm slightly depressed the body weight of the females. Exposures of 250 or 1000 ppm caused a number of deaths and hemangiosarcoma in the liver starting the ninth month. Most rats with hepatic hemangiosarcoma also developed hemangiosarcoma in the lung. Hemangiosarcoma occasionally occurred in other tissues of one or two rats exposed to 50 ppm or higher level of VC. Exposure of mice to 55 ppm of vinylidene chloride (VDC) also caused a few acute deaths and a few hepatic hemangiosarcomas. Inflammatory, degenerative, and mitotic changes occurred in the liver. No mouse exposed to VDC developed any mammary gland tumors. Several mice had bronchioloalveolar adenoma. Exposure of rats to 55 ppm of VDC slightly depressed the body weight. Hemangiosarcoma occurred in the mesenteric lymph node or subcutaneous tissue in two rats.
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PMID:Inhalation toxicity of vinyl chloride and vinylidene chloride. 56 2

Analysis is performed on the observed clinical picture of vinyl-chloride disease in 12 persons, developed at concentrations of toxic substance about MAC after exposure from 5 to 34 years. After enlarged clinical test on individual organs and systems the authors establish that the most frequent result of chronic poisoning with vinyl-chloride is the combination of peripheral neurovegetative symptoms with toxic hepatitis on the background of neurosis-similar (astheno-vegetative) manifestations. In the cases, observed by the authors, the poisoning takes a light course affecting the neurovegetative structures and prevailing of the vegetovasal forms of polyneuropathy ending with Raynaud-similar syndrome, or affecting the distal parts of the peripheral nerves with early electromyographic find. The Raynaud-similar syndrome and the bone changes ad specificity to the clinical picture, but are not constant manifestation of poisoning and can be developed at more continuous occupational exposure. The authors propose a discussion on the legality of the appelation vinyl-chloride disease in the cases, when not all classical clinic symptoms are present.
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PMID:[A clinical observation of vinyl chloride-induced disease]. 136 41

Serum bile acids have been shown to serve as useful indicators of liver disease. We have confirmed these findings and added an analysis of interleukin-1 beta (IL-1 beta) profiles to further differentiate viral hepatitis from toxic liver damage associated with exposure to vinyl chloride (VC) or trinitrotoluene (TNT). The frequency of elevated cholylglycine (CG) was 100%, 75%, and 37.5% in viral hepatitis, VC- and TNT-linked liver injury patients, respectively. The mean levels, expressed in micrograms/dL, were 578, 507, 142, and 65 in hepatitis B, hepatitis non-A non-B, VC and TNT liver injury patients, respectively. Thus, the CG test could detect viral hepatitis and, VC liver injury, and (less frequently) liver injury associated with exposure to TNT. The mean level of IL-1 beta in patients with hepatitis type B was 424 pg/mL and hepatitis non A non B was 384 pg/mL compared with a mean of 33-40 pg/mL in those with VC or TNT-linked liver disease. The IL-1 beta detection test proved further to be an important distinguishing parameter as it was 100% positive in patients with viral hepatitis but only 12.5% to 25% positive in patients with VC/TNT-induced liver damage.
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PMID:Cholylglycine measured in serum by RIA and interleukin-1 beta determined by ELISA in differentiating viral hepatitis from chemical liver injury. 144

A renal transplant recipient presented with bleeding esophageal varices. Needle biopsy, later confirmed by operative wedge biopsy, showed slight periportal fibrosis but no cirrhosis or hepatitis. No etiology for his liver disease could be determined and he could not be differentiated from other reported patients with idiopathic noncirrhotic portal hypertension (IPH). His liver biopsy did show massive hepatic iron deposition. He had received about 115 units of blood while on hemodialysis and had taken oral iron supplementation for 8 years. IPH has been associated with toxin exposure, especially arsenic and vinyl chloride. This case suggests that excessive iron deposition may also lead to IPH and the indiscriminate use of iron supplementation in hemodialysis or renal transplant patients should be avoided.
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PMID:Hemosiderosis without cirrhosis: an unusual case of portal hypertension. 700 99

To quarantine human tumor samples for transplantation into immune deficient mice or tumor xenograft lines established and introduced from other institutions, we performed isolated implantation and passaging of tumors in a vinyl isolator, and microbiological examinations of sentinel mice kept together with tumor bearing mice. We examined 105 pairs of sentinel mice used to quarantine 907 tumors, and found six cases of contamination or infection with Staphylococcus aureus, 20 cases with Pseudomonas aeruginosa and one case with mouse hepatitis virus (MHV). It was, however, possible that Mycoplasma pulmonis contamination was overlooked because the microbe had been isolated from tumors passaged after quarantine, even though the results of the quarantine of these tumors showed no sign of pathogens. Direct culture of tumors for the microbe was recommended to improve the quarantine system.
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PMID:Quarantine for contaminated pathogens in transplantable human tumors or infections in tumor bearing mice. 914 98

Etheno adducts in DNA are formed from the carcinogens vinyl chloride and urethane, and also from products of lipid peroxidation (LPO), such as trans-4-hydroxy-2-nonenal. Using an ultrasensitive detection method, the formation of etheno-DNA adducts in the liver was demonstrated in LEC rats (a strain with hereditary abnormal copper metabolism) that develop hepatitis and hepatocellular carcinoma. Wilson's disease and primary haemochromatosis are human genetic disorders that cause copper or iron accumulation resulting in a high risk for primary liver cancers. Levels of etheno adducts were also significantly elevated in the liver of these patients. In a group of male and female volunteers kept on a controlled diet, the effect of dietary fatty acid composition on the endogenous formation of lipid peroxidation-derived DNA adducts was determined in DNA from white blood cells. Dietary omega-6-polyunsaturated fatty acids greatly increased LPO-derived etheno-DNA adducts in vivo, in females. Thus, exocyclic DNA adducts are promising biomarkers for elucidating the effect of dietary fat intake, oxidative stress and protective dietary antioxidants on endogenous DNA damage and thus may provide a possible mechanistic link with elevated risk for diet-related cancers.
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PMID:Etheno-DNA base adducts as tools in human cancer aetiology and chemoprevention. 949 54

It has been suspected that embryos stored in liquid nitrogen tanks may become contaminated with murine pathogens, if some pathogens had been introduced to the tanks accidentally. To examine this, we stored tubes containing embryos with tubes containing mouse hepatitis virus (MHV) or Pasteurella pneumotropica in liquid nitrogen tanks and examined whether progeny mice derived from the embryos were contaminated with the pathogens or not. After storing for 6 months or 1 year the frozen embryos were thawed and implanted into the oviducts of pseudopregnant female mice, and the mice were bred in vinyl isolators. We could not detect serum antibodies to MHV and isolate Pasteurella pneumotropica in the progeny mice, suggesting that cross-contamination between tubes in a liquid nitrogen tank scarcely occurs.
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PMID:Experimental evaluation of cross-contamination between cryotubes containing mouse 2-cell embryos and murine pathogens in liquid nitrogen tanks. 1263 39


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