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)

1-Amino-2,4-dibromoanthraquinone (ADBAQ), an intermediate in the production of commercial dyes for wool, silk, and synthetic fibers, was selected for toxicology and carcinogenesis studies in two rodent species. In advance of the 2-year studies, 13-week studies were conducted in male and female F344/N rats and B6C3F1 mice which were fed a diet containing ADBAQ at concentrations of 0, 0.25, 0.50, 1.00, 2.50, and 5.00%. ADBAQ stained the skin and fur red at all doses in rats and at 1.00% and higher concentrations in mice. Lethargy and emaciation were noted at the 2.50% and higher doses in rats of both sexes. In general, the absolute weight of the liver and the liver/organ weight ratios increased in both sexes and species at all doses. Treated rats developed a chronic toxic hepatitis characterized by hepatocytomegaly, centrilobular vacuolar degeneration and necrosis, regenerative nodules, acute necrotizing cholangitis, bile duct hyperplasia, chronic active inflammation in periportal areas, and focal pigmentation. The hepatopathy occurred at all doses in males and at 0.50% and higher in females and correlated with elevations of serum glutamic-pyruvic and glutamic-oxaloacetic transaminases, leukocytosis, and neutrophilia. Hyaline droplet degeneration in the proximal convoluted tubules of the kidneys occurred in male rats, and uterine atrophy was observed in female rats at 1.00% and higher. Anemia occurred in both sexes of rats at all doses and thymic atrophy was observed in both sexes of high-dose rats. In male mice minimal dose-related lesions in the liver included centrilobular glycogen depletion at 1.00% and higher and pigmentation at all doses. At comparable doses, ADBAQ was considered to be markedly toxic in rats and of minimal nonlife-threatening toxicity in mice.
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PMID:Thirteen-week toxicology studies of 1-amino-2,4-dibromoanthraquinone in Fischer 344/N rats and B6C3F1 mice. 395 25

A case of acute lead poisoning due to intravenous injection of lead acetate is reported. The patient developed clinical and biochemical symptoms characteristic for acute hepatic porphyrias. Elevated urinary 5-aminolaevulinic acid and low porphobilinogen correlated to a lead-induced inhibition of 5-amino-laevulinic acid dehydrase with diagnostically indicative reactivation rates by zinc and dithiothreitol. Urinary coproporphyrin excretion was also increased. Additional findings included anaemia and toxic hepatitis. Under the influence of elimination therapy with D-penicillamine pathologic parameters normalized. Except for transient neuralgic pains the patient did not experience any neurologic dysfunctions, thus contrasting the findings in chronic lead intoxication.
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PMID:Acute lead intoxication due to intravenous injection. 400 94

Side effects and their relationship with the material used were analyzed in 748 plasma exchanges (PE) performed in 75 patients. The total incidence of acute and mild adverse effects (chills and/or fever, paraesthesias, allergic reactions, acute anaemia, vasovagal reactions, abdominal pain and hypotension) was 18.04%. Two patients developed an episode of left cardiac insufficiency. One patient in whom all PE were performed with fresh frozen plasma (FFP) developed metabolic alkalosis. Three patients developed sepsis during treatment with repeated PE and immunosuppressive drugs; in these three patients a permanent vascular inlet was used (shunt or catheter). All patients in whom only FFP was used as replacement solution developed non-A, non-B hepatitis. Neither haemorrhagic nor thrombotic episodes were observed in these patients. It is of the greatest importance to choose the most suitable material for each patient and to develop a careful technique in order to avoid these complications during treatment with PE.
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PMID:Adverse effects secondary to the treatment with plasma exchange. 403 Jan 33

Although a large number of patients are maintained on chronic dialysis, there is little information regarding the medical care rendered to these patients. We therefore obtained information on health care maintenance policies from 90 dialysis centers (8,104 patients) selected from each End-Stage Renal Disease (ESRD) Network. All centers except one obtained BUN, creatinine, electrolytes, calcium, and phosphorus at intervals of 1 month or less; 85% of centers obtained a multiple-test laboratory panel at monthly intervals. Annual physical examination, ECG, and chest x-ray were performed in 80% or more of the centers. Immunization policies varied with 88%, 64%, and 17% of centers offering influenza, pneumococcal, and hepatitis B vaccine, respectively. Patterns of surveillance for anemia, osteodystrophy, and hepatitis were variable. In view of the high frequency and cost of testing, prospective studies to determine optimal methods of health care maintenance in the chronic dialysis center are indicated.
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PMID:Selected health care maintenance policies in chronic dialysis centers. 405 Jul 81

Chronic intermittent hemodialysis may relieve some medical problems of terminal uremia (for example, azotemia, acidosis, hypertension, neuro-muscular disorders, bleeding, pericarditis) to such a degree that many patients are able to resume their normal activity. There remain, however, problems which are not readily changed by hemodialysis (anemia, peripheral neuropathy, pruritus, sexual impotence, renal osteodystrophy). These, together with medical problems possibly caused by hemodialysis (for example, osmotic disequilibrium, errors in dialysate composition, hepatitis, hemosiderosis, isoimmunization from blood transfusions, shunt problems and psychological problems of dependency upon the artificial kidney) represent a limitation of the present type of hemodialysis therapy.
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PMID:Some medical problems of chronic hemodialysis. 486 55

A case is reported of a 39-year-old woman who had postoperative pulmonary embolism after taking combined oral contraceptives from 1967 to 1970. Her related history included birth of 2 large infants, phlebitis, and varicosities. Her operation for retroverted uterus and tubal sterilization was followed the next day by a severe pulmonary embolism treated with heparin. This treatment resulted in a pelvic hematoma, abundant metrorrhagia, and anemia requiring 4 transfusions. 4 months later she developed jaundice due to hepatitis virus B, which potentiated the effect of the antiprothrombin treatment and precipitated 2 new pelvic masses, fever, and metrorrhagia. She was given hysterectomy, which revealed bilateral hematosalpinx, probably related to endometriosis. 1 year later she was in good health, but her serum lipids were found high in the alpha- and pre-beta-lipoprotein bands. A delay of 2 months between stopping oral contraceptives and surgery is recommended.
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PMID:[Postoperative thromboembolic accident observed during estro-progestative treatment. Apropos of a case]. 516 37

It is essential for an efficient substitution to define the nature of the defect as good as possible. Simple screening tests allow a rapid classification. Prophylactic substitution is recommended in potentially reversible defects (bone marrow aplasia in connection with leukaemia treatment) and/or imminent bleeding (eventually complicated by additional risk factors). If bleeding cannot be stopped surgically therapeutic substitution is indicated. In case of bone marrow failure, a substitution may be particularly promising. In presence of an increased peripheral platelet destruction (disseminated intravascular coagulation, antithrombocytic antibodies) treatment of the basic disease is mandatory. Combined hemostatic defects can be influenced by fresh frozen plasma (FFP). Fresh whole blood (not older than 48 hours) may be considered in cases of thrombocytopenia and concomitant anemia. For isolated defects (e.g. hemophilias with or without antibodies, congenital afibrinogenemia, lack of factor XIII) special preparations are at hand. The clinical effect of substitution depends on the specific activity of the preparation, on the volume of expansion in the recipient and on other pharmacokinetic factors. Hepatitis and antibody-production may be considered as particularly grave side-effects.
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PMID:[Controlled substitution with blood products in hemostatic disorders]. 618 45

A naturally occurring immunodeficiency syndrome has been seen in a captive colony of macaque monkeys. This syndrome is seen primarily in the species Macaca cyclopis. Affected animals died with lymphomas (a rare disease in macaques) or such opportunistic infections as Pneumocystis carinii and noma (necrotizing gingivitis). These M. cyclopis exhibited anemia, neutropenia, and a circulating bizarre immature monocyte. In addition, liver function tests suggested hepatitis. Pokeweed mitogen-, concanavalin A-, and xenogeneic cell-stimulated proliferative responses by lymphocytes of animals with the syndrome were dramatically diminished. The T4 (helper, inducer)/T8 (suppressor, cytotoxic) ratio in the peripheral blood mononuclear T-cell populations of M. cyclopis in this colony are decreased when compared with those from either Macaca mulatta in the same colony or normal humans. Epidemiologic evidence implicates a common source agent in this syndrome. The similarity of this syndrome in macaques to human acquired immunodeficiency syndrome suggests that it may provide an important model for studying the human syndrome.
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PMID:Acquired immunodeficiency syndrome in a colony of macaque monkeys. 622 43

Five cases of the phenytoin syndrome are reviewed here. This hypersensitivity reaction is characterized by fever, eruption, lymphadenopathy, and hepatitis. Anemia, pharyngitis, diarrhea, and nephritis may also be associated. The skin eruption is pleomorphic, presenting as morbilliform eruptions, follicular papules and pustules, erythroderma, or toxic epidermal necrolysis. The management of these patients is made more difficult by the tendency for multiple relapses even after the use of phenytoin has been discontinued.
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PMID:The phenytoin syndrome. 622 59

The case of a 25-year-old patient is reported who suffered from a syndrome similar to immune complex disease following cholera revaccination. The clinical picture included fever, muscle, joint and abdominal pain, vomiting, serositis, hepatitis, suspected myocarditis, anaemia and thrombocytopenia. Clinical symptoms subsided spontaneously within two weeks. This case illustrates a hazard of cholera vaccination so far not reported in the literature.
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PMID:Episode resembling immune complex disease after cholera vaccination. 623 47


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