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)

This summary of adverse reactions to rifampicin has been prepared with the intention that it will be made available to all those involved in the administration of rifampicin in tuberculosis and leprosy control programmes. The reactions covered comprise those to both daily and intermittent administration, namely cutaneous and gastrointestinal reactions, hepatitis, and thrombocytopenic purpura, and those to intermittent administration only, namely "flu" syndrome, shock, shortness of breath, haemolytic anaemia, and renal failure.
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PMID:Adverse reactions to rifampicin. 31 12

Over a period of observation of 4 years maximum, there is no significant difference between the estimated survival time (by actuarial calculation) for patients with single and for those with double prostheses. Wihin the year following operation there is not significant difference between single and double prostheses as regards: the incidence of bacterial endocarditis, of pyrexias of unknown origin, of hepatitis, of haemolytic anaemia, of bleeding complications or incidents, of coronary of peripheral ischaemic episodes, or of reduced cardiac volume. On the other hand, there is a significant difference in the incidence of neurological defects (21% for the double prosthesis group, and 5% for the single prosthesis group, p less than 0.005 and or right ventricular failure (18% and 7% respectively, p less than 0.05) in the two groups.
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PMID:[Intermediate and long-term results of multivalve prostheses]. 82 5

Although M. pneumoniae is a well recognised respiratory pathogen both in children and in young adults, its infections have shown recently some pathomorphism and may also involve other organ systems. The paper reviews the various clinical syndromes in adults by M. pneumoniae, with particular emphasis on those more unusual and nevertheless seen by us. In this connection the possibility of pleural effusions (with a well defined cytology) associated or not with typical Mycoplasma pneumoniae and of chronic bronchopneumonias eventually evolving even in pulmonary fibrosis is stressed. Moreover, the development of M. pneumoniae respiratory infections during the course or hematological malignancies and their characteristics are described in some detail because of the relative rarity of this kind of infections in the above patients. Finally, some less frequently reported manifestations of M. pneumoniae infections, as hemolytic anemia, hepatitis and others are described and discussed.
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PMID:Known and newer manifestations by mycoplasma pneumoniae in adults. 86 Oct 72

With the onset of a remission phase of chronic aggressive hepatitis in a young female patient, two different auto-antibodies were found which had not previously been in evidence. These antibodies were identified as Donath-Landsteiner antibodies, the cause of a secondary auto-immune hemolytic anemia observed during this period, and anti-nuclear antibodies. Both antibodies were of the IgG class, both could be adsorbed onto the patient's own erythrocytes as well as P1-positive test erythrocytes, and both antibodies were present in the subsequent erythrocyte eluate. Separation of the two antibodies present in the serum as well as in the antibody-containing erythrocyte eluate was possible by absorption of the antinuclear factors using preparations of liver and thymus cell nuclei, but the anti-erythrocyte activity was not diminished by this procedure. Rapid remission of the auto-immune hemolytic anemia was achieved by a therapeutic application of corticosteroids. Long-term therapy has resulted in no recurrence of the auto-immune hemolytic anemia until now.
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PMID:[Autoimmune hemolytic anemia with Donath-Landsteiner antibodies and antinuclear factors during the course of chronic-aggressive hepatitis]. 108 45

A patient developed disseminated intravascular coagulation with purpura fulminans 1 month after starting Dilantin therapy for a seizure disorder. In addition, the patient developed exfoliative dermatitis, hepatitis, cutaneous vasculitis, and microangiopathic hemolytic anemia. She was successfully treated with adrenal steroids and heparin for her purpura fulminans. The hepatitic dermatologic, along with hemorrhagic, complications of Dilantin are reviewed, and the possible origin of the vasculitis and disseminated intravascular coagulation is discussed.
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PMID:Dilantin-induced disseminated intravascular coagulation with purpura fulminans. A case report. 114 59

In 35 dogs with spontaneous hepatobiliary liver disease the kinetics and the sources of bilirubin were quantified. The disorders were extrahepatic bile duct obstruction (n = 4), fulminant hepatitis (n = 2), (sub)acute hepatitis (n = 5), chronic active hepatitis (CAH) with cirrhosis (n = 6), hepatic lymphosarcoma (n = 5), centrizonal necrosis secondary to haemolytic anaemia (n = 6) and other (n = 2). The plasma disappearance of [3H]bilirubin was analyzed with a two-compartment model in all dogs. The ratio early labeled/late labeled bilirubin was determined by measuring the incorporation of [14C]glycine into erythrocyte haem and faecal stercobilin. By introducing this relation in the model analysis the bilirubin production rates from erythrocyte destruction (PE), ineffective erythropoiesis (PI) and hepatic haemoprotein (PL) could be quantified. Total bilirubin turnover was increased in both primary haemolytic disease and most cases of hepatobiliary disease. Erythrocyte survival was reduced in all cases but one. The bilirubin clearance was impaired to 30-50% of the normal value in most cases of hepatobiliary disease and also in primary haemolysis. In dogs with fulminant hepatitis, and cirrhosis with or without CAH, the clearance rates were reduced to values below 15% of normal. In these dogs both an impaired clearance and an increased production were important determinants of hyperbilirubinaemia. In other cases plasma bilirubin was primarily determined by increased production. These clearances and production rates were similar in haemolysis and in many cases of primary hepatobiliary disease. The hepatic haemoprotein turnover was quite variable in all subgroups, ranging from 1-74% of the total bilirubin turnover.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The origins and kinetics of bilirubin in dogs with hepatobiliary and haemolytic diseases. 150 35

Altogether 64 young patients with nonconjugated hyperbilirubinemia (NH) underwent clinico-morphological correlations to establish the nosological essence of pigment metabolism disorders revealed. 32 patients showed up the signs of chronic nonspecific hepatitis, including 7 patients with the signs of chronic aggressive hepatitis. The remainder 15 patients were found to have other inflammatory processes in the liver. Only 10 persons examined (15.6%) were diagnosed to have functional hyperbilirubinemia and 7 (10.9%) to have latent hemolytic anemia. The conclusion is made about the necessity of a comprehensive examination of young persons with NH. The morphological examination of the liver is a must to early verify the pathological process manifested by the impairment of pigment metabolism.
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PMID:[Unconjugated hyperbilirubinemia in young people]. 150 73

A Coombs-positive haemolytic anaemia with proof of heat autoagglutinins and autoantibodies against cell nuclei was diagnosed in a girl, now 7 1/2 years of age, in the sixth month of her life as a sequel to jaundice. Shortly afterwards liver biopsy yielded a confirmed diagnosis of giant cell hepatitis. The signs of the disease receded under treatment with decortin and imurek. An attempt to discontinue the medication at 5 1/2 years of age resulted in a histologically confirmed recurrence of autoimmune hepatitis. When the patient was 5 years old, the x-ray revealed a mainly interstitial pneumonia; at 6 years of age, bronchiectases in the region of the left lower lobe were confirmed by bronchography. Resection of the lower lobe was performed after occurrence of atelectasis. Histopathological findings confirmed fibrotic alveolitis associated with giant cells. Based on the overall clinical course and the histological and immunological findings, autoimmune etiology of fibrotic alveolitis must be discussed. Progression of the disease could be avoided during the past 6 months by intensifying the immunosuppressive prednisolone therapy.
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PMID:[Fibrosing alveolitis in a 7-year-old girl with autoimmune hemolytic anemia and autoimmune hepatitis]. 176 5

The clinical history, radiological and histomorphological alterations of the lung parenchyma associated with chronic active autoimmune hepatitis are described. A 6-month-old female infant developed chronic active autoimmune hepatitis associated with autoimmune haemolytic anaemia. She was treated with immunosuppressive drugs, including steroids, for more than 6 years and developed symptoms and radiological signs of interstitial pneumonitis 4 years after onset of the autoimmune hepatitis. Associated bronchiectasis was detected 1 year later. No abnormalities of lung defence mechanisms could be demonstrated. Resection of the sixth left segment and of the basal parts of the left lower lobe revealed honeycombing with changes in the lung parenchyma which included chronic interstitial pneumonitis with multinucleate giant cells, seen predominantly in the distal airways, marked diffuse interstitial mononuclear infiltrates and mild diffuse interstitial fibrosis as well as bronchiectasis and organizing pneumonia. Granulomatous lesions, angiitis and necrotic areas were absent. Immunohistochemistry for immunoglobulins was negative for IgA, IgG and IgM and positive for IgD in the multinucleate giant cells. A strong positive reaction to HLA-DR-specific monoclonal antibody was noted, whereas no specific sugar receptors (endogenous lectins) could be detected by use of biotinylated glyconeoproteins.
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PMID:Alteration of the lung parenchyma associated with autoimmune hepatitis. 187 59

Nitrofurantoin is a widely utilized urinary antimicrobial drug which has been associated with pulmonary fibrosis, neuropathy, and hepatitis as well as hemolytic anemia in glucose-6-phosphate dehydrogenase-deficient individuals. Incubation of freshly isolated rat hepatocytes with nitrofurantoin caused oxygen activation as a result of futile redox cycling. Glutathione disulfide (GSSG) was formed and rapidly exported from the cell resulting in complete glutathione (GSH) depletion followed by cell death. However, fructose prevented the export of GSSG from the cell and GSH levels recovered rapidly without cytotoxicity occurring. Fructose did not affect nitrofurantoin metabolism but rapidly depleted cellular ATP levels by approximately 80% which remained depressed during the incubation period. Fructose, however, did not protect hepatocytes from nitrofurantoin-induced cytotoxicity if GSH was depleted beforehand. Protection by fructose only occurred at concentrations which caused ATP depletion. These results suggest that fructose prevents nitrofurantoin-induced toxicity by depleting ATP and thereby preventing the ATP-dependent GSSG efflux. GSSG is retained enabling NADPH and glutathione-reductase to reduce the GSSG back to GSH, thereby protecting the cell from nitrofurantoin-induced oxidative stress.
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PMID:Prevention of nitrofurantoin-induced cytotoxicity in isolated hepatocytes by fructose. 189 74


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