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)

Gyromitra esculenta (Pers.: Fr.) Fr. and a few other mushrooms have caused severe poisonings and even deaths in humans. Clinical data are characterized primarily by vomiting and diarrhoea, followed by jaundice, convulsions and coma. Gastrointestinal disorders distinguish this poisoning. Frequent consumption can cause hepatitis and neurological diseases. The species of concern are mainly G. esculenta and G. gigas (Kromb.) Cooke (non Phill.). Nevertheless, recent advances in chromatography, biochemistry and toxicology have established that other Ascomycetes species also may prove toxic. Gyromitrin (acetaldehyde methylformylhydrazone, G) and its homologues are toxic compounds that convert in vivo into N-methyl-N-formylhydrazine (MFH), and then into N-methylhydrazine (MH). The toxicity of these chemicals, which are chiefly hepatotoxic and even carcinogenic, has been established through in vivo and in vitro experiments using animals, cell cultures and biochemical systems. When we consider the chemical nature and the reactivity of these natural compounds, we suggest that chemical and biochemical mechanisms may explain their intrinsic biological activity.
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PMID:Poisoning by Gyromitra esculenta--a review. 193 97

We report two cases of fulminant hepatitis which might be due to toloxatone, a new type-A monoamine oxidase inhibitor. Hepatitis occurred 20 days after the beginning of toloxatone administration in the first case and 138 days after the reintroduction of treatment in the second case. Clinical features included vomiting and jaundice, followed by asterixis and coma. Histologically, hepatic cell necrosis was predominant in the centrilobular area in the first case, and affected the entire lobule in the second case. Both patients died despite emergency liver transplantation.
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PMID:[Fatal fulminant hepatitis in 2 women taking toloxatone (Humoryl)]. 236 78

A small proportion of patients with acute viral hepatitis run a progressive fulminant course ending in acute liver failure with encephalopathy, and with a mortality rate of 75-80%. In small children and pregnant women mortality is even higher. We have treated 32 patients of all ages with acute progressive and fulminant hepatitis over the last 7 years in an uncontrolled trial with human interferon-alpha (HulFN-alpha), with i.m. doses of 3 x 10(6) u/day (70,000 u/kg per day for infants) for 8 +/- 3 days (mean +/- SD.) In 17 patients hepatitis was due to hepatitis A virus, in 7 to hepatitis B virus, in 6 to non A-non B virus and in 1 case each to herpes and cytomegalovirus. Sixteen patients (50%) recovered including 9 of 22 (41%) who were in Grades III-IV coma when treatment was started. Only 1 of 8 children less than 4 years of age recovered, whereas 15 of 24 (62%) older children and adults survived. Two of three pregnant women with acute fulminant hepatitis survived. In patients who recovered, improvement was often noted on about the fifth day of IFN treatment: 9 of 16 patients died before completing 5 days of therapy. Our studies of the IFN system response to hepatitis viruses showed that the greater majority of patients produce IFN in the acute stage of the infection. However, a minority have a defective IFN response that is more severe and more common in progressive fulminant hepatitis, and in several of these patients IFN response was completely lacking. It is in these cases that IFN treatment is likely to have the greatest value. On the basis of these encouraging preliminary results, it is suggested that a well-controlled, double-blind study be done to evaluate the effectiveness of HulFN-alpha treatment when given early during the course of acute progressive viral hepatitis.
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PMID:Interferon treatment in acute progressive and fulminant hepatitis. 247 21

Six of seven children with fulminant hepatitis (FH) were treated with a combination of twice daily plasmapheresis and intensive conservative therapy including special amino acid solution, glucagon-insulin therapy, dexamethasone, and so on. The remaining child was treated with intensive conservative therapy only because his condition was not so severe, in spite of being diagnosed as having fulminant hepatitis. Although five patients with biopsy-documented bridging hepatic necrosis or confluent hepatic necrosis in the acute phase made recoveries, the remaining two with massive hepatic necrosis died (the overall survival rate was 71%). The prognostic factors were considered to be the degree and pattern of liver cell necrosis, the degree of coma, and the etiology. The combination of twice daily plasmapheresis and intensive conservative therapy was effective for these pediatric patients with fulminant hepatitis, except those with massive hepatic necrosis.
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PMID:Survival rate in children with fulminant hepatitis improved by a combination of twice daily plasmapheresis and intensive conservative therapy. 250 66

Because of its anatomy, the liver can be divided into two hemilivers suitable for use as two grafts for liver transplantation. The line of division is the main scissure, giving the right hemiliver (segments 5-8) and the left hemiliver (segments 2-4). Segment 1 (caudate lobe) has to be resected. The vessels are divided between the two grafts: the vena cava remains on the right; on the left, the left hepatic vein is sutured into the vena cava of the recipient, which is retained intact. The left graft retains only the left branch of the portal vein, the bile duct and the hepatic artery. The right graft retains the portal trunk, the common bile duct and the right branch of the hepatic artery. This procedure was used for emergency grafting of two patients with fulminant hepatitis when only one donor was available. Both recipients recovered from coma and regained normal liver function. However, both died from causes not specifically related to the operative technique, one from multiple organ failure on the 20th day and the other from diffuse cytomegalovirus infection on the 45th day.
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PMID:Emergency orthotopic liver transplantation in two patients using one donor liver. 267 54

Groups of mice were given 0 mg, 4 mg, or 2 mg of methylprednisolone acetate (MPA) 7 days prior to, the day of, and 7 days after subcutaneous inoculation with 0 or 2 x 10(5) tachyzoites of Neospora caninum. Clinical signs of disease were seen only in mice given both MPA and N. caninum tachyzoites. Mice given 4 mg MPA and N. caninum tachyzoites developed severe disseminated neosporosis and most died or were killed when comatose 11-13 days postinoculation (PI). Acute pneumonia, polymyositis, encephalitis, hepatitis, and pancreatitis were the main lesions in these mice. Mice given 2 mg MPA and N. caninum developed mild pneumonia and many mice began showing neurological signs 14 days PI. Neurological signs consisted mainly of pronounced head-tilting and associated impairment of movement. Grossly visible 1-2-mm single or multiple, white areas of discoloration were seen in the brains of many of these mice. Encephalitis, ganglioradiculoneuritis, pneumonia, and polymyositis were the main changes seen in these mice. Tissue cysts of N. caninum were only seen in mice given 2 mg MPA and were first seen 21 days PI. Tissue cysts were 16-34 by 13-29 microns and had a 1.5-3.0-microns-thick cyst wall. Tissue cysts were seen only in the brain. Mice given 4 mg MPA and tachyzoites and host cells that had been frozen for 1 wk did not develop clinical signs of infection, indicating that freezing kills tachyzoites and that viruses or other agents were not involved in the genesis of disease seen in mice given MPA and viable tachyzoites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neospora caninum (Protozoa: apicomplexa) infections in mice. 279 80

This review covers 42 patients with fulminant hepatitis treated at the Clinic of Infectious Diseases of University of Pavia over a period of 11 years (1975-1985). This group is 1.9% of the 2181 subjects hospitalized for viral hepatitis, and consists of 25 males (59.5%) and 17 females (40.5%) with a mean age of 44 years. 26 patients (62%) had a virus B hepatitis, whereas in the remaining 16 the non-B type was diagnosed. B hepatitis had an overall prevalence of 56.4%. No case of fulminant hepatitis showed prothrombin levels above 23 (overall average 14%) and bilirubin below 17 mg/dl (overall average 24.5 mg/dl). SGOT and SGPT values were 1684 and 1868 UI/l respectively. 24 patients (57.1%) developed coma after admission to hospital and 18 had this diagnosis upon entry. History evidenced a heroin habit for 6 patients (14.2%); antiblastic treatment for 13 (30.9%); a preexisting liver disease for 7 (16.6%); other major pathologies for 6 (14.2%); steroid anabolizers, barbiturates + pirazolone derivatives and oral contraceptives use for 4 (9.5%) respectively. The overall mortality rate was 90.5%. 17 subjects (40.4%) were treated in an intensive care unit with a mortality rate of 75%.
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PMID:An eleven year survey (1975-1985) of fulminant hepatitis: considerations on epidemiology and pathogenesis. 310 92

Patients with agammaglobulinemia are particularly susceptible to chronic enteroviral infections of the central nervous system. Data on 42 patients were obtained by literature review, communications with other physicians, and personal experiences. Thirty-eight patients had congenital immunodeficiencies, most frequently X-linked agammaglobulinemia. Most patients who could be assessed were receiving maintenance therapy with intramuscular gamma-globulin before their enteroviral infection. Seven patients had not been recognized as hypogammaglobulinemic before the onset of infection. The commonest pathogens were echoviruses (37 of 41 cases), especially type 11 (11 cases). Thus far, four patients have had sequential or simultaneous infections with a second enteroviral serotype. Other features of the disease have included weakness, lethargy or coma, headaches, hearing loss, seizures, ataxia, and paresthesias. Some patients have also had nonneurologic manifestations of chronic enteroviral infection, including fever, the dermatomyositis-like syndrome, edema, rashes, and hepatitis. Treatment has consisted primarily of antibody administration, either in intravenous immunoglobulin preparations or in immune plasma. Twelve patients have received intraventricular immunoglobulin through reservoir devices; six of these 12 have improved substantially, as judged by clinical criteria.
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PMID:Chronic enteroviral meningoencephalitis in agammaglobulinemic patients. 329

The toxicities of antimalarial drugs vary because of the differences in the chemical structures of these compounds. Quinine, the oldest antimalarial, has been used for 300 years. Of the 200 to 300 compounds synthesised since the first synthetic antimalarial, primaquine in 1926, 15 to 20 are currently used for malaria treatment, most of which are quinoline derivatives. Quinoline derivatives, particularly quinine and chloroquine, are highly toxic in overdose. The toxic effects are related to their quinidine-like actions on the heart and include circulatory arrest, cardiogenic shock, conduction disturbances and ventricular arrhythmias. Additional clinical features are obnubilation, coma, convulsions, respiratory depression. Blindness is a frequent complication in quinine overdose. Hypokalaemia is consistently present, although apparently self-correcting, in severe chloroquine poisoning and is a good index of severity. Recent toxicokinetic studies of quinine and chloroquine showed good correlations between dose ingested, serum concentrations and clinical features, and confirmed the inefficacy of haemodialysis, haemoperfusion and peritoneal dialysis for enhancing drug removal. The other quinoline derivatives appear to be less toxic. Amodiaquine may induce side effects such as gastrointestinal symptoms, agranulocytosis and hepatitis. The main feature of primaquine overdose is methaemoglobinaemia. No cases of mefloquine and piperaquine overdose have been reported. Overdose with quinacrine, an acridine derivative, may result in nausea, vomiting, confusion, convulsion and acute psychosis. The dehydrofolate reductase inhibitors used in malaria treatment are sulfadoxine, dapsone, proguanil (chloroguanide), trimethoprim and pyrimethamine. Most of these drugs are given in combination. Proguanil is one of the safest antimalarials. Convulsion, coma and blindness have been reported in pyrimethamine overdose. Sulfadoxine can induce Lyell and Stevens-Johnson syndromes. The main feature of dapsone poisoning is severe methaemoglobinaemia which is related to dapsone and to its metabolites. Recent toxicokinetic studies confirmed the efficacy of oral activated charcoal, haemodialysis and haemoperfusion in enhancing removal of dapsone and its metabolites. No overdose has been reported with artemesinine, a new antimalarial tested in the People's Republic of China. The general management of antimalarial overdose include gastric lavage and symptomatic treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and management of poisoning due to antimalarial drugs. 330 66

A 48 year-old-man, with fulminant hepatitis complicated with myocarditis was treated. Despite intensive care, he died of fulminant hepatitis associated with hepatitis B virus infection. Electrocardiography (ECG) showed myocardial infarction-like changes when he went into a deep coma. Microscopically, scattered foci of myocardial cell damage and cell death associated with clusters of inflammatory cells were present in the heart at autopsy. However, there were no findings related to myocardial infarction and staining for hepatitis B surface antigen and core antigen were nil. The concentration of plasma catecholamine was elevated concomitantly with high level of ECG changes. We consider that abnormal ECGs may reflect a hypersecretion of catecholamine and suggest that our patient had a catecholamine cardiopathy.
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PMID:Electrocardiographic changes related to hypersecretion of catecholamine in a patient with fulminant hepatitis. 341 84


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