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)

The chloroquine-resistant strains P. falciparum are widely spread in the countries of South-East Asia, Latin America. Since the middle of the 70s the strains also occurred in Eastern Africa. The given paper is concerned with 4 patients suffering from imported chloroquine-resistant tropical malaria. Of these, 3 patients come from Africa, and one from Vietnam. In the latter patient, the disease ran a grave course and was attended by coma, acute renal insufficiency, hepatitis, and hemolytic anemia. The patient was registered as having grade III resistance of P. falciparum to chloroquine. The schedules of the disease treatment including quinine with fansidar, metakelphin (or with sulphalene and chloridine), mafloquine or tetracycline are presented.
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PMID:[Treatment of imported tropical malaria caused by chloroquine-resistant strains of P. falciparum]. 355 Nov 76

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71

Two cases of the Budd-Chiari syndrome are described in whom the diagnosis was finally confirmed at necropsy. The presentation was with encephalopathy, occurring within eight weeks of first symptoms and coming therefore within the definition of fulminant hepatic failure. In one, thought to have non-A, non-B hepatitis, encephalopathy progressed to grade 4 coma with death 12 days after presentation. In the other, mistakenly thought to have intra-abdominal malignancy, an exploratory laparotomy exacerbated the encephalopathy with death three weeks later. In neither case were non-invasive investigations, such as ultrasound and isotope scanning, carried out which might have facilitated an earlier diagnosis and consideration for orthotopic liver transplantation, probably the most appropriate form of therapy for these very severe cases.
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PMID:Budd-Chiari syndrome presenting as fulminant hepatic failure. 375 22

Beta-interferon was administered by intravenous infusion to 16 patients affected with fulminant hepatitis B virus infection in third or fourth-grade coma. Ten patients presented a superinfection or a co-infection due to the delta (delta)-agent. None had detectable interferon (IFN) activity before therapy was begun. Besides fever, no significant side-effects were observed during treatment. Both the IFN-treated group as well as the "historical" control group, made up of 70 cases of fulminant virus hepatitis, not treated with IFN and observed during a previous ten year-period, received supportive therapy; survival rates were similar in both groups. Furthermore, the presence or absence of the delta-agent did not appear to affect survival rates significantly.
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PMID:Attempted treatment of fulminant viral hepatitis with human fibroblast interferon. 389 68

A 68 year old female patient suffered from postoperative hepatitis and fell in grade III coma with the total bilirubin level of 30 mg/100 ml and prothrombin time of 25%. Plasma exchange using hollow fiber plasma separator was performed and after 10 procedures during 1 month, the patient did fully recover.
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PMID:A case of postoperative liver failure successfully treated with plasma exchange. 404 75

The plasma exchange is an effective measure in the treatment of acute liver failure. The authors report their own first experiences in this field in the management of fulminant viral hepatitis. Four out of 7 treated patients survived. So, the survival rate was augmented from 25 per cent in a control group of 8 patients without plasma exchange to 57.1 per cent. Other necessary therapeutic measures are high energetic nutrition, branched chained amino acids, stimulation of liver cell regeneration, correction of coagulation alterations, and intensive care. The success depends on coma stage in the beginning of treatment. Patients with signs of praecoma should be admitted to specialized centers. The number of such centers should be limited because of the necessary experiences and the high costs of combined plasma exchange treatment of this rare hepatitis complication.
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PMID:[Effectiveness of combined plasma exchange treatment in fulminant viral hepatitis]. 408 89

Liver biopsy was performed in 38 patients with fulminant hepatitis and coma and repeated in 22. Stereological estimation of hepatocyte volume was correlated with levels of clotting factors. Early liver biopsy allowed prognosis in 55% of the cases. All patients with a hepatocyte volume of <35% and thromboplastin time </=10% died; all patients but two with hepatocyte volume >/=35% and thromboplastin time >10% recovered consciousness (n = 9) or at least showed evidence of marked liver regeneration (n = 2). On serial liver biopsy a significant increase in hepatocyte volume and clotting factors was only observed in patients who recovered consciousness. The estimated liver cell mass after regeneration in patients who recovered consciousness was >/=45% and <45% in the patients who did not.
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PMID:Liver biopsy and prognosis in acute liver failure. 478 82

A great deal of interest and speculation has arisen from the discovery of a specific antigen, Australia antigen, in the serum of a high proportion of patients with viral hepatitis. This antigen has been found also in the serum of some patients with other conditions, including Down's syndrome, leukemia, leprosy, chronic renal disorders, and chronic active liver disease. It is not found in the serum of normal persons. Australia antigen has been postulated as the causative agent of viral hepatitis. In most patients the antigen can be detected for less than two weeks during the acute phase of the disease. Its persistence in other conditions may be due to an impairment of the immune response. The course of acute viral hepatitis is usually uncomplicated, full recovery of liver function taking place within four to six weeks, with restoration of normal liver histology within three to four months. Follow-up studies of patients in whom hepatitis has developed during epidemics have failed to reveal evidence of subsequent chronic progressive liver disease. This suggests that most cases of chronic active hepatitis are not the result of preceding acute viral hepatitis. However, the recent finding of Australia antigen in the serum of a small number of patients raises the possibility that sporadic viral hepatitis may be one of the causes of the chronic active hepatitis. Alternatively, the presence of the antigen may be interpreted as being due to an altered immune response. The treatment of acute hepatic coma remains unsatisfactory. Several new forms of therapy have been tried in recent years in an uncontrolled way. These include multiple exchange blood transfusions, isolated pig liver perfusion, human cross-circulation, and cross-circulation with baboons. Transient improvement may follow any of these procedures, but evidence that they influence the final outcome of the disease is lacking. The rapid fluctuations in the neurological status of individual patients makes it difficult to interpret the effects of therapy. Also, until satisfactory objective criteria of degrees of coma are universally accepted it will be impossible to compare one mode of therapy with another.
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PMID:Current concepts in viral hepatitis. 552 Jul 27

The authors report three cases of jaundice which developed during pregnancy and which rapidly resulted in the death of the patients. One case was a fulminant case of cytomegalovirus hepatitis and the other two were cases of acute steatosis of pregnancy. The clinical features are marked by the rapid development of a neurological syndrome resulting in coma and the association of blood dyscrasias due to major hepato-cellular failure resulting in DIC. The rapid progression of the disease generally results in the death of the mother and the child. However, there are some reports of survival with total cure after rapid extraction of the foetus, which justify an active therapeutic attitude.
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PMID:[Severe jaundice with fatal outcome in pregnancy]. 609 54

Hospitalized patients with hepatic insufficiency often suffer from severe catabolic states and are in urgent need of nutritional support during their acute illness. Protein intolerence, however, remains a significant problem with respect to the provision of adequate nutrition, either enterally or parenterally. The following report is an anecdotal series of 63 consecutive patients in a large urban hospital treated prospectively with nutritional support using a prototype high branched-chain amino acid solution (FO80) given by technique of total parenteral nutrition by the subclavian or internal jugular route with hypertonic dextrose. Sixty-three patients, of which 42 had chronic liver disease (cirrhosis) with acute decompensation and 17 with acute hepatic injury as well as four with hepatorenal syndrome, are the subject of this report. All required intravenous nutritional support and were either intolerant to commercially available parenteral nutrition solutions or were in hepatic encephalopathy at the time they were initially seen. The cirrhotic patients had been hospitalized for a mean of 14.5 +/- 1.9 days before therapy, had a mean bilirubin of 13 mg/100 ml, and had been in coma for 4.8 +/- 0.7 days despite standard therapy. Patients with acute hepatitis had been in the hospital for 16.2 +/- 4.1 days before therapy, had a mean bilirubin of 25 mg/100 ml, and had been in coma 5.2 +/- 1.6 days before therapy. Routine tests of liver function, blood chemistries, amino acids, EEGs, and complex neurological testing including Reitan trailmaking tests were used in the evaluation of these patients. Up to 120 grams of synthetic amino acid solution with hypertonic dextrose was tolerated in these patients with improvement noted in encephalopathy of at least one grade in 87% of the patients with cirrhosis and 75% of the patients with hepatitis. Nitrogen balance was achieved when 75 to 80 grams of synthetic amino acids were administered. Survival was 45% in the cirrhotic group and 47% in the acute hepatitis group. Encephalopathy appeared to correlate with individual amino acids differentially in the various groups and with the ratio between the aromatic and the branched-chain amino acids. Ammonia did not correlate with either the degree of encephalopathy or improvement therefrom. In 24 Patients therapy for hepatic encephalopathy was limited to infusion of the branched-chain enriched amino acid solution only, with wake-up in 66% of this group. The results strongly suggest that in protein intolerant patients requiring nutritional support, infusion with branchedchain enriched amino acid solutions is well tolerated with either no worsening of or improvement in hepatic encephalopathy coincident with the achievement of nitrogen equilibrium and adequate nutritional support.
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PMID:Infusion of branched-chain enriched amino acid solution in patients with hepatic encephalopathy. 628 73


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