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)

Two sets of prognostic indicators were recently proposed for selection of patients with acute liver failure for emergency liver transplantation. According to the London criteria, patients with non-paracetamol-induced acute liver failure should be referred for liver transplantation when the prothrombin time is > 100 s or when any three of the following prognostic indicators are present: age < 10 or > 40 yr; non-A, non-B hepatitis, halothane hepatitis or idiosyncratic drug reaction; duration of jaundice before onset of encephalopathy > 7 days; prothrombin time > 50 s; serum bilirubin > 300 mumol/l. According to the Clichy criteria, in acute viral hepatitis, liver transplantation should be decided in patients with coma or confusion, and Factor V < 20% (age < 30 yr) or < 30% (age > 30 yr). To assess the accuracy of these criteria, 81 non-transplanted patients with non-paracetamol-induced acute liver failure were retrospectively studied. The mortality rate was 0.81. The predictive accuracies, respectively on admission and 48 h before death, were 0.80 and 0.79 for the London criteria, and 0.60 and 0.73 for the Clichy criteria. The positive and negative predictive values, 48 h before death, were 0.89 and 0.47 for the London criteria, and 0.89 and 0.36 for the Clichy criteria, respectively. In the 49 patients with acute viral liver failure, the results of the Clichy criteria were similar. In a subgroup of 24 patients who had not received either fresh frozen plasma or sedative-hypnotic drug, the positive predictive values were equal to 1 for the two sets of prognostic indicators, but the predictive accuracies only slightly increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Emergency liver transplantation for acute liver failure. Evaluation of London and Clichy criteria. 844 7

Ischaemic hepatitis, a condition to be distinguished from cardiac liver or stasis cirrhosis, can occur as an acute episode in patients with advanced stage congestive heart failure. The mechanism is massive necrosis in the central lobules resulting from acute hypoxia when low cardiac output reduces oxygen supply further aggravating the underlying condition of congestion due to poor venous outflow. We report 4 cases which illustrate the difficulties in diagnosis and treatment. All four patients (age range 79-86 years) were seen in an emergency situation caused by an acute drop in cardiac output aggravating their underlying heart failure. Clinical signs included jaundice, oligouria, abdominal pain and cardiovascular shock. The first element suggesting the diagnosis of ischaemic hepatitis was a sudden and massive peak in transaminase levels (> 20 times normal) which rapidly returned to normal. Prothrombin and fibrinogen levels fell rapidly and functional renal failure was present in all cases. Viral serology was negative and no hepatotoxic drugs could be incriminated. Despite symptomatic intensive care one patient died on day 15 due to cardiovascular shock. Enzyme movements, together with the lack of evidence for another cause, is the key to diagnosis of acute ischaemic hepatitis which thus is often established after the emergency situation has been controlled. Initially, viral hepatitis or drug-induced hepatotoxicity may be suspected, especially if the episode of low cardiac output goes unrecognized. Cases with signs of encephalopathy may also be difficult to distinguish from fulminating hepatitis and would be the only indication for needle biopsy in this acute situation. Outcome is generally unfavourable with mortality at 6 months estimated at 50%.
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PMID:[Acute ischemic liver]. 854 28

Chronic forms of viral B,C and D hepatitis and fulminant hepatitis represent a serious healthcare problem. The study deals with the changes in the strategy in treating these diseases. During the chronic active hepatitis caused by the B hepatitis virus, the main aim of treatment is to cease multiplication of viruses, eliminate the clinical symptoms, prevent the development of cirrhosis, or the origin of hepatocellular carcinoma. The authors analyze the possibilities of the application of corticosteroids, viricidal drugs (vidarabin and interferons) and other medicaments (acyclovir, zidovudin, duramin, gancyclovir, chinacrin, and others) besides corticosteroids, interleukin 2 and tymozin from the group of immunomodulators were tested. The testing included the factor stimulating the colonies of granulocytes and myeloblasts and other substances. The therapy of acute protracted B hepatitis by means of interferon still requires controlled studies. Superinfection by D virus in chronic carriers of HBsAG causes chronic hepatitis which quickly leads to the development of cirrhosis. The therapy on basis of alpha interferon decreases the RNA virus D hepatitis serum level and leads to an improvement in the development of chronic hepatitis in half of the patients. Therapy of chronic C hepatitis on basis of corticosteroids is ineffective, and can be dangerous. Acyclovir is proved to be ineffective as well. The open study indicated certain positive results in application of interferon. The fulminant hepatitis can be defined as a development of encephalopathy and a decrease of the prothrombin time to less than 50% in the course of acute hepatitis. The break-point in the therapy of fulminant hepatitis took place in association with the performance of the transplantation of the liver. Impossibility to transplant the liver means that the effect of therapy of fulminant hepatitis is merely of supportive value. Majority of patients die due to neurologic complications, namely unmanageable oedema of the brain. But still, neither the antioedema therapy, e.g. on basis of manitol, as well as by means of corticosteroids, hemodialysis, hemofiltration, plasmapheresis and hemoperfusion, nor the treatment on basis of E1 prostaglandine improved the survival of patients. (Tab. 2, Ref. 82).
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PMID:[Treatment of viral hepatitis]. 855 59

A further series of 41 adult patients with late-onset hepatic failure was investigates with respect to aetiological factors, particularly hepatitis C and E, which have been identified since our earlier report of this condition. The increased use of transplantation and its impact on survival overall is assessed. Comparison is made with 64 patients admitted over the same period with fulminant hepatic failure of non-A, non-B aetiology. Screening for the hepatitis viruses revealed three cases of hepatitis A and one case of Epstein Barr virus hepatitis. There were no cases of hepatitis C or hepatitis E virus detected by enzyme immunoassay and reverse transcriptase/polymerase chain reaction techniques, although three patients had positivity for IgG anti-hepatitis E virus, demonstrating previous exposure. Serum autoantibodies in a titre greater than or equal to 1:40 were present in 29% of samples tested and in three cases, titres of SMA or ANF were greater than 1:320. In a further five cases, a potentially hepatotoxic agent had been given within 3 months of the onset of symptoms, leaving the majority of patients (29) with no identifiable cause for their disease. The frequency of symptoms, however, including nausea, abdominal discomfort with the subsequent development of ascites, encephalopathy and renal impairment suggest a similar disease process in these patients. Analysis of liver biopsy material showed similar patterns on all cases of map-like necrosis with nodular regeneration and without other additional features of aetiological significance. Differences in clinical and histological changes for the non-A, non-B fulminant hepatic failure comparison group reflect the tempo of disease process rather than the nature and cause of the liver damage. The introduction of transplantation has led to a marked improvement in survival (39% overall in the earlier series). In the 21 patients in whom transplantation was carried out, the 1-year actuarial survival is currently 55%. Treatment of late-onset hepatic failure with corticosteroids and the use of Prostaglandin E1 and interferon in individual cases has been disappointing, and the emphasis in management should be placed on teh early referral of such patients to a centre offering transplantation.
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PMID:Late-onset hepatic failure: clinical features, serology and outcome following transplantation. 865 52

Eight cases of ecstasy related acute liver damage referred to a specialised liver unit are described. Two patients presented after collapse within six hours of ecstasy ingestion with hyperthermia, hypotension, fitting, and subsequently disseminated intravascular coagulation with rhabdomyolysis together with biochemical evidence of severe hepatic damage. One patient recovered and the other with evidence of hyperacute liver failure was transplanted but subsequently died, histological examination showing widespread microvesicular fatty change. Four patients presented with acute liver failure without hyperthermia. All four fulfilled criteria for transplantation, one died before a donor organ became available, and two died within one month post-transplantation of overwhelming sepsis. Histological examination showed submassive lobular collapse. Two patients presented with abdominal pain and jaundice and recovered over a period of three weeks; histological examination showed a lobular hepatitis with cholestasis. Patients developing jaundice or with evidence of hepatic failure particularly encephalopathy and prolongation of the international normalised ratio, or both, whether or not preceded by hyperthermia, should be referred to a specialised liver unit as liver transplantation probably provides the only chance of recovery.
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PMID:Acute liver damage and ecstasy ingestion. 867 2

We report the case of a patient who developed jaundice, encephalopathy, a marked increase in serum aminotransferase activity and a decrease in prothrombin and proaccelerin levels, after 6 weeks' treatment with carbimazole and propranolol for hyperthyroidism. The patient ultimately underwent orthotopic liver transplantation. This case strongly suggests that carbimazole may occasionally induce fulminant hepatitis and that careful monitoring of liver enzymes may be useful during the treatment of hyperthyroidism with this drug.
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PMID:Fulminant hepatitis after carbimazole and propranolol administration. 872 32

Epidemic emergencies have shown increasing trend in India and most parts of the country appear to be vulnerable to these emergencies. In this paper we present a profile of epidemic emergencies attended by the National Institute of Communicable Diseases in the last five years, to delineate aspects that will promote better preparedness and management. Water borne and water related disease epidemics constituted more than 70% of the epidemic emergencies in India. Non 01 cholera epidemics constituted one fourth of total cholera epidemics during 1991-95. Most of the hepatitis outbreaks were attributed to Non A Non B. The source of infection in majority of the cholera and jaundice epidemics was contaminated water. Dengue and resistant typhoid fever were among other emergencies reported during last five years. Some of these epidemic were reported to local health authorities as mysterious diseases due to lack of public health laboratory facilities. Encephalitis and encephalitis like epidemics in the form of Liquor poisoning and chronic Heat syndrome encephalopathy were also observed. The re-emerging disease epidemics like plague in Beed, Pneumonic plague in Surat and malaria in Rajasthan were also investigated during 1994. These observations indicate the weakness in the epidemiological and laboratory surveillance besides inadequacy in water management practices and other socio environmental reasons.
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PMID:Profile of epidemic emergencies in India during 1991-95. 881 Jan 49

Spontaneous bacterial peritonitis (SBP) is a frequent complication of cirrhosis with ascites. As clinical symptoms are often mild or lacking, the condition may not be perceived in otherwise severely ill patients. This study focuses on diagnostic and prognostic aspects in 25 patients with 26 episodes of SBP. A microbiological diagnosis was established in 18 patients by positive culture of ascitic fluid or positive gram stain. In 8 episodes the diagnosis was presumed on the basis of an elevated polymorphonuclear leukocyte (PMN) count in the ascitic fluid (> 250 PMN/microliters). The mean (+/- SD) age of the 11 women and 14 men was 55 +/- 14 years; 16 were attributed to Child grade C, 9 to Child grade B liver dysfunction. In 19 cases, cirrhosis was confirmed histologically. The underlying liver disease was Laennec's cirrhosis in 13 cases, hepatitis-B virus associated chronic liver disease in 7 cases and primary biliary cirrhosis in 2 cases. At the time of diagnosis, 6 of 25 patients had no fever, 13 of 25 patients had no abdominal pain, 10 of 24 patients showed no abdominal tenderness upon palpation and 5 of 26 patients had no fever or abdominal pain. 17 of 26 patients showed signs of portosystemic encephalopathy. The total white blood cell count in the ascitic fluid was 3627 +/- 3978/microliters with 71 +/- 29% polymorphonuclear cells in the group with microbiologically proven peritonitis and 5105 +/- 2860 cells/microliters (80 +/- 13%) in the group with negative ascitic fluid culture, respectively. Gram stains were positive in 8 cases and culture in 16 of 25 patients. E. coli was cultured in 8 episodes and Str. pneumoniae in two. In-hospital mortality was 61% in the group with microbiologically proven peritonitis and 14% in the group with negative ascitic fluid culture (p = 0.062); 6-month mortality rate was 78% and 86% respectively (p = 0.91). Prognosis was worse in patients Child grade C (p = 0.027), in patients lacking symptoms or signs of peritoneal irritation (p = 0.017), in patients with septic shock (p = 0.018) and in patients with elevated serum-creatinin levels at the time of diagnosis (p = 0.05). SBP is a treatable complication with high mortality of advanced liver disease. Clinical manifestations may be non-specific or absent. We recommend that diagnostic paracentesis be performed in all patients with cirrhosis and ascites if their clinical condition is rapidly worsening.
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PMID:[Spontaneous bacterial peritonitis: diagnostic and prognostic aspects]. 884 98

Forty children with Reye syndrome (RS) or Reye-like illnesses were investigated to elucidate the underlying aetiologies. Extensive biochemical studies including patterns of organic acids and amino acids, liver histopathology, and, if available, a DNA approach were performed. In addition to classical RS (n = 10), the causes of Reye-like conditions included hereditary organic acidaemias (n = 13), urea cycle defects (n = 4), mitochondrial disorders (n = 3), fulminant hepatitis (n = 2), tyrosinaemia (n = 1), valproate-associated hepatotoxicity (n = 1), and other non-specific generalized organic acid disorders (n = 6). It is important to collect specimens when encephalopathy with liver dysfunction of unknown causes is noted. When the underlying inherited metabolic disorders are confirmed, the prevention of the recurrence by adequate diet control and medications, and genetic counselling become possible.
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PMID:Metabolic function and liver histopathology in Reye-like illnesses. 888 17

Patients presenting with clinical and laboratory features consistent with a diagnosis of acute non-A, non-B hepatitis were evaluated for evidence of hepatitis C or hepatitis E infection and for evidence of severe or prolonged disease. Antibody to hepatitis C virus (anti-HCV) was detected in 75 of 108 (69%) patients, antibody to hepatitis E virus (anti-HEV) in three patients (3%), and neither antibody in 31 (29%) patients. One patient had both anti-HCV and anti-HEV. HCV RNA was not detected in sera from any of 20 patients with seronegative (non-ABCDE) hepatitis, but in all 10 patients with anti-HCV who were tested by polymerase chain reaction (PCR). Compared with patients with acute hepatitis C, those with non-ABCDE hepatitis had a lower incidence of parenteral risk factors (6% vs. 70%; P < .001), higher peak serum bilirubin levels (45% vs. 5% with peak levels > 15 mg/dL; P < .001), more prolonged jaundice (25% vs. 0% with peak bilirubin >5 weeks after onset; P < .01), more severe prothrombin time abnormalities (26% vs. 0% with >3 second prolongation; P < .001), more severe hypoalbuminemia (39% vs. 9% with albumin <3 g/dL; P < .01), and more frequent major clinical complications (13% vs. 0% with encephalopathy; P < .01; 10% vs. 0% with death or transplant; P = .024). Patients with acute non-ABCDE hepatitis were less likely to develop chronic hepatitis than those with acute hepatitis C (23% vs. 68%; P < .05). Thus, patients with acute non-ABCDE hepatitis are epidemiologically distinct from those with acute hepatitis C and have a significantly more severe acute illness.
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PMID:Acute sporadic non-A, non-B, non-C, non-D, non-D, non-E hepatitis. 902 67


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