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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the usefulness of muscle biopsy to obtain a diagnosis of Reye syndrome (RS), muscle biopsies were performed in 10 patients, with definite RS (1 patient) and mimicking RS (9 patients) (Table 1). The muscle biopsy results were compared with those of liver biopsies in 7 patients including one patient with definite RS and 6 with mimicking RS. In 3 clinical RS patients, only a muscle biopsy was performed. In the patient with definite RS, oil red O positive lipid droplets were mildly increased in type 1 fibers, with no morphological abnormality of muscle mitochondria, whereas the liver biopsy specimen showed both centrinuclear fatty metamorphosis and mitochondrial abnormality, i.e., a typical RS pathology. Marked lipid accumulation in type 1 fibers and morphological abnormality of muscle mitochondria were observed in two patients with systemic carnitine deficiency and one of two patients with fulminant hepatitis without jaundice who showed mimicking RS clinically. Therefore, it is difficult to make a diagnosis of RS simply on the basis of the clinical findings and muscle morphology.
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PMID:The differential diagnosis of Reye syndrome: muscle biopsy evaluation. 344 23

Serious hepatotoxicity is uncommon with the proper therapeutic use of non-narcotic analgesics but experience with new non-steroidal anti-inflammatory drugs (NSAIDs) is limited. Drugs such as ibufenac, fenclofenac and benoxaprofen were withdrawn from the market because of hepatotoxicity, and liver damage has been reported on occasion with virtually all non-narcotic analgesics. However, a clear pattern of toxicity with characteristic clinical, biochemical and histopathological abnormalities has emerged with relatively few. With the exception of acute hepatic necrosis following overdosage of paracetamol, little is known of the mechanisms of liver injury induced by non-narcotic analgesics. Involvement of the liver in a generalised drug reaction does not imply specific hepatotoxicity. About 50% of patients given aspirin regularly in anti-inflammatory doses develop mild, dose-dependent reversible liver damage as shown by elevation of the plasma aminotransferase activity. Liver damage is more severe in a small minority and it may rarely be complicated by disseminated intravascular coagulation and encephalopathy with a fatal outcome. There have also been isolated reports of chronic active hepatitis associated with the use of salicylates. Salicylate hepatitis has been reported most often in young females with connective tissue diseases. Many patients with Reye's syndrome have been given aspirin during the prodromal phase, and this serious condition closely resembles subacute salicylate intoxication in children. Salicylate probably has a causal or contributory role in Reye's syndrome, but many refuse to accept this and the issue is the subject of heated debate. Paracetamol in overdosage causes acute hepatic necrosis, and liver damage has been attributed to its therapeutic use. However, most reports have involved chronic alcoholics who took excessive doses and in these patients the clinical, biochemical and pathological findings were typical of paracetamol overdosage. Many authors have failed to make the distinction between therapeutic use and a therapeutic dose. In other cases liver damage could have been caused by exposure to other agents, viral infection or naturally occurring liver disease. If these cases are excluded, there are very few reports of liver damage associated with the proper therapeutic use of paracetamol. In some cases, the picture resembled chronic active hepatitis but no causal relationship has been established between this condition and paracetamol use. Paracetamol does not cause deterioration in liver function in patients with chronic liver disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of non-narcotic analgesics on the liver. 355 80

We report the case of a 32 year old man who present two weeks after a typical varicella an alteration of consciousness with pleocytosis in the cerebrospinal fluid and abnormalities of EEG and CT Scan. An hepatic dysfunction with cytolysis and a high level of transaminases and ammonia was noted. About this case the author precise the encephalitic complication of varicella, and the different liver abnormalities, such as Reye's syndrome, hepatitis with parcellar necrosis, or hepatitis with hyperammonemia but without cytolysis or necrosis, as in our own.
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PMID:[Encephalitis and hepatitis after varicella. Relations with Reye's syndrome]. 383 44

Dengue hemorrhagic fever/dengue shock syndrome is a serious manifestation of dengue fever, which is observed predominantly in the tropical regions of the West Pacific and in Southeast Asia and is associated with secondary infections, mainly in children under age 15. A concomitant microangiopathic coagulopathy has been described; moreover, encephalopathy and even Reye's syndrome have been rarely reported. This report describes a 51-year-old man with secondary dengue infection who presented with clinical evidence of severe hepatitis, encephalopathy, cranial nerve palsy, and microangiopathic coagulopathy and who had a favorable outcome. A careful surveillance for the occurrence of secondary dengue in the Western Hemisphere is proposed, and dengue is suggested as a diagnostic possibility in obscure febrile illnesses presenting as either hepatitis, encephalopathy, or coagulopathy in places in which the mosquito vector, Aedes aegypti, is present.
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PMID:Dengue and hepatic failure. 406 82

In a one-year prospective study we assessed the incidence of Reye's syndrome in children presenting with the acute onset of vomiting after a prodromal upper-respiratory-tract infection or varicella, and with serum alanine or aspartate aminotransferase levels at least three times higher than normal, and a paucity of neurologic findings. Of 25 patients meeting the above criteria, 19 had liver biopsies yielding adequate tissue for diagnostic purposes. Biopsy specimens from 14 of these 19 patients (74 per cent) were diagnostic of Reye's syndrome, according to rigorous light-microscopical, histochemical, and ultrastructural criteria. None of the biopsy specimens contained evidence of other acute pathologic processes, including hepatitis. A wide spectrum of mitochondrial alterations existed at the ultrastructural level, ranging from mild to severe lesions that were indistinguishable from those seen in comatose patients with Reye's syndrome. Our findings suggest that the clinical complex of vomiting, hepatic dysfunction, and minimal neurologic impairment after varicella or an upper-respiratory-tract infection usually represents Reye's syndrome. This syndrome occurs more frequently than previously recognized.
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PMID:Grade I Reye's syndrome. A frequent cause of vomiting and liver dysfunction after varicella and upper-respiratory-tract infection. 686 12

Varicella hepatitis has been reported frequently in immunocompromised patients and occasionally in adults with varicella pneumonia and/or systemic involvement. However, hepatitis is not generally known to occur in otherwise uncomplicated varicella. Six children are described who had typical varicella in association with transient elevation of liver enzymes. No CNS abnormalities were noted, and all recovered uneventfully. Such patients have previously been described as representing stage I of Reye's syndrome. The authors postulate that hepatitis complicating varicella may well represent a distinct entity which bears no relationship to Reye's syndrome.
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PMID:Varicella hepatitis without neurologic symptoms or findings. 724 56

The case of a young man of 20 who, after aspecific prodromic symptomatology of viral type, presented a clinical picture characterised by encephalitis and hepatitis classifiable in Reye's syndrome is reported. Bioenzymatic data and therapeutic outlook are discussed.
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PMID:[Clinical picture of Reye's syndrome in an adult]. 739 75

We report the pattern of childhood liver disease revealed by a study of 134 biopsies obtained from 128 infants and children below the age of 16 years seen in this hospital during a 3-year period. The most common histological diagnoses were neonatal hepatitis syndrome in 23, storage disorders in 11, and cirrhosis in 26 children. Less common diagnoses included Reye's syndrome in four, fatty liver in seven, granulomas in four, and chronic active hepatitis, fulminant hepatitis, congenital hepatic fibrosis and neoplasms in two children each. Miscellaneous specific diagnoses were made in 16 cases. Twenty-three per cent of the liver biopsies were non-diagnostic. The study has provided background information on the occurrence of specific histological diagnoses in liver biopsies in infants and children in this tropical region and identifies a group with cirrhosis and copper deposition which was not typical of either Indian childhood cirrhosis or Wilson's disease.
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PMID:The pattern of liver disease in Indian children: a review of 128 biopsied cases. 768 12

Fulminant hepatic failure (FHF) is a poorly understood condition in which total liver failure occurs and is thought to be caused by a variety of conditions including Reye's syndrome, hepatitis, drug overdoses, and vascular insufficiency. While this condition is an uncommon one, it carries with it a high fatality rate and must therefore be diagnosed as rapidly as possible. Six patients have been observed over a two-year period with biopsy and/or autopsy-confirmed FHF: one with acute hepatitis B-delta; three with histories of alcoholism, two of them with cirrhosis; one with acute tylenol overdose; and one with hepatic vascular insufficiency. All of these patients, except one, exhibited a rapid, fatal downhill course after onset of symptoms. In all of these patients, a consistent elevation was observed in serum levels of aspartate aminotransferase (AST) or serum glutamate oxaloacetate transaminase (SGOT) and alanine aminotransferase (ALT) or serum glutamate pyruvate transaminase (SGPT) such that the ratio of AST to ALT was significantly greater than 1 and in serum levels of ammonia. Other liver function tests were found to be abnormal but not in so consistent a pattern, although total protein and albumin were found to be significantly decreased in all of these patients. The stereotypical elevation of the transaminases with high AST-to-ALT ratios and the rise in ammonia appear to characterize this life-threatening illness most reliably.
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PMID:Serum analyte pattern characteristic of fulminant hepatic failure. 820 19

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


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