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

Neonatal hepatitis is closely related to human cytomegalovirus infection in Taiwan, a conclusion based on serological and urine culture studies. To obtain more direct evidence further relating cytomegalovirus to the pathogenesis of neonatal hepatitis, the cytomegalovirus genome was studied in the liver tissues of 50 infants with neonatal hepatitis using the polymerase chain reaction (PCR). Liver tissues from 26 infants with biliary atresia and another 30 infants and children with diagnoses other than neonatal hepatitis, cholestasis, or hepatitis were also studied for comparison. Sequences from the immediate early gene 1 and 2 regions were used as primers. The liver tissues from 23 (46%) of the 50 infants with neonatal hepatitis were positive for cytomegalovirus genome, whereas those of 2 of the 26 infants with biliary atresia and none of the liver tissues from 30 infants and children without neonatal hepatitis were positive for cytomegalovirus genome, by PCR. The results of PCR correlated well with that of serology and urine culture. This study provides further evidence of cytomegalovirus in the pathogenesis of neonatal hepatitis.
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PMID:Polymerase chain reaction to detect human cytomegalovirus in livers of infants with neonatal hepatitis. 132 96

Syndrome of Neonatal hepatitis and atresia of extrahepatic bile ducts are the most frequent causes of jaundice with conjugated bilirubin in the small infant. The neonatal hepatitis is diagnosed by its plurietiologic character, onset in the first 3 months, subacute or chronic, potentially cirrhogenous, evolution, conjugated hyperbilirubinemia and mainly, gigantocellular hepatic transformation--the essential characteristic of the diagnosis. Etiology of neonatal hepatitis has extremely diverse causes: infectious causes, genetic diseases of metabolism, toxic causes, post-hemolytic states, neonatal acute hepatic necroses, parenteral nutrition, chromosomal anomalies, familial syndromes, etc.; there exists also a form with nonspecific cause (idiopathic form). Practically, neonatal hepatitis might often be mistaken for atresia of the extrahepatic bile ducts. In the latter case, the temporization of the surgery (bilidigestive anastomosis) for more than 2 months of cholestasis evolution leads to the appearance of hepatic cirrhosis lesions. The authors analyze various clinical, biological and histopathological elements which permit the differentiation in due time of the two situations that require different therapeutic attitudes. Except for certain situations, which allow an etiologic treatment, the main therapeutic element (pathogenic) is corticotherapy and several additional measures. The paper concludes with appreciations on the evolution, prognosis and prophylaxis possibilities.
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PMID:[The neonatal hepatitis syndrome]. 212 14

Neonatal hepatitis and biliary atresia are disorders of early infancy that represent variable expressions of one entity. Clinical and extensive laboratory evaluation are unsatisfactory in distinguishing between the two diseases. The usefulness of hepatobiliary ultrasonography in the evaluation of neonatal jaundice is described in four infants. Ultrasonic diagnosis was substantiated by laparotomy, liver biopsy or autopsy. The performance of hepatobiliary ultrasonography is recommended in all cases of neonatal jaundice in order to differentiate between extrahepatic biliary obstruction and neonatal hepatitis.
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PMID:Hepatobiliary ultrasonography as a diagnostic aid in neonatal jaundice. 714 55

The risk of a mother transmitting hepatitis B virus infection to her child is virtually 100% when she develops acute HBs and HBe-positive hepatitis during the last three months of pregnancy or if she is a carrier of these two antigens while expecting the baby. The risk is lesser, though not negligible (20%) for children of mothers with HBs-positive and HBe-negative antigens. Most infants contaminated during the perinatal period become themselves carriers of the HBs antigen. Neonatal hepatitis can be prevented by either seroprophylaxis or immunization. To provide maximum and long-lasting protection for children born of HBs-positive mothers, the authors advocate a combination of hepatitis B vaccine and specific anti-HBs immunoglobuLins, the so-called serovaccination.
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PMID:[Mother-to-infant transmission of hepatitis B virus. Towards the prevention of neonatal infection]. 714 88

Six patients with post-infantile giant cell hepatitis (PIGCH) are reported. The age of the patients ranged from 12 to 74 years. One patient had acute giant cell hepatitis and complete restitution was established by biopsy. In five patients, giant cell formation was seen in chronic aggressive hepatitis with cirrhosis. Cirrhosis was demonstrated 5-11 months after the onset of hepatitis. All of these cases later became inactive, but in only one was evidence of inactivity obtained by liver biopsy. Giant cell hepatitis occurred in 0.25% of patients with post-infantile hepatitis; however, all but one of the PIGCH-cases were seen between 1972 and 1974. Hepatitis B markers were negative in all tested cases. The possibility of a special type of infection is discussed.
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PMID:Post-infantile giant cell hepatitis. 716 39

Neonatal hepatitis is a syndrome of unknown etiology occurring in children with viral liver disease, as well as children with unidentified disorders of bile salt synthesis and other poorly understood metabolic diseases. It is characterized by jaundice, giant cell hepatitis and rare liver failure necessitating liver transplantation. In the present investigation, the outcome of liver transplantation performed in 16 children with neonatal hepatitis at the investigators' institution was determined from 1 January 1989 to 31 December 1991. The results were compared to those obtained in 288 children transplanted for biliary atresia and 66 children transplanted for recognized metabolic liver disease. The children transplanted for neonatal hepatitis (4.1 +/- 1.3 years) and metabolic liver disease (5.8 +/- 0.6 years) were older than those transplanted for biliary atresia (3.3 +/- 0.2 years) (p < 0.01), but did not differ in terms of sex, ABO type, UNOS status or year in which the transplant procedure was performed. Interestingly, first allograft survival was equal in the children with neonatal hepatitis (74%) and those with metabolic liver disease (74%), but was greater than that for children transplanted for biliary atresia (68%) (p < 0.01). Despite this significant difference in first graft survival, no differences in 5-year survival were seen for the three groups (81% for neonatal hepatitis, 68% for biliary atresia and 79% for metabolic liver disease).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver transplantation for neonatal hepatitis as compared to the other two leading indications for liver transplantation in children. 769 24

Giant cell hepatitis is a rare disorder after the newborn period. Drugs, autoimmunity, and viruses (lately, paramyxovirus infection) have been implicated in its etiology. Without treatment, liver dysfunction is progressive and fatal. Immunosuppression with steroids and azathioprine has been demonstrated to sustain improvement in the disease. In this report, a one-year-old boy who has giant cell hepatitis with Coombs' positive hemolytic anemia and anti-smooth muscle antibodies is presented, and the course of the disease and the patient's response to treatment with steroid and azathioprine is reviewed.
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PMID:Combination of steroid with azathioprine in treatment of giant cell autoimmune hepatitis. 943 62

The occurrence of plasmodial giant cells in the liver is probably a morphological reaction pattern with the most diverse causes. In babies and infants, these changes occur in particular in neonatal hepatitis and intrahepatic and extrahepatic bile duct atresia. Viral infections and/or autoimmune reactions are discussed etiologically in giant cell hepatitis in adults (adult gaint cell hepatitis, AGCH), which is much rarer. In some of the cases, there were conspicuously high titers against paramyxoviruses. Giant cell hepatitis can occur in the course of HIV infection. These both indicate an infectious cause. However, the disease cannot be transmitted to chimpanzees. Apart from our case, only one further case is described in the literature in which a completed hepatitis A infection could be demonstrated serologically. In addition, the titer of antinuclear antibodies was raised in our patient. This autoimmune phenomenon is probably of crucial pathogenetic significance in our patient, especially since a hepatitis A infection on its own does not afford an adequate etiological explanation for the form of chronic and active hepatitis with consecutive cirrhotic transformation observed here.
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PMID:[Adult giant cell hepatitis with fatal outcome. Clinicopathologic case report and reflections on pathogenesis]. 964 48

Giant cell hepatitis (GCH) in adults is a rare event. The diagnosis of GCH is based on findings of syncytial giant hepatocytes. It is commonly associated with either viral infection or autoimmune hepatitis type I. A patient with GCH due to autoimmune hepatitis type II (LKM1+) is described, a combination that has not been previously reported. Corticosteroid therapy was effective in decreasing serum liver enzymes; however, the patient deteriorated rapidly and developed subfulminant hepatic failure. Although an emergency orthotopic liver transplantation was performed, the patient died because of reperfusion injury. Interestingly, only a few giant hepatocytes were noted in the explanted liver. This case stresses the association of GCH with autoimmune disorders, the possible immune mechanism involved in the formation of giant cell hepatocytes, and illustrates the rapidly progressive course and unfavorable prognosis that these patients can develop.
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PMID:Syncytial giant-cell hepatitis due to autoimmune hepatitis type II (LKM1+) presenting as subfulminant hepatitis. 1071 79

Syncytial giant cell hepatitis in the neonatal period has been associated with many different etiologic agents and may present initially as cholestasis. Infectious causes are most common and include: (1 ) generalized bacterial sepsis, (2) viral agents, (3) toxoplasmosis, (4) syphilis, (5) listeriosis, and (6) tuberculosis. Viral hepatitis may be due to cytomegalovirus, rubella virus, herpes simplex, HHV-6, varicella, coxsackievirus, echovirus, reovirus 3, parvovirus B19, HIV, enteroviruses, paramyxovirus, and hepatitis A, B, or C (rare). Giant cell hepatitis may result in fulminant liver failure with massive hepatocyte necrosis and severe liver dysfunction leading to death, resolution with severely compromised liver function, or liver transplantation. The authors report a 6-week-old male who had an unremarkable perinatal period, became jaundiced after developing diarrhea, and subsequently developed liver dysfunction with massively increased liver enzymes and a coagulopathy. Open wedge and core liver biopsies were performed to determine if the patient should be listed for liver transplantation. Giant cell hepatitis with a significant mixed lymphocytic and neutrophilic infiltrate was present on both the wedge and core biopsies. The residual 60% of hepatocytes had ballooning degeneration and many possessed pyknotic nuclei. The hepatocytes were arranged in a pseudoacinar pattern. Electron microscopy showed paramyxoviral-like inclusions in the giant cells, characterized as large inclusions with fine filamentous, beaded substructures (18-20 nm). Paramyxoviridae are nonsegmented, negative-sense, single-stranded RNA viruses. This family is divided into the Paramyxovirinae subfamily containing respirovirus (Sendai virus, parainfluenza virus type 3), rubulavirus (mumps, parainfluenza virus type 2), and morbillivirus genera (measles); and Pneumovirinae subfamily (pneumovirus genus [respiratory syncytial virus]). Supportive care to determine if hepatic function resolves following the viral episode, liver transplantation with fulminant liver failure, and ongoing evaluation in those who recover to assess chronic liver disease are necessary. Ultrastructural evaluation may unmask the etiologic agent for hepatitis and direct therapy.
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PMID:Neonatal syncytial giant cell hepatitis with paramyxoviral-like inclusions. 1129 22


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