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

A multiparameter ultrasonic tissue characterization system has been developed and tested on several types of diffuse liver disease. The four tissue characterization parameters used are based on the first and second order statistics of the B-scan image. Performance of the system was evaluated using receiver operating characteristic (ROC) analysis and was compared with the performance of experienced human observers viewing B-scan images. The machine-based multiparameter system achieved an area under the ROC curve (Az) of 0.88 for detection of chronic hepatitis in more than 100 proven cases of the disease. This was dramatically better than the performance of human observers (Az = .64, P less than .05) and compares favorably to the performance of other accepted diagnostic tests such as head CT and the PAP smear. For detection of Gaucher's disease, the Az for the system was .92, whereas for separating hepatitis from Gaucher's disease Az was .84. Human observers also did well at these tasks (P greater than .8) using organomegaly as their major criterion for diagnosing Gaucher's disease. For primary biliary cirrhosis the system Az was .80, for glycogen storage disease Az was .94. These results suggest that use of multiparameter tissue characterization can significantly increase the usefulness of ultrasound for evaluation of diffuse liver disease.
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PMID:Quantitative ultrasonic detection and classification of diffuse liver disease. Comparison with human observer performance. 266 36

The liver in an infant or child is as liable to the same pathologies afflicting the adult liver but with certain differences in prevalence and causes. Genetic disorders are more likely to present in the paediatric age group where many involve metabolic processes such as galactosemia, phenylketonuria, glycogen storage disease and others. Many of these present in the newborn period. However, neoplasms and hamartomas also present in the newborn period, such as congenital neuroblastoma with an enormously enlarged liver, hepatoblastoma and haemangioma. The latter may present with intractable cardiac failure as a result of considerable shunting of blood. Acquired liver lesions often present in the newborn period or early infancy and this includes hepatitis and biliary atresia. The difficulties in the differentiation of the two lesions will be discussed together with the management of biliary atresia. As the child grows older, Reyes encephalopathy with microvesicular fat in the liver is not uncommon. The pathophysiology of Reyes encephalopathy as seen locally will be described. The choledochal cyst with direct (Caroli's disease) or indirect effect on the liver will be described. Problems of childhood portal hypertension as well as congenital hepatic fibrosis will be described. Hemosiderosis of the liver is chiefly seen in homozygous beta-thalassaemia patients who have been kept alive with repeated blood transfusions. Amoebic and pyogenic hepatitis, fatty liver due to protein malnutrition, biliary ascariasis, etc, which are common in tropical and subtropical countries are rarely seen now in Singapore children.
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PMID:Paediatric liver disorders in Singapore. 346 38

To assess whether hepatic peptidyl prolyl hydroxylase (PPH) activity could serve as a practical quantitative indicator of hepatic fibrosis or aid in the categorization, diagnosis or prognosis of hepatobiliary disorders in infancy and childhood, the activity of this enzyme has been determined prospectively by a tritium release method in 97 biopsies from 94 infants and children with the following conditions: acute hepatitis of infancy, 10 patients; extrahepatic biliary atresia, 13; previous hepatitis of infancy, 8; alpha-1-antitrypsin deficiency, 6; chronic active hepatitis, 17; chronic persistent hepatitis, 5; glycogen storage disease, 5; and 25 patients with a miscellanea of other liver disorders. PPH activity was considered in relation to diagnosis, biochemical and histological abnormality and subsequent prognosis over a 4-year period. Five liver biopsies which showed no histological abnormality were considered as "controls" having PPH values of 0.72 +/- 0.47 (mean +/- S.D.). PPH activity was significantly elevated in acute hepatitis of infancy, 9 of the 10 infants having PPH greater than 1.66 units (i.e., mean +/- 2 S.D. of the "control" value). Nine infants (70%) with extrahepatic biliary atresia also had PPH activity above this value, as did two with alpha-1-antitrypsin deficiency and 12 patients all in different diagnostic categories. PPH activity did not correlate with hepatic fibrosis as indicated by hepatic hydroxyproline concentration or by histological assessment, or with biochemical tests of liver function within any diagnostic group or in the series as a whole. PPH activity was similar in biopsies with and without histological features of cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic peptidyl prolyl hydroxylase activity and liver fibrosis--a prospective study of 94 infants and children with hepatobiliary disorders. 632 86

Cystic fibrosis (CF) is an autosomal recessive disorder that is reported frequently among Caucasians. In view of the high rate of consanguinity in Saudi Arabia and the high number of children dying so young, many Saudi infants with CF remain undiagnosed owing to lack of clinical suspicion and proper diagnostic facilities. Over a 6-year period (1986-1992), we have made a diagnosis of CF in 36 cases. The aim of this report is to increase awareness of the hepatic presentation of CF in the developing word. Nine patients (25%) were originally referred to us as having liver disorders but subsequent investigations confirmed the diagnosis of CF. The referral diagnoses, number of patients in parentheses, were jaundice for investigation (four), glycogen storage disease (three), hepatomegaly for investigation (one) and neonatal hepatitis (one). Liver biopsies, obtained in five cases, demonstrated portal fibrosis and some steatosis. Consanguinity was present in eight cases, two were siblings. Four patients died. Three families had previously lost seven siblings during infancy with clinical features consistent with CF. It is concluded that hepatic presentation among Saudi patients with CF is relatively common, with serious sequelae.
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PMID:Cystic fibrosis and the liver--a Saudi experience. 782 91

Flutamide, an oral nonsteroidal, antiandrogenic, anilid compound which inhibits the uptake and binding of androgens to nuclear receptors in the prostate, is used with or without LH-RH analogues for treatment of patients with metastatic carcinoma of the prostate. Clinically significant hepatotoxicities such as toxic hepatitis, cholestatic hepatitis, hepatic failure, and even death have rarely been reported in the English literature, but no case has been reported in Korea. A 75-year-old man with metastatic carcinoma of the prostate had taken flutamide (750 mg/day) for 7 months and suddenly developed jaundice and general weakness. The findings of blood chemistries were compatible with cholestatic hepatitis, but ultrasonography, viral marker and auto-antibody studies did not reveal any attributable causes. Histologic examination of a sono-guided liver biopsy only disclosed centrilobular cholestasis, nuclear glycogenosis and mild sinusoidal lymphocytic infiltration. Discontinuation of flutamide resulted in an almost full recovery of the patient's liver function in 2 months. We, herein, report a case of flutamide-induced acute choestatic hepatitis with a brief review of the literature.
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PMID:A case of flutamide-induced acute cholestatic hepatitis--a case report. 882 89

We present a series of 8 patients (6 males, 2 females) with hepatocellular carcinoma (HCC) and glycogen storage disease type Ia (GSD Ia). In this group, the age at which treatment was initiated ranged from birth to 39 years (mean 9.9 years). All patients but one were noncompliant with treatment. Hepatic masses were first detected at an age range of 13-45 years (mean 28.1 years). Age at diagnosis of HCC ranged from 19 to 49 years (mean 36.9 years). Duration between the diagnosis of liver adenomas and the diagnosis of HCC ranged from 0 to 28 years (mean 8.8 years, SD = 11.5). Two patients had positive hepatitis serologies (one hepatitis B, one hepatitis C). Alpha-fetoprotein (AFP) was normal in 6 of the 8 patients. Carcinoembryonic antigen (CEA) was normal in the 5 patients in which it was measured. Current guidelines recommend abdominal ultrasonography with AFP and CEA levels every 3 months once patients develop hepatic lesions. Abdominal CT or MRI is advised when the lesions are large or poorly defined or are growing larger. We question the reliability of AFP and CEA as markers for HCC in GSD Ia. Aggressive interventional management of masses with rapid growth or poorly defined margins may be necessary to prevent the development of HCC in this patient population.
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PMID:Hepatocellular carcinoma in glycogen storage disease type Ia: a case series. 1587 4

This prospective study analyzes the clinical features and histopathological findings in liver biopsies of pediatric patients presenting to the hospital with liver disease during a 10 year period. Only those patients in whom liver biopsy was performed for a tissue diagnosis were included. Fifty patients were investigated, all below the age of 12 years, of whom 36 were male and 14 female. Thirty-two were of neonatal-infantile group, 11 had a diagnosis of neonatal giant cell he hepatitis of infections origin and an intact biliary tree. Two had septic shock and one had leishmaniasis. The remaining 18 patients of the neonatal-infantile group constituted five case of glycogen storage disease, six of infantile obstructive cholangiopathy (biliary atreasia), four of fatty change and one each of congenital hepatic fibrosis, neuroblastoma and nonspecific reactive hepatitis. The eighteen older children had the following diagnoses: thalassemia in five, sickle cell disease in four, two each of Reye syndrome and hepatoblastoma. The remaining were one each of glycogen storage disease, Rotor syndrome, cirrhosis, fatty change and non-Hodgkin lymphoma (NHL). These findings are presented and discussed.
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PMID:Pediatric liver disease in the eastern province of Saudi Arabia: A clinicopathological study. 1758 93

Of hepatocellular carcinomas (HCC), 15-20% occur in the non-cirrhotic liver. All factors which cause HCC when liver cirrhosis (LC) is present, can also lead to HCC without LC. On the basis of the relative frequency, HCC can be roughly differentiated into 3 groups: 1) HCC, rarely occurring without cirrhosis (e.g. virus hepatitis, alcohol abuse). 2) HCC, frequently occurring without LC (alpha1-antitrypsin deficiency, hemochromatosis, non-alcoholic fatty liver disease). 3) HCC, consistently occurring without LC (glycogen storage disease type 1, consumption of oral contraceptives/anabolic steroids). In groups 1 and 2 the level of hepatocellular toxicity necessary to reach LC is not yet achieved but the carcinogenic effect is already strong enough to induce HCC, possibly owing to the influence of additional carcinogens or host factors. In group 3, the carcinogenic effect is mediated by a long-standing alteration of the hepatocellular metabolism that is of low toxic effect and does not lead to cell death, but is nevertheless carcinogenic. In these cases, the initial formation of hepatocellular adenomas that subsequently transform into HCC is a common finding (adenoma-carcinoma sequence).
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PMID:[Hepatocellular carcinoma in the non-cirrhotic liver]. 1805 36

Liver retransplantation carries a significantly higher morbidity and mortality compared with patients after single transplantations. The aim of this study was to review our outcomes in liver retransplantations. From February 1984 to February 2007, 409 liver transplantations were performed on 396 patients, including 13 retransplantations (3.2%) in 12 patients. The mean follow-up was 1.6 +/- 0.4 years (range, 0.1-5.2). The mean duration between the first and the second transplantation was 2.8 +/- 1.0 years (range, 15 days-11.6 years). The indications for the first liver transplantation included biliary atresia (n = 3), hepatitis B virus (HBV)-related cirrhosis with hepatoma (n = 3), fulminant hepatic failure (n = 2), HBV-related end-stage liver disease (n = 1), hepatitis C virus (HCV)-related end-stage liver disease (n = 1), neonatal hepatitis (n = 1), and glycogen storage disease (n = 1). The indications for retransplantations were secondary biliary cirrhosis (n = 3), veno-occlusive disease-related liver failure (n = 2), hepatic arterial occlusion and graft failure (n = 2), chronic rejection with hepatic graft failure (n = 2), recurrent HBV (n = 1) and de novo HBV-related decompensated cirrhosis (n = 1), and idiopathic graft failure (n = 1). There were 4 living donor and 9 deceased donor liver retransplantations. The cumulative survival rate was 71.4 +/- 14.4%, with an estimated mean survival time of 3.9 +/- 0.7 years. Our results showed that minimizing the rate of retransplantation was critical to enhance overall patient survival. Moreover, living donor liver retransplantation is another option within the short, yet critical, waiting period, after failure of the first graft. Provided that a suitable living donor is available, we recommend early retransplantation to minimize the risk of morbidity and mortality.
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PMID:Retransplantation for end-stage liver disease: a single-center Asian experience. 1892 80

Hepatic lesions in nondomestic felids are poorly characterized. The purpose of this study was to evaluate hepatic lesions in 90 captive, nondomestic felids including tigers, cougars, and lions. Hepatic lesions were histologically characterized as vacuolar change (lipidosis or glycogenosis), biliary cysts, biliary hyperplasia, hepatitis, necrosis, neoplasia, fibrosis, veno-occlusive disease, cholestasis, hematoma, congestion, or hemorrhage. Stepwise logistic regression analyses were performed for vacuolar change, benign biliary lesions, hepatitis, lipogranulomas, extramedullary hematopoiesis, and hepatic stellate cell hypertrophy and hyperplasia, with species as the outcome variable. Ninety cats met the inclusion criteria. Seventy livers (78%) contained 1 or more lesions. Hepatocellular vacuolar change (41/90 [46%]) was the most common lesion overall. Extramedullary hematopoiesis, lipogranulomas, and hepatic stellate cell hyperplasia were also common. One snow leopard had veno-occlusive disease. Tigers were more likely than other felids to have no significant hepatic histologic lesions (odds ratio [OR], 12.687; P = .002), and lions were more likely to have biliary cysts (OR, 5.97; P = .021). Six animals (7%) died of hepatic disease: cholangiocellular carcinoma (n = 2) and 1 each of hepatic lipidosis, hepatocellular necrosis, pyogranulomatous hepatitis, and suppurative cholecystitis. Hepatocellular iron and copper accumulations were present in 72 of 90 (80%) and 10 of 90 (11%) sections, respectively. Sinusoidal fibrosis was common (74/90 [82%]) and primarily centrilobular (65/74 [88%]). Hepatocellular iron, copper, and fibrosis were not significantly associated with hepatic lesions. Primary hepatic disease was not a common cause of death in nondomestic felids in this study.
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PMID:Hepatic lesions in 90 captive nondomestic felids presented for autopsy. 2478 21


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