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)

A program of twice yearly testing of Alaska Native carriers of hepatitis-B surface antigen (HBsAg), for alpha-fetoprotein elevations as an indicator of early hepatocellular carcinoma has been established in Alaska. Because many HBsAg carriers live in remote regions of Alaska, logistical and cost considerations complicate the efficiency of this program. We evaluated the feasibility of using blood spotted onto mail-in cards as a system of blood collection and commercial assays for alpha-fetoprotein and HBsAg testing. We compared alpha-fetoprotein levels and the detection of HBsAg in both plasma and blood spots from HBsAg-positive carriers, normal volunteers, and pregnant females. There was good correlation between serum and blood spot AFP levels (r = 0.94, p < 0.001) over a wide range of serum alpha-fetoprotein levels. alpha-fetoprotein and HBsAg remained detectable in blood spots stored at room temperature for more than 8 weeks. The sensitivity of detection of HBsAg in blood spots was not as great in blood spots when compared to plasma levels. This system has been incorporated into the hepatocellular carcinoma screening program in Alaska. It should also prove feasible and economical for such screening to be undertaken in developed countries and possibly make alpha-fetoprotein screening affordable in those developing countries where the prevalence of hepatitis-B virus infection is high.
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PMID:Detection of alpha-fetoprotein and hepatitis-B surface antigen in blood spotted on filter paper: use as a screen for hepatocellular carcinoma in Alaska Natives. 888 34

In this paper, we describe a clinicopathological study of primary hepatocellular carcinoma (HCC) associated with alcoholic liver disease without hepatitis virus infection. In 180 HCC patients who were admitted to Asahikawa Medical College Hospital from 1987 to 1995, 10 patients (6%) had HCC associated with pure alcoholic liver disease (Al-HCC), whereas the HCC in 165 patients was associated with chronic viral liver diseases, in 2 with primary biliary cirrhosis, in 1 each with coexistence of the hepatitis C virus infection and hemochromatosis, and in 2 with cirrhosis of unknown origin. In the Al-HCC group, all patients were male. The diagnosis of HCC was obtained at the age of 54 to 67 years old, and the duration of ethanol intake was 33 to 40 years. Four cases had a history of temperance. As an underlying liver disease, liver fibrosis was found in three cases and liver cirrhosis in seven cases. HCC was diagnosed histologically in all cases. Serum alpha-fetoprotein and PIVKA-II were positive in patients with advanced HCC. In cases with small HCC, the tumor was resected surgically in three cases and percutaneous ethanol injection was performed in two cases. In four cases with small HCC, the patients were alive without tumor recurrence during the observation period. In advanced HCC, transcatheter arterial chemolipiodolization was performed. In the analysis of genetic polymorphism of ALDH 2, all Al-HCC had ALDH 2(1)/2(1).
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PMID:Hepatocellular carcinoma associated with alcoholic liver disease: a clinicopathological study and genetic polymorphism of aldehyde dehydrogenase 2. 898 42

We describe a HBsAg-positive patient with non-Hodgkin's lymphoma who underwent aggressive chemotherapy. After discontinuation of chemotherapy, he developed jaundice due to a reactivation of the hepatitis B. Serum HBeAg and HBV DNA turned positive, indicating active virus replication. Abdominal CT-scan showed a large solitary tumour mass in the liver and the serum alpha-fetoprotein level was extremely high, suggesting HBV-related hepatoma. After discontinuation of chemotherapy, the patient died of non-Hodgkin's lymphoma and hepatocellular carcinoma. Throughout treatment of HBsAg-positive patients with cytotoxic or immunosuppressive therapy, careful monitoring of serum aminotransferase levels and HBV DNA is essential. Aggressive chemotherapy may have to be discontinued or changed to a milder regimen if hepatitis occurs.
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PMID:Acute hepatic injury after discontinuation of chemotherapy in a patient with non-Hodgkin's lymphoma and chronic hepatitis B virus infection. 899 Aug 63

Subfractionation of serum alpha-fetoprotein (AFP) is a useful method to discriminate between yolk sac tumors, hepatic malignancies, and benign liver diseases in adults but has not been validated in infants and children. AFP subfractionation was performed on AFP-positive sera from 73 infants and children. AFP subfraction profiles were classified into three common types: (1) yolk sac type, (2) hepatoblastoma type, and (3) benign hepatic type, according to the reactivity of individual AFP samples to lectins. In 68 of 73 samples (93.2%), AFP subfraction profiles were accurately classified into these three types, and an atypical AFP subfraction profile resembling the hepatoblastoma type was found in sera from five infants (6.8%). Differentiation between hepatoblastoma and hepatitis when patients are very young can be difficult. Subfractionation is more accurate when patients are older. This technique was found to be useful in the diagnosis of neonatal ovarian tumors, in recurrent hepatoblastoma/ yolk sac tumor with low serum AFP, and in the differential diagnosis of hepatic mass (malignancy versus hyperplastic nodule) in the liver with long-standing cholestasis. Estimation of serum AFP subfraction profiles facilitates the differential diagnosis of various AFP-positive pediatric diseases, such as hepatoblastoma, hepatoma, hepatitis or germ cell tumors. This test is inexpensive, can be carried out within 48 hours, and should be performed for the differential diagnosis of pediatric liver disease.
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PMID:The role of subfractionation of alpha-fetoprotein in the treatment of pediatric surgical patients. 909 31

Immunohistochemical study was carried out on D-galactosamine hydrochloride (GaIN)-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1Nts strain (Mini rats), in which the expression of growth hormone gene is suppressed by the presence of an antisense transgene. Mini rats were given 1000 mg/kg of GaIN once a week for 4 consecutive weeks and killed at 1, 2, 3 and 4 weeks after the first administration. At 1 week after the first administration, proliferation of small epithelial cells positive for both alpha-fetoprotein and cytokeratin 7, i.e. so-called oval cells, was observed in the whole area of each hepatic lobule, and prominent deposition of fibronectin, laminin and type IV collagen was detected around these oval cells. Together with these extracellular matrix components, many activated Ito cells positive for both desmin and alpha-smooth muscle actin were observed. With time, most of the oval cells formed duct-like structures and lost their positive stainability for alpha-fetoprotein, and many Ito cells became inactive. Deposition of fibronectin decreased rapidly from 2 weeks after the first administration. At 4 weeks after the first administration, deposition of laminin was detected only around the duct-like structures, where that of type IV collagen was also still prominent. These results suggest that a large population of oval cells differentiated into bile duct epithelial cells and that Ito cells and extracellular matrix components might play a role in this process.
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PMID:Immunohistochemical study on galactosamine-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1 Nts strain (Mini rats). 925 Apr 81

Histopathological and immunohistochemical studies were carried out on D-galactosamine (GalNAc)-induced acute hepatitis in rats of the JCI: Wistar TgN (ARGHGEN) 1 Nts strain (Mini rats), in which expression of the growth hormone gene is suppressed by an antisense transgene. Hepatitis characterized by hepatocellular acidophilic necrosis with inflammatory cell infiltration was most prominent at 2 days after GalNAc (1000 mg/kg)-injection, when proliferation of Ito cells and deposition of fibronectin and laminin were found along the sinusoidal linings. At 72 hours after GalNAc-injection, Ito cell proliferation with deposition of laminin and fibronectin became more prominent, and marked proliferation of small epithelial cells was observed in the periportal area. At 7 days after GalNAc-injection, quite a number of alpha-smooth muscle actin-positive Ito cells, surrounded by abundant fibronectin, laminin and type IV collagen, were still observed in close juxtaposition to rapidly proliferating small epithelial cells. The small epithelial cells were found to be positive for both alpha-fetoprotein and cytokeratin 7 and were therefore considered to be so-called oval cells. The results suggest that there may be some relation between oval cell proliferation, Ito cell activation and extracellular matrix accumulation in GalNAc-induced acute hepatitis in Mini rats.
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PMID:Prolonged oval cell proliferation with Ito cell activation and extracellular matrix accumulation in galactosamine-induced acute hepatitis in mini rats. 930 54

Little is known about the coincidence of hepatitis C virus infection (HCV) and non-Hodgkin's lymphoma, although there is an increased incidence of chronic HCV infection with cryoglobulinemia type II and, interestingly, low-grade non-Hodgkin's lymphoma (NHL) in a few patients. We therefore report on a 74-year-old white male with known chronic hepatitis C virus infection who was admitted to the clinic due to weight loss and pain in the right upper quadrant. Ultrasound examination was performed for suspected hepatocellular carcinoma since a lesion in the left lobe of the liver was seen. X-ray of the lungs showed a few scattered lesions, suggestive of metastases. The ultrasound-guided fine-needle puncture revealed a high-grade malignant B-cell NHL While alpha-fetoprotein was normal, both cryoglobulin type II and the polymerase chain reaction (PCR) for HCV were positive. After six cycles of chemotherapy consisting of CHOP, the patient showed complete remission over three years. Ultimately, he died due to a sudden myeloic blast crisis. In summary, we discuss the possible etiopathologic role of the hepatitis viruses in the occurrence of non-Hodgkin's lymphoma. As we and others showed that HCV infects peripheral mononuclear blood cells (PBML), the infected PBML not only may be a source for reinfection after orthotopic liver transplantation, but also could be the cause for transformation and monoclonal propagation of lymphomatous tissue.
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PMID:Primary hepatic high-grade non-Hodgkin's lymphoma and chronic hepatitis C infection. 939 1

Alpha-1-6 fucosylated alpha-fetoprotein (AFP) is known to be elevated in patients with primary hepatoma and has been suggested as being useful as an early indicator and predictor of the poor prognosis for hepatoma. Although GDP-L-fucosyl-N-acetyl-beta-D-glucosaminide alpha-1-6 fucosyltransferase (alpha-1-6 FucT), is the key enzyme involved in alpha-1-6 fucosylation of AFP, when and how the expression of alpha-1-6 FucT is enhanced during hepatocarcinogenesis is unknown. Recently, we established a convenient assay method for this enzyme and were successful in the purification and cDNA cloning of alpha-1-6 FucT from human gastric cancer, as well as from porcine brain. In the present study, levels of alpha-1-6 FucT activity and mRNA expression have been determined during hepatocarcinogenesis in LEC rats which spontaneously develop hereditary hepatitis and hepatoma. The fetal liver contained the highest enzymatic activity, which tended to increase in inverse proportion to gestation. The enzymatic activity was significantly increased in hepatoma tissues as compared with uninvolved adjacent tissues. Northern-blot analysis revealed high expression of alpha-1-6 FucT mRNA in hepatoma tissues, whereas the expression was fairly low in normal, hepatitis and uninvolved adjacent liver tissues. While the fetal liver had the highest enzymatic activity, the expression of alpha-1-6 FucT mRNA was low, suggesting that another alpha-1-6 FucT is induced in fetal liver or that post-translational modification occurs. High expression of alpha-1-6 FucT was also observed in 3'-MeDAB-induced rat hepatomas and some rat hepatoma cell lines. Collectively, alpha-1-6 FucT was strongly enhanced from an early stage of hepatocarcinogenesis and was maintained at a high level in rat hepatomas.
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PMID:High expression of alpha-1-6 fucosyltransferase during rat hepatocarcinogenesis. 945 7

With advances in lectin affinity electrophoresis of alpha-fetoprotein (AFP), the detection of significant changes in serum AFP at low levels in cirrhotics has become important for early detection of hepatocellular carcinoma. Serum AFP levels of 616 healthy individuals without abnormal liver function tests or virus markers of hepatitis B and C were determined by enzyme immunoassay with IMx-AFP Dainapack using automated IMx apparatus set at twice the ordinary sensitivity and compared with those of 241 individuals with abnormal liver function tests and/or positive hepatitis virus markers. The coefficient of variation in this assay was less than 10% at AFP levels as low as 0.2 ng/ml with a lower detection limit of 0.1 ng/ml. The AFP level of healthy population showed a Gaussian distribution curve after logarithmic transformation with a median and 2.5-97.5 percentile reference range of 2.2 (0.6-5.6) ng/ml. There was no significant difference in the AFP level between males and females. Individuals with abnormal liver function tests alone showed no significant increase in serum AFP unless they were associated with positive hepatitis virus markers.
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PMID:Serum alpha-fetoprotein levels in healthy Japanese adults. 966 42

Family history is a risk factor for hepatocellular carcinoma (HCC). However, the risk of first-degree relatives is not known. To investigate the risk of HCC among the first-degree relatives of probands and whether screening can lead to early diagnosis of HCCs in these relatives, we conducted a screening program. The probands' first-degree relatives who were >20 years old were included. Serum aminotransferase, hepatitis viral marker, alpha-fetoprotein, and abdominal sonography were done. HCCs were found in 20 (1.9%) of the 1,046 first-degree relatives, especially in the male siblings. Eighty-five percent of these 20 HCC patients were hepatitis B virus carriers. Forty percent of these 20 HCC patients had tumors <5 cm. Approximately 55% of these 20 HCCs were resectable. The 1-year survival rate in these 20 HCC patients with resectable HCCs was 72.7%. However, the overall 1-year survival rate was only 40%. We found HCC in 1.9% of the first-degree relatives of HCC patients. The male relatives, especially the older brothers, were the group at highest risk. The familial HCCs were closely related to the hepatitis B virus infection. To detect HCCs early, initial screening should be done as early as possible on the HCC family members.
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PMID:Clinical impact of screening first-degree relatives of patients with hepatocellular carcinoma. 980 52


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