Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lysosomal enzyme beta-hexosaminidase was elevated in different forms of hepatitis. The enzyme level was correlated to the aminotransferases in the acute stage of hepatitis A and B. In hepatitis B there was also a correlation to ALP and bilirubin. In chronic hepatitis B a significant correlation was found only to ALAT. The elevated beta-hexosaminidase levels are attributed to defective non-parenchymal liver cell function in hepatitis.
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PMID:beta-Hexosaminidase level in serum from patients with viral hepatitis as a measure of reticuloendothelial function. 645 81

This article reports the clinical characteristics of 38 cases of patients with hepatitis B (HB) which developed into primary hepatocyte carcinoma (PHC), during a period of observation for 2-28 years (average 11.4 years). These patients were admitted repeatedly for 2 to 12 times (average 3.4 times). The clinical characteristics of the development of the symptoms in these patients were as follows: 1. Liver function fluctuated again and again. Ninety percent of these patients with HB developed liver cirrhosis (LC). Subsequently they developed into PHC. 2. HBV markers were positive over a long period of observation. During the phases of LC and PHC the rates of positive anti-HBe were 23.5% and 54.5%, respectively (P < 0.05). Comparing with anti-HBe, the rate of positive HBeAg was lower. 3. During the phase of HB, 21.0% of these patients had elevated alpha FP (mean titer 80.0 ng/ml). During the phase of PHC, 65.8% of the patients had abnormal alpha FP (mean titer 635.9 ng/ml) (P < 0.01). Sustained high level of gamma-GT and the ratio of gamma-GT/ALT higher than 1.5 were dangerous signals (P < 0.05). The level of ALP in these patients with HB was below 170 u/L. But 50% of them had high level of ALP when they developed into PHC. During the phase of LC these patients were detected regularly with ultrasonic waves.
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PMID:[The study on clinical characteristics of the development of primary hepatocyte carcinoma induced by hepatitis B]. 751 49

Liver cirrhosis (LC) in habitual drinkers is divided into three categories: (1) alcoholic LC, (2) LC due to hepatitis C virus and alcohol, and (3) LC due to hepatitis C virus. In Japan, the frequency of LC related to hepatitis B virus in habitual drinkers is comparatively low. Although making a distinct differentiation is very difficult, it is possible to point out some characteristics which ars due to either alcohol or hepatitis C virus: (1) multiple spider angioma, acne rosacea, and palmar erythema are more frequently found in categories 1 and 2 than in 3, (2) levels of AST/ALT, gamma-GTP, TG, ALP, lactate, and UA are higher in category 1 than in 3, (3) enlargement of both lobes is observed in category 1, and (4) abnormality due to alcohol improves relatively soon after abstinence of alcohol.
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PMID:[Differentiation alcoholic liver cirrhosis from viral liver cirrhosis]. 790 45

We report a case of hyperphosphatasemia in a 35-year-old patient with hepatitis B who underwent an orthotopic xenogeneic liver transplant. Marked increases in total alkaline phosphatase (ALP; EC 3.1.3.1) activity began 5 days posttransplantation (six times human normal) and increased to approximately 17 times normal at day 11. Increased ALP persisted for > 40 days and steadily increased to 75 times normal in the patient's last 30 days. Gel electrophoresis detected both liver (LALP) and biliary (high-molecular-mass, BALP) isoforms. LALP measured with ion-exchange columns revealed an activity time course pattern similar to that of total ALP. Results for BALP activity also obtained with ion-exchange columns exhibited broad variability, ranging from 2 to 428 times normal.
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PMID:Changes in biliary (high-molecular-mass) and liver isoforms of alkaline phosphatase after baboon-to-human liver transplantation. 791 70

We measured serum PIVKA-II concentrations in 18 patients with alcoholic liver cirrhosis. Alcoholic liver disease was diagnosed by the history of ethanol intake of more than 900 ml/day for over 10 years. Liver cirrhosis was diagnosed histologically. Infections with hepatitis B and C viruses were ruled out by assaying serum virus markers. No tumor was detected in liver by ultrasonography and computed tomography during observation period. None of the patients studied were positive for alpafetoprotein (AFP). Eight out of 18 (44.4%) patients with alcoholic liver cirrhosis showed elevated serum PIVKA-II levels. In contrast, only eight out of 93 (8.6%) patients with nonalcholic liver cirrhosis had elevated serum PIVKA-II levels. PIVKA-II is well known as a tumor marker of hepatocellular carcinoma (HCC). The rates of positive PIVKA-II found in alcoholic liver cirrhosis approached its rates in HCC. However, the time course for the elevation of serum PIVKA-II levels was different each other in alcoholic liver cirrhosis and HCC. In HCC, serum PIVKA-II "levels" continued to elevate until therapy. In contrast, its elevation was transient and its levels returned to baseline in alcoholic liver cirrhosis. The values of ALT (GPT), gamma-GTP, and ALP correlated poorly with serum PIVKA-II levels in patients with alcoholic liver cirrhosis. To investigate the mechanism by which elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis occurred, we studied the effect of vitamin K on production of PIVKA-II and AFP by hepatocytes. Hepatocytes(Alexander PLC/PRF/F cell line) were cultured in the presence of various concentrations of vitamin K (Kaytwo, Eisai, Tokyo). Vitamin K had no effect on AFP production. In contrast, PIVKA-II production was inhibited by addition of vitamin K in a dose dependent manner. Moreover, elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis was suppressed by administration of vitamin K (Kaytwo) to these patients. Taken together, these results suggest that vitamin K may have a role in the mechanism of PIVKA-II elevation in sera of these patients. Then, we measured serum concentrations of vitamin K(PK, MK-4, MK-7) in these patients. There was no correlation observed between vitamin K and PIVKA-II in these patients. This result suggests that elevation of serum PIVKA-II in these patients may not be due to vitamin K deficiency. One question not answered here is how serum PIVKA-II levels in these patients are suppressed by treatment with vitamin K (Kaytwo). More detailed analysis of the mechanism of elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis is needed.
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PMID:[Studies on the mechanism of elevation of serum PIVKA-II levels in alcoholic liver cirrhosis]. 1198 59

The aim of this study was to determine the existence of immune activation by measuring neopterin in HBV (Hepatitis B virus) carriers with viral load (HBV DNA) less than 5 pg/ml. Forty-three subjects and 56 healthy controls were included in the study. Neopterin levels of were compared. ALT and ALP levels in one patient and AST levels in two patients were found minimally higher than upper limit, and GGT levels were within the reference range in all patients. Neopterin levels in the patient group and in the controls were 159.97+/-13.39 and 84.10+/-11.45 nmol/l, respectively (P<0.0001). The difference between the two groups was statistically significant (P<0.0001). In conclusion, the increased neopterin levels of HBV carriers might be the indicators of the effect of cellular immunity. This increase might also implicate a background inflammation based on mainly cellular immunity that exists within the liver.
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PMID:Neopterin levels in nonreplicative HBV carriers. 1224 88

Mycophenolate mofetil (MMF) is a potent immunosuppressive agent used in renal transplantation. Gastrointestinal and hematological side effects are commonly observed, but hepatotoxicity has not been reported. In this study, we assessed MMF-related hepatotoxicity in renal transplant recipients. A total of 124 renal transplantation recipients (RTRs) were evaluated for elevated liver enzymes associated with MMF, and 79 patients were enrolled to the study. Patients used MMF 2 g/day. The patients who had progressive increase in liver enzymes after renal transplantation and their AST, ALT, GGT, ALP, bilirubin levels, hepatitis, cytomegalovirus (CMV), abdominal ultrasonography, duration of hepatotoxicity, and decreased dosage or withdrawal of MMF were recorded. Also, we evaluated their liver enzymes while the patients were on the waiting list. Of the 79 patients, 11 patients (13.9%) had a progressive increase in liver enzymes. The median (min-max) age of the patients with MMF-hepatotoxicity was 29 (19-54) and 72.7% of them were male. None of the patients had hepatitis B or C, CMV infection, or other possible causes for elevated liver enzymes and their abdominal ultrasonography were normal. High liver enzyme levels regressed after the withdrawal (n=6) or reduce dosage (n=5) of MMF. The median time of the increase in liver enzymes was 28 (4-70) days and after 50% reduction or withdrawal of MMF, returned to normal values in 16 (4-210) days. The median levels of ALT in waiting list (I), before (II), and after (III) reduction dosage or withdrawal of MMF were 22.0 (3-22), 222.0 (51-508), and 33.0 (21-64) U/L, respectively (p I-II=0.004,p I-II=0.013, andp II-III=0.005). There were no differences for ALP, GGT, total bilirubin, and direct bilirubin levels. Also, the correlation between recovery time of ALT and persistence time of ALT elevation before adjustment of MMF was significant (r=0.739, p=0.009). Consequently, after renal transplantation, hepatotoxicity can occur due to a lot of reason including MMF usage. If hepatotoxicity related to MMF is not considered, especially in the early period of renal transplantation, resolution of hepatotoxicity can be required long term.
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PMID:Uncommon side effect of MMF in renal transplant recipients. 1615 98

Multitransfused beta-thalassaemic patients constitute a population having a higher prevalence of hepatitis C virus (HCV) infection because of its transmission from infected blood collected during seronegative window period. HCV genotyping in thalassaemic patients is mainly useful for the clinical management of the patients and for facilitating decisions on therapy. Thus, the aim of the present study was to identify the genotypes that are prevalent in thalassaemic patients and to correlate these with gender, age, number of blood transfusions and the liver function test profiles. Reverse transcription-polymerase chain reaction (RT-PCR) was carried out in 80 beta-thalassaemic patients (58 men and 22 women) for detection of HCV RNA who were seronegative for hepatitis B virus or human immunodeficiency virus antibodies. HCV genotyping was carried out by restriction fragment length polymorphism (RFLP) method of Chinchai et al. Type-specific PCR followed by direct sequencing was also used to confirm the mixed-genotype infection. Among the 80 thalassaemic patients, 20 and eight patients were infected with genotypes 3 and 1, respectively, whereas two cases had infection with HCV genotype1c/5a. The serum levels of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were found to be significantly altered between the two groups of HCV-infected and noninfected thalassaemic patients. No significant correlation was observed between genotypes when compared with gender, age and number of blood transfusions, except significantly higher level of ALP in genotype 1 than in genotype 3. Genotype 3 alone was the predominant type in beta-thalassaemic patients, with approximately 45% being infected with mixed type. Hence, detection of HCV RNA would help in decreasing the transmission of HCV-infected blood collected during the seronegative window period, whereas determination of genotypes would provide help in adoption of different treatment policies for better management of thalassaemic patients.
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PMID:Distribution of hepatitis C virus genotypes in beta-thalassaemic patients from Northern India. 1716 74

Data about hepatic effects of ethylene glycol ethers had been limited and inconsistent. In this study, we determined whether ethylene glycol monoethyl ether acetate (EGEEA) was a hepatotoxin in exposed workers. Workers from one silk-screening shop (n=29), using EGEEA as the major cleaning solvent, were recruited as high exposure group. Another group of workers with indirect and low exposure to EGEEA (n=57) were selected as the comparison group. Air concentration of EGEEA was measured by 8-h personal sampling. The mean of air EGEEA concentration in the high exposure group was 7.41-16.5 ppm. The mean of air EGEEA concentration in the low exposure group was 0.07-3.62 ppm. Liver function profiles showed that the AST, ALT, ALP and gamma GT in both male and female EGEEA-exposed workers were not significantly different from those in the comparison group. After adjustment for potential confounders such as gender, body mass index, hepatitis B status, and duration of employment, no difference in hepatic dysfunction were found between exposed and comparison groups. In addition, a two-year follow-up study of these EGEEA-exposed workers, no significant change in hepatic function was noted either. The findings suggest that EGEEA is not a hepatotoxin in this workplace.
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PMID:Hepatic effects among workers exposed to ethylene glycol monoethyl ether acetate. 1884 Sep 36

Hepatitis B virus (HBV) reactivation is well documented in individuals with cancer who receive certain cytotoxic or immunosuppressive therapies including rituximab treatment. As a general rule, the risk is greatest upon withdrawal of chemotherapy. The risk ranges from approximately 20 to 50% among HBsAg-positive carriers. A 67-year-old man was diagnosed with inoperable multiple hepatocellular carcinoma accompanied by an increase in alpha-fetoprotein and protein induced by vitamin K absence or antagonist II level. Eighteen weeks after starting on the oral multi-tyrosine kinase inhibitor TSU-68, laboratory investigations showed a substantial increase in serum transaminase levels (AST: 302 IU/l; ALT: 324 IU/l) and an elevation of the HBV-DNA level (6.9 log copies/ml). The diagnosis was that the cause of the acute hepatitis was HBV reactivation and we immediately administered entecavir. Two months after the initiation of daily entecavir treatment, laboratory findings showed that the serum levels of transaminases and ALP had improved (AST: 18 IU/l; ALT: 10 IU/l; ALP: 197 U/l). When the HBV markers were examined 4 months later, they were altered: HBeAg was negative and HBeAb was positive. Entecavir treatment was discontinued after 6 months. Although reactivation with rituximab has been reported, reactivation with a tyrosine kinase inhibitor is extremely unusual in a patient who is HBsAg negative but anti-HBc positive. This is the first report describing HBV reactivation with an increasing HBV-DNA level in a HBsAg-negative/HBcAb-positive/HBsAb-positive patient who was treated with TSU-68 for hepatocellular carcinoma.
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PMID:Hepatitis B Virus Reactivation during Treatment with Multi-Tyrosine Kinase Inhibitor for Hepatocellular Carcinoma. 2313 64


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