bluuebunny/crossref_metadata_2025_split huggingface dataset:
Value of Ascitic Lipids in the Differentiation Between Cirrhotic and Malignant Ascites
Authors: Jüngst Dieter , Gerbes Alexander L. , Martin Robert , Paumgartner Gustav 
Published: March 2007

Ascitic fluid concentrations of cholesterol, triglycerides and phospholipids, were compared with ascitic fluid total protein in 40 patients with chronic liver disease, 51patients with various neoplasms and 1 patient with cardiac failure. Seven patients withboth chronic liver disease and malignancy were considered separately. The first 54 patients (23 cirrhotic and 31 with malignancy) were used to determine median values and ranges and to define the most suitable cutoff concentrations between both groups. Median values for cholesterol (75 mg per dl), phospholipids (0.79 mmole per liter), triglycerides (75 mg per dl) and protein (3.8 gm per dl)were higher in malignant ascites compared to ascitic fluid concentrations of cholesterol (20 mg per dl), phospholipids (0.33 mmole per liter), triglycerides (51 mg per dl) and protein (1.9 gm per dl) in patients withcirrhosis. The best discrimination values were 48 mg per dl for cholesterol, 0.6 mmole per liter for phospholipids, 65 mg per dl for triglycerides and 2.5 gm per dl for protein. Application of these cutoff points to 38 subsequent patients (17 cirrhotic, 1 with cardiac failure and 20 with malignancy) revealed an efficiency of 86.8% for cholesterol, 86.8% for phospholipids, 68.4% for triglycerides and 79.0% for protein. From the data of all 92 patients, an efficiency of 92.3% forcholesterol, 79.4% for phospholipids, 72.8% for triglycerides and 79.4% for protein was calculated.
We conclude that ascitic fluid cholesterol determination offers an excellent, cost–effective discrimination of ascites due to cirrhosis vs. ascites caused by malignancies.
The hemodynamic effect of verapamil on portal hypertension in patients with postnecrotic cirrhosis
Authors: Kong Chi-Woon , Lay Chii-Shyan , Tsai Yang-Te , Yeh Ching-Lan , Lai Kwok-Hung , Lee Shou-Dong , Lo Kwang-Juei , Chiang Benjamin N. 
Published: March 2007

Wedged hepatic venous pressure, free hepatic venous pressure and cardiac index were measured before and 1 hr after i.v. administration as well as 1 month and 3 months after chronic oral administration of verapamil in 10 patients with HBsAg-positive cirrhosis.
The gradient between wedged hepatic venous pressure and free hepatic venous pressure was decreased 14% at 1 hr after i.v. administration of 10 mg verapamil, and the sustained decrease in hepatic venous pressure gradient was also demonstrated in the patients after 1 month, and in six patients after 3 months of continuous oral administration of verapamil. The mean arterial pressure significantly decreased (p<0.01) 1 hr after the administration of verapamil. There was no significant change in other hemodynamic values. We conclude that chronic oral administration of verapamil can reduce the hepatic venous pressure gradient in patients with compensated HBsAg-positive cirrhosis and portal hypertension.
Hepatic transport of fluorescent molecules: In Vivo studies using intravital TV microscopy
Authors: Sherman I. A. , Fisher M. M. 
Published: March 2007

Experiments were undertaken to evaluate the role of intravital epifluorescent TV microscopy in the study of the hepatic transport of sodium fluorescein and fluorescently labeled sodium glycocholate in rats and hamsters.
It was found that the apparent sinusoid to canaliculus transport time for fluorescently labeled sodium glycocholate was only half of that for sodium fluorescein, 0.50 and 0.92 sec, respectively. The sinusoid to bile transport time was 35 sec for fluorescently labeled sodium glycocholate and 90 sec for sodium fluorescein. There were also marked differences in zonal clearance of these two substances. Sodium fluorescein was removed from Zone 1 much faster than from Zone 3, while fluorescently labeled sodium glycocholate was cleared at the same rate by hepatocytes in all three acinar zones.
This study provides direct evidence that there are zonal differences in hepatic transport rates for certain compounds. It also demonstrates that epifluorescent TV microscopy has the potential to provide quantitative data on the transport rates of bile acids and other molecules into, through and out of the liver.
Effect of combined treatment with 2,3,7,8-tetrachlorodibenzo- p -dioxin and phototherapy on bilirubin metabolism in the jaundiced gunn rat
Authors: Cohen Arnold N. , Kapitulnik Jaime , Ostrow Donald J. , Webster Cecile C. 
Published: March 2007

2,3,7,8-Tetrachlorodibenzo-p-dioxin, a potent inducer of microsomal cytochrome P448-dependent monoxygenases, and phototherapy both accelerate bilirubin metabolism and decrease jaundice in Gunn rats. The effects of combined treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and light were studied in these rats by applying phototherapy for 65 hr, beginning 5 days after induction with 2,3,7,8-tetrachlorodibenzo-p-dioxin.
2,3,7,8-Tetrachlorodibenzo-p-dioxin pretreatment caused a 75% decline in plasma bilirubin in 5 days, with no change thereafter, whether or not the rats were exposed subsequently to phototherapy. In the uninduced rats, plasma bilirubin levels declined by 55% after 40 hr of phototherapy. As determined by [14C]bilirubin kinetics, both 2,3,7,8-tetrachlorodibenzo-p-dioxin and phototherapy increased fractional bilirubin turnover and decreased the total bilirubin pool. In the 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced rats, the contracted bilirubin pool shifted from skin to liver, but these tissue pools did not change further during phototherapy. By contrast, in uninduced rats, phototherapy decreased the cutaneous bilirubin pool, which is the main target of phototherapy. 2,3,7,8-Tetrachlorodibenzo-p-dioxin was more effective than phototherapy in diminishing plasma bilirubin levels and the total bilirubin pool, but the combined treatment (2,3,7,8-tetrachlorodibenzo-p-dioxin followed by phototherapy) was no more effective than 2,3,7,8-tetrachlorodibenzo-p-dioxin alone.
Halothane hepatitis: A double defect?
Authors: Ranek Leo 
Published: March 2007

We studied susceptibility to halothane hepatitis with an in vitro test that detects cell damage from electrophilic drug intermediates. Metabolites of phenytoin were generated by incubation of phenytoin with rat hepatic microsomes in the presence of the epoxide hydrolase inhibitor 1,1,1-trichloropropene oxide (TCPO), which prevents the further metabolism of phenytoin to an inert metabolite. In lymphocytes exposed to this system, cytotoxicity was measured by trypan blue dye exclusion and was expressed as the percentage increase in trypan blue-positive cells after the addition of TCPO. In the presence of TCPO, lymphocytes from 11 patients with halothane hepatitis exhibited an increase in cytotoxicity at 0.06 mM phenytoin that was eight times greater than the increase in healthy controls (54 ± 10 per cent [mean ± S.E.M.] vs. 7.1 ± 2.2 per cent, p<0.001). Patients with other liver diseases and persons recently exposed to halothane without adverse effects did not differ from healthy controls. In three patients with halothane hepatitis who were studied serially, the lymphocyte abnormality was still present after 13 months. Family studies revealed abnormal results on 10 cytotoxicity tests among 19 members of four families.
We propose that there is a familial, constitutional susceptibility factor that predisposes persons to halothane hepatitis.
Noninvasive measurement of the pressure of esophageal varices using an endoscopic gauge: Comparison with measurements by variceal puncture in patients undergoing endoscopic sclerotherapy
Authors: Bosch Jaime , Bordas José M. , Rigau Joaquín , Viola Carmen , Mastai Ricardo , Kravetz David , Navasa Miguel , Rodés Joan 
Published: March 2007

Measurements of variceal pressure with a noninvasive endoscopic pressure gauge and by direct variceal puncture were performed in 20 cirrhotic patients with portal hypertension in the course of the first session of therapeutic sclerotherapy following an episode of variceal bleeding.
Endoscopic gauge measurements of the pressure of esophageal varices gave similar values (15.5 ± 2.7 mm Hg) than measurements by variceal puncture (15.4 ± 2.4 mm Hg; not statistically significant), and there was a highly significant linear correlation between both measurements (r = 0.9, p < 0.001). Azygos blood flow, that was markedly increased in these patients (852 ± 399 ml per min), was directly related to variceal pressure (r = 0.73, p < 0.01). Variceal pressure was significantly lower than portal pressure (18.8 ± 5.0 mm Hg) (p < 0.05), indicating that measurements of variceal pressure cannot substitute measurements of portal pressure.
The study demonstrates that the noninvasive endoscopic gauge technique allows an accurate estimation of variceal pressure in patients with portal hypertension. This technique may provide additional useful information in the evaluation of portal hypertension as well as on the mechanism of variceal bleeding.
Evaluation of aztreonam in the treatment of spontaneous bacterial peritonitis in patients with cirrhosis
Authors: Ariza Javier , Gudiol Francisco , Dolz Carlos , Xiol Javier , Liñares Josefina , Bosch Jorge , Pallares Roman 
Published: March 2007

To determine the efficacy of aztreonam in the treatment of spontaneous bacterial peritonitis in patients with hepatic cirrhosis, 14 patients (7 males, 7 females) with 16 Gram-negative infective episodes (12 Escherichia coli and 4 Klebsiella pneumoniae) were treated with aztreonam infusions at doses of 1 gm per 8 hr for a planned 14-day period. Ages ranged from 40 to 75 years with a mean of 57 ± 10 years.
All organisms were highly susceptible to aztreonam (minimal inhibitory concentration ≤ 0.06 to 0.12 μg per ml). Serum antibiotic levels were 61.9 ± 25.5 μg per ml (peak) and 27 ± 18.5 μg per ml (trough). Ascitic fluid antibiotic levels were 33.6 ± 22.5 μg per ml (peak) and 32.7 ± 16.8 μg per ml (trough).
Although the symptoms of infection were controlled within 3 days and ascitic fluid cultures became negative after 48 hr, 10 patients (62.5%) died, with hepatorenal syndrome and digestive tract hemorrhage as the principal causes of death. Three patients developed streptococcal superinfections during treatment; Streptococcus faecalis peritonitis in one case and spontaneous bacteremia due to Streptococcus equinus and Streptococcus mutans in the other two.
Aztreonam was well tolerated and clinically and bacteriologically efficacious in controlling the infection. Serum and ascitic fluid levels were considerably higher than the minimal inhibitory concentration for the causative organisms, suggesting that lower doses may achieve suitable therapeutic levels.
A negative aspect of the antibiotic therapy was the superinfections. The high mortality rate was attributable to the generally poor underlying condition of the patients.
Medium-chain and long-chain acyl CoA dehydrogenase deficiency: Clinical, pathologic and ultrastructural differentiation from Reye's syndrome†
Authors: Treem William R. , Witzleben Camillus A. , Piccoli David A. , Stanley Charles A. , Hale Daniel E. , Coates Paul M. , Watkins John B. 
Published: March 2007

The clinical and pathologic findings in 12 patients with medium-chain acyl CoA dehydrogenase deficiency and three patients with long-chain acyl CoA dehydrogenase deficiency are summarized. Although these inborn errors of intramitochondrial β-oxidation of fatty acids present with similar findings to Reye's syndrome, there are clinical, laboratory and hepatic histologic differences. Younger age at presentation, history of unexplained sibling death, a previous episode of lethargy, hypoglycemia or acidosis precipitated by fasting stress and only mildly elevated serum transaminases with normal or only mildly prolonged prothrombin time may all suggest an acyl CoA dehydrogenase deficiency. Long-chain acyl CoA dehydrogenase deficiency is differentiated from medium-chain acyl CoA dehydrogenase deficiency by younger age at presentation, more profound cardiorespiratory depression, evidence of cardiomyopathy, and sequelae of muscle weakness, hypotonia and developmental delay. Definitive diagnosis is made by assay of medium-chain or long-chain enzyme activity in cultured skin fibroblasts or in leukocytes.
Hepatic light microscopic alterations are essentially limited to steatosis, which may be either macro- or microvesicular. The cases with microvesicular steatosis can be differentiated morphologically from Reye's syndrome by electron microscopy, showing the absence of the mitochondrial changes characteristic of Reye's. Four of seven cases of acyl CoA dehydrogenase deficiency showed some variations from normal in the appearance of the hepatocyte mitochondria. The relationship of these variations to the basic metabolic defect(s) remains to be determined.
Type D hepatitis: The clinical significance of hepatitis D virus RNA in serum as detected by a hybridization-based assay
Authors: Smedile Antonina , Rizzetto Mario , Denniston Katherine , Bonino Ferruccio , Wells Frances , Verme Giorgio , Consolo Fausto , Hoyer Bill , Purcell Robert H. , Gerin John L. 
Published: March 2007

Hepatitis D virus is a defective human pathogen that requires hepatitis B virus for its replication. A hybridization-based assay for the 1.75 kb RNA genome of hepatitis D virus was developed using as probe a radiolabeled transcript of a cloned cDNA fragment (pKD3 hepatitis D virus DNA). Sera from 120 chronic carriers of HBsAg with confirmed hepatitis D virus infection were analyzed for the presence of hepatitis D virus RNA. Serum hepatitis D virus RNA was detected in 43 of 74 (58%) patients with chronic liver disease; some patients were positive for hepatitis D virus RNA in multiple samples over a period of several years. Serum hepatitis D virus RNA was present in 17 of 28 (61%) patients during the acute phase of clinical hepatitis and was not detected after recovery from acute disease or in 18 asymptomatic chronic HBsAg carriers with antibody to hepatitis D virus. The presence of hepatitis D virus RNA correlated with other known markers of active hepatitis D virus replication; all chronic active liver disease patients with serum hepatitis D virus RNA were positive for antihepatitis D antigen IgM, and 34 of 37 (92%) had hepatitis D antigen in their liver biopsy specimens.
The assay for hepatitis D virus RNA provides a direct and noninvasive method for the detection of hepatitis D virus in serum and will be useful in the study of the natural history of type D hepatitis, the identification of chronic hepatitis D virus carriers likely to transmit hepatitis D virus and the selection and monitoring of patients for potential antiviral therapy.
A histological study of hepatitis delta virus liver disease
Authors: Verme Giorgio , Amoroso Pietro , Lettieri Gennaro , Pierri Paola , David Ezio , Sessa Fausto , Rizzi Roberto , Bonino Ferruccio , Recchia Serafino , Rizzetto Mario 
Published: March 2007

The histopathology of hepatitis delta virus disease was studied in carriers of HBsAg with chronic hepatitis delta antigen-positive hepatitis and in serial biopsies of patients with acute hepatitis delta virus hepatitis that progressed to chronicity.
There was no histologic feature distinctive of hepatitis delta virus from other types of viral hepatitis. Biopsy specimens of patients with chronic disease exhibited portal and periportal inflammation with piecemeal necrosis, conforming to a picture of aggressive hepatitis often accompanied by cirrhosis. Characteristic was a marked intralobular infiltration by mononuclear cells and a degenerative eosinophilic change of the hepatocytic cytoplasms conducive to the formation of acidophilic bodies.
Liver specimens from patients with hepatitis delta virus hepatitis exhibited aspects of focal, confluent and bridging necrosis. The disease progressed to chronicity irrespective of the original histological features.
The expression of intrahepatic hepatitis delta antigen was reduced in the phase of the acute hepatitis but increased in parallel with the development of chronic active liver disease. In late-stage cirrhosis, expression of hepatitis delta antigen was usually low.
A pilot study on the effects of prednisone withdrawal on serum hepatitis B virus DNA and HBeAg in chronic active hepatitis B
Authors: Nair Prem V. , Tong Myron J. , Stevenson Douglas , Roskamp Deborah , Boone Cissy 
Published: March 2007

We investigated the efficacy of a short course of prednisone therapy in 20 patients with histologic evidence of chronic active hepatitis B. Sixteen of 20 prednisone-treated patients who were initially serum hepatitis B virus DNA-positive had a transient elevation of their serum ALT activity on withdrawal of prednisone. Subsequently, 14 of these 16 patients (87.5%) became persistently negative for serum hepatitis B virus DNA, and 10 also lost their HBeAg. In addition, there was a significant fall in serum ALT levels and HBsAg titers up to 12 months of follow-up in the prednisone-treated group. Five of 20 (25%) prednisone-treated patients experienced a transient episode of hepatic decompensation coinciding with the peak of enzyme elevation.
To contrast, only 3 of 15 (20%) initially hepatitis B virus DNA-positive matched untreated patients followed during the same time period became negative for serum hepatitis B virus DNA, and no significant changes in serum ALT values or HBsAg titers were noted over the 12-month study period. Thus, patients with chronic active hepatitis B appear to be responsive to immunologic manipulation with prednisone as indicated by a pronounced rebound immune response and clearance of hepatitis B virus DNA with improvement in liver disease activity.
If the proper study of mankind is man, the proper study of cholesterol is the liver
Authors: Tint G. S. 
Published: March 2007

A two-year-old boy presented with severe failure to thrive, developmental delay, anemia, hepatosplenomegaly, central cataracts, and dysmorphic features. Quantitative analyses of urinary organic acids revealed massive excretion of mevalonic acid, a metabolic precursor of cholesterol and nonsterol isoprenes: 46,000 to 56,200 mmol per mole of creatinine, as compared with 0.2 to 0.3 mmol per mole in normal children. The mevalonic acid concentration in plasma was also greatly increased at 440 μmol per liter (normal, <0.05). The activity of mevalonate kinase, the enzyme that catalyzes the first step in mevalonate metabolism, was severely deficient in the patient's fibroblasts, lymphocytes, and lymphoblasts.
In the subsequent pregnancy of the patient's mother, gas chromatography-mass spectrometry demonstrated a marked elevation of mevalonic acid in the mother's urine and a 3000-fold elevation, as compared with control levels in the amniotic fluid, suggesting that the fetus was affected. The diagnosis was confirmed by demonstration of the deficiency of mevalonate kinase in amniocytes and ultimately in liver from the abortus. Intermediate activities of the enzyme in both parents indicated an autosomal recessive mode of inheritance. These observations identify an inherited disorder of cholesterol and nonsterol isoprene biosynthesis in humans.
Occurrence and ultrastructural localization of duck hepatitis B virus in the liver of ducks after experimental infection
Authors: Uchida Toshikazu , Suzuki Koyu , Esumi Mariko , Arii Masayuki , Oomura Masashi , Shikata Toshio 
Published: March 2007

A sequential study was performed to investigate the occurrence and localization of duck hepatitis B virus in the liver of domestic ducks utilizing the indirect immunoperoxidase method and electron microscopy. Seventeen ducklings were injected intravenously with duck hepatitis B virus-positive serum within 24 hr after hatching and were subsequently sacrificed on the 2nd, 3rd, 4th, 5th, 27th and 44th day after injection. Nine ducklings were not injected and were used as a negative control.
Duck hepatitis B virus DNA by spot hybridization using a [32P]-labeled probe occurred in trace amounts on the 2nd day and in large amounts on the 4th day after inoculation. Immunoreactivity for DHBV was seen in the hepatocytes, sporadically on the 2nd day and diffusely on the 4th day, and also in the biliary epithelial cells on the 27th day. Both kinds of cells revealed staining in the cytoplasm but not in the nucleus.
Virus particles were recognized by electron microscopy in the hepatocytes beginning on the 4th day. The hepatocytes had many incomplete virus particles, 40 to 61 nm in diameter, and a few complete virus particles, 40 nm in diameter, in the cisternae of the rough and smooth endoplasmic reticula. Such particles and the endoplasmic reticulum showed reaction products for duck hepatitis B virus by immunoelectron microscopy. There were clusters of core particles, 27 nm in diameter, in the hyaloplasm around peroxisomes where an assembly of cores appeared to occur. No conspicuous virus particles were recognized in the biliary epithelial cells. The similarities and differences in virus localization between duck hepatitis B virus and hepatitis B virus are discussed.
Subtypes of antimitochondrial antibodies in primary biliary cirrhosis before and after orthotopic liver transplantation
Authors: Haagsma Elizabeth B. , Manns Michael , Klein Reinhild , Grond Joris , Huizenga Johannes R. , Slooff Maarten J. H. , Zum Büschenfelde Karl-Hermann Meyer , Berg Peter A. , Gips Chris H. 
Published: March 2007

Antimitochondrial antibodies are markers for primary biliary cirrhosis and probably reflect a specific defect in immunoregulation underlying this disease. Antimitochondrial antibodies and their primary biliary cirrhosis-specific subtypes were tested before and up to 6 years after orthotopic liver transplantation. Sera from 31 consecutive patients were tested, 15 patients had primary biliary cirrhosis and 16 non-primary biliary cirrhosis. Antimitochondrial antibodies were investigated under code by immunofluorescence, and primary biliary cirrhosis-specific subtypes were determined by radioimmunoassay (anti-p62, anti-p48) and complement fixation test (anti-M2, anti-M4, anti-M8). Before orthotopic liver transplantation, antimitochondrial antibodies were detected by immunofluorescence in 13 of 15 patients with primary biliary cirrhosis. Of these patients, 12 were positive for anti-p62 and 8 for anti-p48. Ten patients were positive for anti-M2, 4 patients for anti-M4 and 7 patients for anti-M8. Two primary biliary cirrhosis patients and all non-primary biliary cirrhosis patients were negative with all tests. One month after orthotopic liver transplantation, antimitochondrial antibodies titers declined or became negative by antimitochondrial antibodies immunofluorescence, 3 patients became negative by radioimmunoassay for anti-p62 and 1 for anti-p48. With complement fixation test, 4 patients became negative for anti-M2, 2 for anti-M4 and 4 for anti-M8. Antimitochondrial antibody titer reduction observed 1 month after orthotopic liver transplantation remained unchanged in most sera during the following years. A rise was observed in two patients after 4 and 5 years.
We conclude that antimitochondrial antibodies titers detected by immunofluorescence and their primary biliary cirrhosis-specific subtypes decline after orthotopic liver transplantation or become negative. Subtypes after orthotopic liver transplantation are the same as before. Antimitochondrial antibody titer height does not influence long-term results. A recurrence of primary biliary cirrhosis was not observed in our primary biliary cirrhosis patients after orthotopic liver transplantation. Disappearance of antimitochondrial antibodies may be either due to prednisolone treatment or to a cure of the disease by orthotopic liver transplantation.