bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Randomized Comparison of Metoclopramide and Domperidone on Plasma Aldosterone Concentration and on Spironolactone–Induced Diuresis in Ascitic Cirrhotic Patients
Authors: D-Arienzo Agesilao , Ambrogio Gabriella , Siervi Pasqualina Di , Perna Enzo , Squame Giovanni , Mazzacca Gabriele 
Published: March 2007

The effect of metoclopramide and domperidone, two dopamine antagonists, administered to cirrhotic patients with ascites and secondary hyperaldosteronism, was examined to evaluate the changes in plasma aldosterone levels and in spironolactone–induced diuresis.
In 15 patients with ascites and secondry hyperaldosteronism, the intravenous administration of 10 mg metoclopramide significantly increased plasma aldosterone levels (23%, p < 0.01). This effect was observed when an equivalent dose of domperidone was administered.
In 20 ascitic patients treated with spironolactone (300 mg per day), the administration of metoclopramide (20 mg) significantly reduced urinary output (24%, p < 0.001) and urinary sodium (35%, p < 0.001) while simultaneously increasing urinary potassium (24%, p < 0.001) and plasma aldosterone (40%, p < 0.001). This effect was not observed with domperidone in an equivalent dose.
Therefore, it is recommended that metoclopramide should be avoided during diuretic therapy in cirrhotic patients with ascites. In these circumstances, domperidone is preferred.
Effect of Glycoursodeoxycholate on Precipitation of Calcium Carbonate
Authors: Marteau Chantal , Portugal Henri , Pauli Anne-Marie , Gerolami André 
Published: March 2007

The potential role of bile salts in preventing calcium carbonate precipitation was investigated by studying their interaction of Ca2 and their inhibitory effects on calcium carbonate formation.
Glycochenodeoxycholate micelles bound more calcium than did glycocholate. At bile salt concentrations exceeding 12.5 mM, glycoursodeoxycholate bound calcium as well as glycochenodexycholate did. Similar results for calcium binding were observed in mixed micelles of bile salts and lecithin. In bicarbonate (25 or 50 mM) and CaCl2 (10 mM) solutions, calcium carbonate formation was inhibited by the bile salts. Glycoursodeoxycholate and glycochenodeoxycholate (25 mM) prevented calcium carbonate formation which was delayed by glycocholate. This effect is not due to differences between both series of bile salts for calcium binding since glycoursodeoxycholate or glycochenodeoxycholate (25 mM) more efficiently prevented calcium carbonate precipitation than did 35 mM glycocholate in spite of the same Ca2+ binding.
These results suggest that some bile salts may have a specific role in preventing calcium precipitation in bile. The mechanism is unknown. The physical properties of glycoursodeoxycholate and glycochenodeoxycholate do not support a role for CaCO3 precipitation in gallstone calcification during litholytic therapy.
Hepatic Hemodynamics and Oxygen Consumption in Alcoholic Fatty Liver Assessed by Organ–Reflectance Spectrophotometry and the Hydrogen Clearance Method
Authors: Kasahara Akinori , Hayashi Norio , Kurosawa Kazuhei , Sasaki Yutaka , Sato Nobuhiro , Kamada Takenobu 
Published: March 2007

Hepatic blood flow and estimated hepatic oxygen consumption were studied in rats treated chronically with ethanol by organ–reflectance spectrophotometry and the hydrogen clearance method.
In the withdrawal state from ethanol, the concentration of hemoglobin in the hepatic tissue (ΔEr569—650), the estimated hepatic oxygen consumption (estimated VO2) and the regional liver blood flow decreased significantly in rats treated chronically with ethanol in comparison with their controls. On the other hand, there was no significant difference in the estimated oxygen saturation of the hepatic blood hemoglobin (estimated SO2) between both groups. That is, an increase in oxygen extraction, which was exhibited by a decrease in the estimated SO2, did not occur in rats treated chronically with ethanol in spite of a decrease in blood supply.
Thus, in the withdrawal state from ethanol, both oxygen delivery to the liver and oxygen utilization in the liver weredisturbed at the stage of alcoholic fatty liver.
Short–Term Effects of Propranolol on Portal Venous Pressure
Authors: Garcia-Tsao Guadalupe , Grace Norman D. , Groszmann Roberto J. , Conn Harold O. , Bermann Max M. , Patrick Michael J.C. , Morse Steven S. , Alberts Jeanne L. 
Published: March 2007

The present study was designed to investigate the effect of propranolol on portal pressure of patients with alcoholic cirrhosis and portal hypertension and to correlate these effects with clinical and laboratory parameters. The mean baseline hepatic venous pressure gradient in the 50 patients studied was of 18.2 ± 4.1 mm Hg. It decreased significantly2 hr after the oral administration of 40 mg of propranolol to 15.7 ± 4.2 mm Hg (a mean reduction of 13.4 ± 17%). This reduction in hepatic venous pressure gradient resulted mainly from a decrease in mean wedged hepatic venous pressure. There was no correlation between the decrease in hepatic venous pressure gradient and the decrease in heart rate. When results were analyzed individually, only 15 (30%) showed a large decrease in hepatic venous pressure gradient (>20%), 15 (30%) showed a moderate decrease (10 to 19%), and in 20 patients (40%) there was no reduction or an increase in hepatic venous pressure gradient. Comparison of “responders” (those that reduced hepatic venous pressure gradient >10%) and “nonresponders” (hepatic venous pressure gradient reduction <10%) showed no significant differences in baseline laboratory and hemodynamic parameters, in the severity of the liver disease, in theheart rate and blood pressure response to propranolol, nor in the propranolol plasma levels achieved 2 hr after propranolol administration. Propranolol plasma levels correlated with the reduction in heart rate but not with the reduction in hepatic venous pressure gradient. Of 14 nonresponders to 40 mg of propranolol who received additional doses, six showed a reduction inhepatic venous pressure gradient.
We conclude that, although propranolol reduces the mean portal pressure in patients with alcoholic cirrhosis and portal hypertension, this response is not uniform. Twenty percent of cirrhotic patients do not show any reduction in portal pressure even after maximal doses of propranolol. There is no clear explanation for this variable response; pharmacologic and/or hemodynamic factors may be involved. Neither the heart rate response to propranolol nor the propranolol plasma concentrations were found to be useful in assessing the portal pressure response to propranolol.
Differential Distribution of Hepatitis B Core and E Antigens in Hepatocytes: Analysis by Monoclonal Antibodies
Authors: Mondelli Mario , Tedder Richard S. , Ferns Bridget , Pontisso Patrizia , Realdi Giuseppe , Alberti Alfredo 
Published: March 2007

Current knowledge on the expression of HBeAg in hepatocytes is incomplete because of difficulties in obtaining monospecific antisera devoid of anti–HBc reactivity. In this study, we have examined by immunofluorescence the expression of HBcAg and HBeAgin cryostat liver sections from 25 chronic carriers of HBsAg using monoclonal antibodies.
Although virtually all liver biopsies displayed concordance for HBeAg and HBcAg expression, the pattern of fluorescence differed markedly. Thus, monoclonal anti–HBcgave nuclear staining in all 13 reactive biopsies, while cytoplasmic staining was observed in only two of these. In contrast, monoclonal anti–HBe showed cytoplasmic reactivity coexisting with nuclear reactivity in 10 of 13 reactive biopsies. Hepatitis B virus DNA polymerase activity in the serum appeared to correlate better with the presence of HBcAg in hepatocytes rather than HBeAg.
These results provide further evidence that HBeAg is expressed both in the nuclei and in the cytoplasm of infected hepatocytes. The observation that the number of cells expressing HBeAg exceeds those expressing HBcAg in carriers with active virus replication would suggest that assembly of core particles occurs in only a proportion of infectedhepatocytes expressing HBeAg.
Pyridoxal–5′–Phosphate and Alkaline Phosphatase
Authors: Lumeng Lawrence 
Published: March 2007

Markedly increased circulating concentrations of pyridoxal–5′–phosphate (PLP) were found in each of 14 patients representing all clinical forms of hypophosphatasia, an inborn error characterized by deficient activity of the tissue–nonspecific (bone/liver/kidney) isoenzyme of alkaline phosphatase (AP). The mean PLP concentration in plasma was 1,174 nM (range, 214 to 3,839 nM) in the patients and 57 ± 26 nM (mean ± S.D.) in 38 control subjects. In four affected children, urinary excretion of the PLP degradation product, 4–pyridoxic acid, was unremarkable during consumption of normal quantities of dietary vitamin B6.
Our findings identify increased circulating PLP concentration as a marker for hypophosphatasia and provide further evidence that tissue–nonspecific AP acts in vitamin B6 metabolism. Tissue–nonspecific AP appears to function as an ectoenzyme to regulate extracellular but not intracellular levels of PLP substrate. Performing assays of circulating PLP concentrations alone to assess vitamin B6 nutrition may be misleading in disorders associated with altered AP activity.
Effects of a new loop diuretic (muzolimine) in cirrhosis with ascites: Comparison with furosemide
Authors: Bernardi Mauro , De Palma Rossana , Trevisani Franco , Santini Costanza , Patrono Daniela , Motta Roberto , Servadei Donatella , Gasbarrini Govanni 
Published: March 2007

Muzolimine is a loop diuretic with both the dosedepend increasing effectiveness of loop diurexctics and the long-lasting effect of thiazides. This is a potential advantage in the treatment of ascites in advanced cirrhosis since these patients have a low tolerance to sudden reductions of blood volume.
Equivalent single, oral doses of furosemide (40 mg) and muzolimine (30 mg) were given to 10 cirrhotic patients with ascites and reduced renal perfusion (glomerular filtration rate=30 to 75 ml per min). The study was preceded by 4 days of equilibration (dietary sodium 40 mmoles per day), and the drugs were alternated via a single-blind, cross-over protocol after a wash-out period of 3 days. Renal function was monitored under basal conditions and after diuretic administration through 4-hr clearance periods for 24 hr. The reninaldosterone axis was evaluated before diuretic administration and after 8 and 24 hr. Muzolimine led to a 12-hr cumulative diuresis [AUC0−2=2.52 ± 0.42 (S.E.) ml per min] and natriuresis (5.14 ± 1.05 mmoles per hr), which were comparable to those of furosemide (2.85 ± 0.29 ml per min and 6.75 ± 1.63 mmoles per hr). Its effect, however, was distributed over a longer period (8 hr) than furosemide (4 hr). Muzolimine activity mainly-differed from furosemide because of: significantly lower 12-hr potassium excretion (AUC0−2=0.28 ± 0.82 vs. 2.69 ± 0.46 mmoles per hr; p<0.005); greater sodium/ chloride excretion ratio (0.45 ± 0.08 vs. 0.26 ± 0.06; p<0.025), and absence of rebound phenomena. These were clearly evident with furosemide, involving both the glomerular filtration rate and renal ion excretions from the third clearance period. Finally, plasma renin activity significantly increased 24 hr after furosemide (from 1.66 ± 0.40 to 2.35 ± 0.60 ng per ml per hr; p<0.05), whereas it was not affected by muzolimine administration. These findings suggest that muzolimine use in the treatment of ascites in cirrhosis may be followed less easily by complications, such as diureticinduced uremia and metabolic alkalosis, as compared to other loop diuretics.
The ontogeny of liver copper metabolism in the guinea pig: Clues to the etiology of Wilson's disease
Authors: Srai Surjit K. S. , Burroughs Andrew K. , Wood Bernard , Epstein Owen 
Published: March 2007

The normal human neonate has a copper profile indistinguishable from Wilson's disease, and we have previously postulated that this disease is caused by genetic failure to switch from the fetal to adult mode of copper metabolism. This study validates the developing guinea pig as a suitable animal in which to study copper ontogeny. At birth, liver copper concentrations are 7 times higher than in adults and serum copper and ceruloplasmin are 27 and 21% of adult values, respectively. A 53% fall in liver copper occurs in the 4 days after birth. This is associated with a marked increase in bile copper output, which does not parallel increasing bile flow. Liver copper falls, and serum copper and ceruloplasmin increase to near adult levels in the 30 days after birth. Until the sixtieth day of gestation, liver copper was significantly increased in copper-stressed littermates, although paradoxically at birth, concentrations were significantly lower. In copper-stressed fetal animals, bile copper output increased markedly before birth.
Metallothionein was the dominant copper-binding protein in the fetal liver but a minor component in the adult. Superoxide dismutase activity only developed after birth. We conclude that the postnatal switch from the fetal to adult mode of copper metabolism involves activation of biliary excretion and ceruloplasmin export as well as changes in the association of copper with hepatic copper proteins. Similarities between the fetus and Wilson's disease suggest that this disease is caused by failure of this postnatal adaptation process.
Bile infection documented as initial event in the pathogenesis of brown pigment biliary stones
Authors: Cetta Francesco M. 
Published: March 2007

Findings in two patients having brown pigment bile stones, recurrent 18 and 36 months after cholecystectomy, are reported. Present data suggest that bile infection precedes rather than follows the formation of brown stones. The present data are part of a prospective study of 600 consecutive patients who underwent operation for gallstones and in whom clinical and laboratory findings, intra- and postoperative bile culture and bile pH were related to the analysis of stone composition by X-ray diffractometry and infrared spectroscopy.
Both patients during the first operation underwent cholecystectomy, sphincterotomy and T-tube drainage. Bile culture was negative both at operation and in the first 3 to 5 samples obtained from the T-tube every 2 days, while Escherichia coli was found, starting from the tenth and fourteenth postoperative days, respectively. At the second operation, typical recurrent “earthy” brown stones, easily crushed with the fingers, with no central nucleus of a different structure were found. Previous sphincterotomy became stenotic, and E. coli was found in the operative bile in a concentration higher than 106 per ml. It is suggested that bile infection by E. coli, in addition to bile stasis, plays a crucial role in the pathogenesis of brown pigment stones.
Quantitation, tissue distribution and proliferation kinetics of kupffer cells in normal rat liver
Authors: Bouwens Luc , Baekeland Marijke , de Zanger Ronald , Wisse Eddie 
Published: March 2007

In normal rat liver, Kupffer cells were unequivocally identified using peroxidase cytochemistry by light microscopy in semithin plastic sections. The Kupffer cell population was found to constitute 31% of the sinusoidal cells and by morphometry and serial sectioning, a mean absolute number of 14 to 20 × 106 Kupffer cells per g liver was calculated. The mean distribution of Kupffer cells in the liver lobules was 43% in the periportal, 28% in the midzonal and 29% in the central area of the lobule. Administration of latex particles labeled only 64% of all Kupffer cells, and in particular centrally located cells, showed a lower activity of latex uptake, even at overloading doses. Furthermore, the latter cells were of smaller size than periportal Kupffer cell profiles.
The mean number and distribution of latex-labeled Kupffer cells did not change over a period of 3 months, indicating a long lifetime for these resident macrophages. This slow population turnover was supported by the observed small mitotic index, 0.06% after a 6 hr arrest by vinblastine, and by the small [3H]thymidine labeling index which did not change over a period of 3 weeks after administration of the label. It is proposed that the Kupffer cell population, under physiologic conditions, is a long-living and self-renewing population, the kinetics of which substantially differ from those of other sinusoidal cell types.
Nonsyndromatic paucity of interlobular bile ducts: Light and electron microscopic evaluation of sequential liver biopsies in early childhood
Authors: Kahn Ellen , Daum Fredric , Markowitz James , Teichberg Saul , Duffy Lynn , Harper Rita , Aiges Harvey 
Published: March 2007

Liver biopsies and/or autopsy specimens from 17 children (ages 1 week to 5 years) with nonsyndromatic paucity of the interlobular bile ducts were studied by light and electron microscopy. Initial biopsies were obtained before 90 days of age from all patients, and two or more specimens were available from nine. No specific underlying condition was found in nine infants. The remaining cases were associated with Down's syndrome (n = 2), hypopituitarism (n = 2), cystic fibrosis (n = 1), α1-antitrypsin deficiency (n = 1), cytomegalovirus (n = 1) and Ivemark syndrome (n = 1).
Before 90 days of age, portal changes included duct paucity and fibrosis. Lobular changes were nonspecific, consisting of cholestasis, giant cell transformation, extramedullary hematopoiesis and perisinusoidal fibrosis. Duct paucity, portal fibrosis and perisinusoidal fibrosis persisted after 90 days. Cholestasis was mild or no longer apparent. Portal changes before 90 days of age appear to be sufficiently distinctive to microscopically distinguish nonsyndromatic from syndromatic paucity.
Electron microscopic findings suggest that paucity in nonsyndromatic patients may result from a primary ductal insult: ultrastructural studies revealed bile duct destruction characterized by undulation and breaks in the basal lamina and infiltration of the epithelium by lymphocytes. Bile canalicular dilatation with blunting of microvilli and electron-dense material in the lumen, predominantly seen before 90 days, also reinforces the hypothesis of a primary ductal defect.
Simultaneous passive and active immunization against hepatitis B: Noninterference of hepatitis B immune globulin with the anti-HBs response to reduced doses of heat-inactivated hepatitis B vaccine
Authors: Lelie Nico P. , Reesink Henk W. , Grijm Rob , de Jong-Van Manen Sonja Th. , Reerink-Brongers Eveline E. 
Published: March 2007

The effect of simultaneous administration of hepatitis B immune globulin on the antibody response to a low dose of heat-inactivated hepatitis B vaccine was investigated in 175 health care workers. Subjects were divided into four groups: Groups I and II received 3 monthly injections of a reduced dose (0.6 μg) of a heat-inactivated hepatitis B vaccine (the usual dose being 3 μg) along with 500 IU of hepatitis B immune globulin simultaneously with the first injection of vaccine; Groups III and IV received the vaccine only. In addition, Groups I and III received a final booster injection with 0.6 μg of the vaccine 8 months after the initial injection.
Anti-HBs passively acquired from hepatitis B immune globulin did not interfere with the development of an active antibody response to the vaccine: the anti-HBs conversion rates were similar in persons treated with the combined regimen (89%) as in those who received the vaccine only (91%). At 3 and 5 months after the first injection, however, anti-HBs titers in the recipients of vaccine alone were slightly but statistically significantly higher than those of persons who received both hepatitis B immune globulin and vaccine; but at 8 months, this difference was no longer statistically significant. After a booster inoculation at 8 months, the geometric mean titer of anti-HBs increased 7- to 8-fold in antibody-positive vaccinees, regardless of whether hepatitis B immune globulin had been given earlier. Moreover, 6 of 13 nonresponders to the initial three vaccine injections developed anti-HBs after the booster inoculation.
Thus, passively acquired anti-HBs does not interfere with an active antibody response to hepatitis B vaccine even when a low dose of vaccine is used. Furthermore, a final booster vaccine inoculation, several months after the initial series of injections, is important in providing high response rates and sustained high titers of anti-HBs.
In situ distribution of major histocompatibility complex products and viral antigens in chronic hepatitis B virus infection: Evidence that HBc-containing hepatocytes may express HLA-DR antigens
Authors: van den Oord Joost J. , De Vos Rita , Desmet Valeer J. 
Published: March 2007

Using a double-staining immunohistochemical procedure, the topographical relationship between viral antigens on the one hand and the expression of major histocompatibility complex products by hepatocytes on the other hand was analyzed in a series of 19 liver biopsies from patients with chronic hepatitis B virus infection.
In areas of piecemeal necrosis, periportal hepatocytes demonstrated Class I major histocompatibility complex products or HLA-A, B and C antigens, but did not show a preferential expression of either HBcAg or HBsAg. The cellular infiltrate of piecemeal necrosis consisted of helper/inducer and suppressor/cytotoxic T-lymphocytes, and was admixed in four cases with branching dendritic processes of sinusoidal lining cells which strongly expressed Class II major histocompatibility complex products or HLA-DR antigens. The latter surrounded small groups of periportal hepatocytes.
In areas of spotty necrosis, the hepatocytes expressed HLA-A, B and C antigens in all cases, and were admixed with variable numbers of suppressor/cytotoxic T-lymphocytes. In 14 cases, the clustered hepatocytes in areas of spotty necrosis expressed HLA-DR antigens, associated in 11 of the cases with immunoreactive HBcAg in the nuclei of some of the HLA-DR-positive hepatocytes. Immunoelectron microscopy, performed in one such case, demonstrated the presence of HLA-DR antigen in a discontinuous pattern at the plasma membrane of some hepatocytes, together with the presence of core particles in the nucleus of HLA-DR-positive hepatocytes.
Our findings further contribute to the growing evidence that HBcAg represents the major target antigen for T-cell attack in areas of spotty necrosis. It is suggested that lymphokines, e.g., γ-intereron, secreted by nearby lymphocytes represent the eliciting agent for HLA-DR production and expression by hepatocytes in areas of spotty necrosis in chronic hepatitis B virus infection.