bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of metoclopramide and domperidone on azygos venous blood flow in patients with cirrhosis and portal hypertension†
Authors: Mastai Ricardo , Grande Luis , Bosch Jaime , Bruix Jordi , Rigau Joaquim , Kravetz David , Navasa Miguel , Pera Cristobal , Rodés Joan 
Published: March 2007

The effects of pharmacological manipulation of the lower esophageal sphincter pressure on the esophageal circulation in patients with cirrhosis and portal hypertension were investigated in 33 patients by measuring the azygos venous blood flow, which is an index of blood flow through esophageal varices and periesophageal collaterals draining into the azygos venous system. Measurements were performed in baseline conditions and after the blind administration of metoclopramide (20 mg i.v.) (12 patients), domperidone (10 mg i.v.) (12 patients) and placebo (9 patients).
Both metoclopramide and domperidone caused a significant reduction of azygos blood flow, that decreased by 11.5% (p < 0.01) and 15.6% (p < 0.02) respectively, while no change was observed in patients receiving placebo (+1.4%, not statistically significant). Reduction of azygos blood flow represents a selective effect of metoclopramide and domperidone on the esophageal circulation, since portal pressure, hepatic blood flow, cardiac output, heart rate and arterial blood pressure were unchanged by the administration of metoclopramide, domperidone or placebo.
These results indicate that the administration of drugs that increase the lower esophageal sphincter pressure may reduce the inflow of blood into the esophageal varices in cirrhotic patients with portal hypertension.
Epidemiologic aspects of Santa Marta hepatitis over a 40-year period
Authors: Buitrago Bernardo , Hadler Stephen C. , Popper Hans , Thung Swan N. , Gerber Michael A. , Purcell Robert H. , Maynard James E. 
Published: March 2007

“Santa Marta” hepatitis has been recognized as an unusual type of severe hepatitis occurring in northern Colombia since 1930. Liver specimens from a historic viscerotomy series, used by Gast-Galvis to identify cases and describe epidemiologic features of this disease, were available for review and histopathologic staining for δ-virus. Of 86 liver specimens examined from cases of fulminant Santa Marta hepatitis, 81 showed a distinct histopathologic picture, in various stages of progression, with features of eosinophilic necrosis, microvesicular fat infiltration of the liver parenchyma and morula cells; 69% were positive for δ-antigen by immunoperoxidase staining. This disease occurred predominantly in several small towns within 50 km of Santa Marta, with mortality reaching 1.25 per 1,000 inhabitants per year during the 1940′s. Children under age 15 were most commonly affected and males affected twice as frequently as females. Liver specimens obtained from children, or within 15 hr of death, or which showed early histologic stages of disease were most likely to be positive for δ-antigen.
This and the accompanying study confirm the existence of a distinct type of fulminant hepatitis in Colombia for over 50 years. The epidemiologic and histopathologic features are comparable to severe hepatitis in Venezuela Indians and in the Amazon basin of Brazil, suggesting that all are caused by δ-superinfection of hepatitis B virus carriers.
Virological significance of HBeAg subtypes (HBeAg/1 and HBeAg/2) in patients with type B hepatitis
Authors: Kanno Atsushi , Ohori Hitoshi , Matsuda Keizaburoh , Nakayama Haruo , Miyazaki Yutaka , Ishii Motoyasu , Suzuki Hiroshi , Ohtsuki Masao , Goto Yoshio 
Published: March 2007

In order to establish the virological significance of HBeAg subtypes (HBeAg/1 and HBeAg/2) during hepatitis B virus infection, HBsAg, HBeAg and hepatitis B virus DNA in serum and HBeAg in liver were determined quantitatively in relation to the detection of HBeAg subtypes in agar gel diffusion. Thirty-eight chronic HBsAg carriers with HBeAg, including 16 non-specific reactive hepatitis, 8 chronic persistent hepatitis, 11 chronic active hepatitis and 3 liver cirrhosis, who were seen at Tohoku University Hospital from 1983 to 1985, were examined. Significantly larger amounts of HBsAg, HBeAg and hepatitis B virus DNA in serum and HBeAg in liver were found in patients positive for both HBeAg/1 and HBeAg/2 in serum than in those positive for only HBeAg/1 or negative for both subtypes. These results suggest that the presence of HBeAg/2 in serum may reflect the occurrence of active viral replication.
When the detection pattern of HBeAg subtypes was examined during serial follow-up for at least 1 year, three groups of patients were classified with respect to the presence of HBeAg/2, i.e., Type I, consistently positive for HBeAg/2, Type II, consistently negative for HBeAg/2, and Type III, intermittently positive for HBeAg/2. More than 80% of Type I patients were histologically diagnosed having as nonspecific reactive hepatitis, while more than 80% of Type II and III patients had more progressive liver diseases such as chronic persistent hepatitis, chronic active hepatitis and liver cirrhosis. These results suggest that the serial examination of HBeAg subtypes in serum may be important for more detailed evaluations of type B hepatitis.
Primary hepatocellular carcinoma and hepatitis B infection during childhood
Authors: Wu Tzee Chung , Tong Myron J. , Hwang Betau , Lee Shou-Dong , Hu Mu Mei 
Published: March 2007

Twenty pediatric patients with primary hepatocellular carcinoma in Taiwan were tested for HBsAg, and all were found to be positive. The youngest case was 8 months of age, five cases occurred between 9 and 10 years of age, and 14 cases occurred between 11 and 16 years of age. The serum α-fetoprotein was elevated in all 20 primary hepatocellular carcinoma patients, and the average survival of these cases after diagnosis was 4.7 months.
Seventy per cent of the mothers of the pediatric primary hepatocellular carcinoma cases and 52.9% of their siblings who were tested also were positive for HBsAg. In addition, two families had clustering of primary hepatocellular carcinoma cases.
The occurrence of primary hepatoceullar carcinoma in the pediatric age group suggests the need for close follow-up of young HBsAg-positive carriers. Also, prevention of perinatal transmission of hepatitis B virus by immunoprophylaxis will significantly decrease both the hepatitis B virus carrier rate and the incidence of primary hepatocellular carcinoma in the asian population.
Bile salts induce calcium uptake in vitro by human erythrocytes
Authors: Oelberg David G. , Dubinsky William P. , Sackman Jeffrey W. , Wang Leslie B. , Adcock Eugene W. , Lester Roger 
Published: March 2007

At high concentrations, bile salts induce hemolysis by comicellization of lipid components of the cell membrane. However, bile salts are also associated with hemolysis at lower concentrations by mechanisms which have not been characterized. To investigate the possibility that bile salts promote calcium uptake by red blood cells and that bile salt-associated hemolysis is, in part, calcium-mediated, calcium uptake by red blood cells was measured in the presence of individual bile salts, and hemolysis dependence upon calcium availability was examined.
Washed human red blood cells with or without ATP depletion were incubated with 1 mM CaCl2 and tracer amounts of 45CaCl2 in the presence of selected bile salts at concentrations (0.01 to 0.3 mM reported to be below critical micellar concentrations. Calcium uptake (defined for the purposes of this study as 45Ca retained in red blood cells) was monitored over 5 hr, after which hemolysis and membrane phospholipid content were determined. The presence of bile salts stimulated calcium uptake 4- to 25-fold—the magnitude of which was partly related to the lipid solubility of the bile salts. ATP depletion or exposure to trifluoperazine, procedures which inhibit calcium pump activity in red blood cells, enhanced bile salt-induced calcium uptake relative to controls. The percentage of associated hemolysis (2 to 14%) at the end of 5 hr correlated directly with the observed calcium uptake. Removal of calcium from the extracellular space reduced hemolysis in the presence of bile salts to control levels. After red blood cells exposed to bile salts and calcium were hemolyzed, 10% of the measured calcium uptake by intact cells and 60% of the measured bile salt uptake by intact cells remained with the membrane fraction. Overall, the above results are compatible with the hypothesis that, at concentrations below critical micellar concentrations, bile salts are associated with calcium-dependent hemolysis which results, in part, from increased calcium uptake by cells.
An extrahepatic bile duct growth factor: In vivo effect and preliminary characterization
Authors: Glaser Joy H. , Morecki Rachel , Fallon-Friedlander Sheila , Horwitz Marshall S. 
Published: March 2007

Rabbit sera injected intraperitoneally into BALB/c mice were noted to produce a considerable and selective enlargement of extrahepatic bile ducts. The gallbladder, intrahepatic ducts, liver and other organs showed no stimulaion of growth. Duct enlargement leading to widening of its outer diameter which, on average, was 3.6 times that of normal, was due entirely to an increased number of epithelial cells with prominent proliferation of intramural glandular components. There was no evidence of inflammatory bile duct injury, fibrosis or obstruction. All of the above changes were reversible and regressed slowly after discontinuation of injections. The bile duct growth-promoting factor was detected in sera of many animal species including humans and birds. Host response to this factor was determined by the number of injections and appeared to be strain-related since it was not observed in C57BL or C3H mice. The sex and age of the donor or recipient were not of any relevance to the growth response.
In order to isolate and characterize the bile duct growth factor, rabbit serum was separated into various fractions, and the effect of each fraction was tested in the animal model. Proteins in the 33 to 65% ammonium sulfate precipitate of whole rabbit sera had activity equal to that of native sera. Activity was abolished by treating this serum fraction with 1% sodium dodecyl sulfate plus proteinase K, suggesting that the bile duct growth factor is a protein. Lipids extracted from whole sera using chloroform:methanol or ultracentrifugation were devoid of activity.
These studies point to the existence of a serum protein which acts as a selective in vivo growth factor for extrahepatic bile ducts in genetically susceptible mice.
Anticalmodulin autoantibody in liver diseases: A new antibody against a cytoskeleton-related protein
Authors: Ikeda Yusei , Toda Gotaro , Hashimoto Naoaki , Aotsuka Shin-Ichi , Yokohari Ryuichi , Maruyama Toshiyuki , Oka Hiroshi 
Published: March 2007

An ELISA has been developed for detection of auto-antibodiees against calmodulin. There was a significantly increased frequency (63.1%) of autoantibodies against calmodulin in 103 patients with chronic liver diseases as compared to that (30%) of patients with systemic lupus erythematosus and to that (6.9%) of normal subjects (p < 0.01). IgG autoantibodies against calmodulin were detected in the patients with acute hepatitis (37.9%), chronic liver disease (45.6%) and also in the patients with systemic lupus erythematosus (30%). IgM autoantibodies against calmodulin were frequently found in patients with liver cirrhosis (52.2%), primary biliary cirrhosis (50%) and autoimmune chronic active hepatitis (38.7%), but rarely in patients with acute hepatitis (13.8%), chronic persistent hepatitis (9.5%) and systemic lupus erythematosus (0%). IgA autoantibodies against calmodulin were frequently found in liver cirrhosis (33.3%), primary biliary cirrhosis (452.9%) and autoimmune chronic active hepatitis (53.6%), but rarely in chronic persistent hepatitis (15.8%), chronic active hepatitis (14.3%) and systemic lupus erythematosus (0%).
The occurrences of autoantibodies against calmodulin correlated neither with those of antismooth muscle antibody, antinculear antibody and antimitochondrial antibody, nor with serum IgG concentrations. Autoantibodies against calmodulin did not cross-react with troponin, myosin light chain, calf thymus DNA and actin. The titer of autoantibodies against calmodulin was decreased by absorption of serum with calmodulin and the liver plasma membrane fraction. The immunoblotting experiment revealed the bidning of autoantibodies against calmodulin to calmodulin. IgG fraction from a patient with autoimmune chronic active hepatitis inhibited the activation of phosphodiesterase by calmodulin. These results provide us with valuable information to elucidate the immunological abnormality in liver diseases.
Interaction of natural and synthetic albumin polymers with hepatocytes
Authors: Wright Teresa L. , Lysenko Nina , Ockner Robert K. , Weisiger Richard A. 
Published: March 2007

The hepatitis B virus binds avidly to albumin polymers which in turn may mediate the initial binding of viral particles to the liver cell. However, the interaction of albumin polymers with the liver remains poorly characterized, and the possibility that hepatic binding reflects an artifact of polymerization with glutaraldehyde has not been excluded. We therefore characterized the binding of 125I-labeled natural and synthetic albumin polymers to suspensions of rat hepatocytes.
Saturable binding was demonstrated for all preparations of monomeric and polymeric albumin studied. Glutaraldehyde-polymerized albumin (mean polymerization number = 15) bound much more avidly than naturally occurring albumin polymers (mostly dimers and trimers) or monomeric albumin. Competition between monomer and synthetic polymer was not observed. Reduction of free aldehyde groups on the synthetic polymer decreased nonsaturable binding without affecting saturable binding. Autoradiography confirmed binding of polyalbumin to hepatic parenchymal cells. Glutaraldehyde-polymerized ovalbumin, a protein unrelated to serum albumin, also bound hepatocytes saturably.
We conclude that hepatic binding of synthetic albumin polymers is not due to residual aldehyde groups on the polymer and is much more avid than for natural polymer. This difference may reflect the higher degree of polymerization or chemical modification of the synthetic polymer. The hepatic binding sites for synthetic polymer appear distinct from those previously described for monomeric albumin and may not be specific for albumin.
Long-term follow-up study of asymptomatic hbsag-positive voluntary blood donors in austria: A clinical and histologic evaluation of 242 cases
Authors: Dragosics Brigitte , Ferenci Peter , Hitchman Eva , Denk Helmut 
Published: March 2007

Two hundred forty-two voluntary blood donors, referred after detection of HBsAg positivity, underwent clinical evaluation and liver biopsy and were prospectively followed for an average of 3.5 years. At initial testing, 65% of HBsAg carriers had normal laboratory findings; during follow-up, 26% of these carriers developed abnormal test results, at least transiently. Liver histology was normal in 31.4%, revealed nonaggressive liver disease in 63.6% and chronic active hepatitis or cirrhosis in 5%, only. All except one case of chronic active hepatitis or cirrhosis were associated with abnormal blood biochemical tests. Sequential liver biopsies obtained in 56 HBsAg carriers after a minimal interval of 4 years showed mitigation of inflammatory changes in 5.4% and developing chronic active hepatitis in three cases (5.4%). One carrier died of primary hepatocellular carcinoma.
Upon follow-up, HBsAg persisted in 98%. Anti-HBe was found in 90% of all carriers already at the initial testing. HBeAg positivity (7.5%) was associated with chronic active hepatitis as well as nonaggressive liver disease; clearance of HBeAg occurred in 40% after 2 to 8 years. Because of the subclinical progression of liver disease and the increased risk for developing primary hepatocellular carcinoma in asymptomatic HBsAg carriers, routine blood testing, including α-fetoprotein screening, as well as abdominal ultrasound surveillance are indicated. Liver biopsy, however, should be restricted to carriers with abnormal biochemical findings.
Depression of peripheral blood monocyte aryl hydrocarbon hydroxylase activity in patients with liver disease: Possible involvement of macrophage factors
Authors: Peterson Theresa C. , Williams Noel C. 
Published: March 2007

Aryl hydrocarbon hydroxylase activity was detectable in cultured macrophage monolayers of peripheral blood monocyte origin. Peripheral blood monocytes were isolated from patients with biopsy-confirmed liver disease and healthy volunteers. Macrophage monolayers were prepared and incubated at 37°C. After 24 hr, the aryl hydrocarbon hydroxylase activity and cellular protein concentration were assayed on cell homogenates. The monocyte aryl hydrocarbon hydroxylase activity in cultured macrophages from normal volunteers was 1.23 ± 0.16 (n = 19). The aryl hydrocarbon hydroxylase activity in macrophage cultures from patients with biopsy-confirmed liver disease was 0.48 ± 0.05 (n = 20). This represents a significant (61%) decrease in monocyte aryl hydrocarbon hydroxylase compared to controls. The 20 patients have established cirrhosis or early stage liver disease. The established cirrhosis group includes α1-antitrypsin deficiency-associated cirrhosis; primary biliary cirrhosis; alcoholic (Laennec's) cirrhosis; cryptogenic cirrhosis, and hemochromatosis. Early stage liver disease is attributed to methotrexate (Stage III), early stage primary biliary cirrhosis and α1-antitrypsin deficiency. Our results indicate that the depression in monocyte aryl hydrocarbon hydroxylase activity is greater in patients with established cirrhosis than early stage liver disease.
Our results further suggest that cultured monocytes from patients with liver disease spontaneously release soluble factors into the culture medium. Incubation of this medium, containing macrophage factors, with isolated hepatocytes significantly depress hepatocyte aryl hydrocarbon hydroxylase activity compared to medium obtained from cultures of monocytes from normal volunteers.
We propose that cultured monocyte aryl hydrocarbon hydroxylase activity mimics the hepatic enzyme and reflects the status of the hepatic enzyme in severe liver disease. Consequently, monocyte aryl hydrocarbon hydroxylase activity may be a useful noninvasive measure of hepatic enzyme function.
Liver cell dysplasia: What is its significance?
Authors: Anthony Peter B. 
Published: March 2007

Liver cell dysplasia (LCD) was investigated for hepatitis B virus (HBV) markers, alpha-fetoprotein (AFP) and ferritin by serologic and immuno-histochemical methods in 101 patients with cirrhosis. LCD was found in 30 cases (29.7%), with the highest incidence in cases of posthepatitic cirrhosis (67%). In the group of dysplastic cirrhosis (DC) 46.6% of the patients had active HBV infection (hepatitis B surface antigen [HBsAg] serum positivity) compared with 7% of the patients with nondysplastic cirrhosis (NDC) (P < 0.01). The mean serum AFP concentration was significantly raised in the DC group compared with that in the NDC group (P < 0.05). In seven patients with LCD at the initial biopsy, the histologic follow-up showed the persistence of LCD in all cases, and the development of hepatocellular carcinoma (HCC) in three cases. In serologic HBsAg-positive cases, dysplastic cells, at variance with the surrounding liver parenchyma, were almost always negative for tissue HBsAg, and always negative for tissue hepatitis B core antigens (HBcAg). AFP was never detected in either normal or dysplastic cells. Ferritin was found in all cases, but dysplastic foci displayed a lesser amount of this protein. These serologic and immunohistochemical data strongly suggest a preneoplastic significance of LCD. The importance of monitoring cirrhotic patients with LCD and particularly those with HBV infection and/or increased AFP levels with more aggressive follow-up is also stressed.
An assessment was made of the frequency of liver cell dysplasia and the mean age of each group in 56 normal, 13 cirrhotic, and 50 hepatocellular carcinoma (HCC) patients, 40 with cirrhosis, from southern Africa. Dysplasia increased from 7.1% in normal subjects to 38.5% in cirrhotic, 40% in non-cirrhotic HCC, and 52.5% in cirrhotic HCC patients, three statistically similar frequencies. Average patient ages were as follows: patients with normal livers, 37.3 years; with cirrhosis, 42.4 years; with noncirrhotic HCC, 36.5 years; and with cirrhotic HCC, 34 years, the mean age with dysplasia being lower than that of the whole group. With no increase in frequency of dysplasia from cirrhosis to HCC with cirrhosis, with a similar high frequency in HCC without cirrhosis, and with a mean age of all HCC patients 8 years less than that of cirrhotics and 3 years less than normals, chronologic evolutionary progression from cirrhosis to dysplasia to HCC in southern Africa cannot be demonstrated.
Interrelationship between splenic and superior mesenteric venous circulation manifested by transient splenic arterial occlusion using a balloon catheter
Authors: Nishida Osamu , Moriyasu Fuminori , Nakamura Takefumi , Ban Nobuyuki , Miura Kensuke , Sakai Masahiko , Uchino Haruto , Miyake Takeo 
Published: March 2007

We examined the hemodynamic changes induced by transient splenic arterial occlusion using a balloon catheter to investigate the hemodynamic effect of transcatheter splenic arterial embolization—a procedure that has been used since its introduction in 1973 as therapy for hypersplenism and more recently for portal hypertension. The blood flow volume was measured in 20 patients with liver disease using an ultrasonic duplex system (Toshiba SAL50A/SDL-01A). The portal venous pressure was also measured via a 3F catheter using a transducer. The catheter was placed in position by substituting it for a 25-gauge needle that had been inserted into the portal vein under ultrasonic guidance percutaneously and transhepatically.
Splenic arterial occlusion caused a drop in splenic venous blood flow from 708 ± 487 to 241 ± 155 ml per min, in portal venous blood flow from 993 ± 439 to 807 ± 419 ml per min and in portal venous pressure from 17.4 ± 7.2 to 14.4 ± 6.1 mm Hg. The latter two reductions were less than expected from the decrease in the splenic venous blood flow volume. This phenomenon was caused by an increase in the mesenteric venous blood flow from 475 ± 126 to 630 ± 270 mm per min.
This increase may be due to a compensatory mechanism under the control of a regulatory loop in the liver or portal vein, and there seems to be a relationship between splenic and intestinal circulation in portal hypertension that maintains hepatic circulation.