bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hepatic Expression of Intercellular Adhesion Molecule–1 (Icam–1) in Viral Hepatitis B
Authors: Volpes Riccardo , van den Oord Joost J. , Desmet Valeer J. 
Published: March 2007

The in situ distribution patterns of intercellular adhesion molecule–1 and human leukocyte antigen–DR antigens were studied in serial sections of 61 liver biopsy specimens from patients with hepatitis B virus infection using immunohistochemical techniques. In addition, the topographical relationship between the display of HBcAg on one hand and the expression of intercellular adhesion molecule–1 by hepatocytes on the other was analyzed with a double–staining immunohistochemical procedure in 14 selected liver biopsy samples showing chronic persistent or chronic active hepatitis and signs of active hepatitis B virus replication as reflected by the presence of variable amounts of HBcAg in a nuclear or cytoplasmic pattern of immunoreactivity.
Coexpression of intercellular adhesion molecule–1 and human leukocyte antigen–DR antigens by hepatocytes correlated positively with the site and extent of the inflammatory infiltrate, which was composed of lymphocytes expressing lymphocyte function-associated antigen–1. In healthy HBsAg–positive carriers without inflammatory liver disease, no intercellular adhesion molecule–1 or human leukocyte antigen–DR expression was found on hepatocytes; in acute hepatitis, intercellular adhesion molecule–1 and human leukocyte antigen–DR were strongly expressed throughout the liver parenchyma on liver cell membranes and on sinusoidal lining cells. In chronic persistent and chronic active hepatitis and in active cirrhosis, intercellular adhesion molecule–1 and human leukocyte antigen–DR showed membranous positivity on focal clusters of hepatocytes in areas of periportal or intraacinar inflammation.
Double–staining for HBcAg and intercellular adhesion molecule–1 revealed variable numbers of HBcAg–positive hepatocytes expressing intercellular adhesion molecule–1 on their cell membranes; these cells may represent the “cytotoxic” model, in which cell–cell interactions between lymphocyte function-associated antigen–1-positive lymphocytes and hepatitis B virus-infected hepatocytes are facilitated. Furthermore, intercellular adhesion molecule–1-positive hepatocytes lacking HBcAg were found in areas of inflammation, indicating that the virus itself does not directly trigger intercellular adhesion molecule–1 expression. These intercellular adhesion molecule–1-positive, HBcAg–negative liver cells might “guide” lymphocytes through the parenchyma toward virally infected target cells. Finally, in many cases, variable numbers of HBcAg–positive liver cells lacked membranous intercellular adhesion molecule–1 expression; these cells may represent the “tolerogenic” model, in which incomplete clearance of virally infected hepatocytes adds to the chronic nature of hepatitis B virus infection. (Hepatology 1990;12:148-154).
Auxiliary Liver Transplantation: A Negative Viewpoint
Authors: Shaked Abraham A. , Busuttil Ronald W. 
Published: March 2007

Auxiliary heterotopic liver transplantation is theoretically attractive because it leaves the recipient's liver in place. The surgical trauma of hepatectomy is avoided, and failure of the graft does not necessarily lead to the death of the patient or a second, emergency transplantation. Another advantage is that matching the body sizes of the donor and the recipient is not mandatory, which increases the number of possible donors. However, previous clinical results of auxiliary liver transplantation have been poor.
We performed auxiliary partial liver transplantation in six consecutive patients with end–stage chronic liver disease who were not accepted for orthotopic liver transplantation because they had massive ascites, deficient clotting function, cachexia, or poor pulmonary reserve. The donor liver was transplanted to the right subhepatic region after removal of segments II and III, and it was provided with portal and arterial blood. There were no major changes in hemodynamic measurements during surgery. The mean hospital stay after transplantation was 22.7 days (range, 14 to 29). After a mean follow–up period of 14 months (range, 5 to 23), all patients were alive, with good graft function as demonstrated by scintigraphy, Doppler ultrasonography, and synthesis of clotting factors.
From these observations we conclude that auxiliary partial liver transplantation is an attractive alternative to orthotopic liver transplantation in high–risk patients. Its role in other patients who need liver transplants remains to be defined.
Microscopic Incipient Hepatocellular Carcinoma Found Incidentally in A Routine Liver Biopsy Specimen
Authors: Hirooka Noboru , Nitta Yoshiro , Tsunoda Takabumi , Kitazawa Eiji , Sato Junichi , Machii Akira , Murakami Yoshitsugu , Takahashi Manabu , Kondo Fukuo 
Published: March 2007

A microscopic atypical focus suggestive of hepatocellular carcinoma is reported. The lesion, 0.3 mm in diameter, was found by chance in a liver biopsy specimen taken from a cirrhotic patient; it was characterized histologically by cytoplasmic basophilia, hypercellularity (high nucleus–to–cell ratio) and microacinar structures. The reticulin framework of the focus was relatively sparse compared with the surrounding noncancerous area. The focus had developed in a regenerative nodule apparently no different from other regenerative nodules of the cirrhosis and showed no accompanying preneoplastic lesion such as adenomatous hyperplasia.
A thorough search for the primary lesion, including ultrasonographic imaging and superselective hepatic arteriography, demonstrated no mass lesion in the liver.
Therefore, the lesion may have been an incipient de novo hepatocellular carcinoma, and this may be the first report of such a lesion discovered in a biopsy sample. (Hepatology 1990;12:291-294).
Ursodeoxycholic acid-induced changes of plasma and urinary bile acids in patients with primary biliary cirrhosis
Authors: Stiehl Adolf , Rudolph Gerda , Raedsch Richard , Moller Bernd , Hopf Ulrich , Lotterer Erich , Bircher Johannes , Fölsch Ulrich , Klaus Jürgen , Endele Richard , Senn Martin 
Published: March 2007

Ursodeoxycholic acid treatment of patients with primary biliary cirrhosis may lead to relief of pruritus and improvement of biochemical liver tests. The changes in serum and urinary bile acids induced by ursodeoxycholic acid treatment were studied. After 29 patients with primary biliary cirrhosis were treated with ursodeoxycholic acid (750 to 1,000 mg/day) for 6 to 12 mo because of an increase in ursodeoxycholic acid, total plasma bile acids increased from 30.5 ± 6 μmol/L (mean ± S.E.M.) to 52.7 ± 11.7 μmol/L (p < 0.01). The increase in total plasma bile acids correlated significantly with concentrations of plasma bile acid before treatment (p < 0.01). The concentrations of endogenous bile acids decreased, mainly because of a decrease of cholic acid. During treatment, glycine conjugation increased and taurine conjugation decreased, whereas sulfation and glucuronidation of bile acids were unchanged.
In 10 patients with primary biliary cirrhosis in stages III and IV, urinary excretion of bile acids was also studied. After treatment, ursodeoxycholic acid and its 3-β isomer and C-1-hydroxylated and C-6-hydroxylated derivatives were also excreted. During treatment, urinary excretion of endogenous bile acids decreased.
The increase of ursodeoxycholic acid and the decrease of endogenous bile acids may both be related to the improvement of biochemical liver tests in precirrhotic stages of the disease. In cirrhosis, endogenous bile acids in plasma remained high and changes in liver tests were small. (Hepatology 1990;12:492-497).
Mechanisms of transport of nontransferrin-bound iron in basolateral and canalicular rat liver plasma membrane vesicles
Authors: Wright Teresa L. , Lake John R. 
Published: March 2007

Although most iron in plasma is bound to transferrin, recent evidence suggests that the nontransferrin-bound fraction contributes to hepatic iron loading and toxicity seen in iron-overload disorders. Our studies of isolated perfused rat liver previously demonstrated saturable uptake of nontransferrin-bound iron that continues despite hepatic iron overload. To further characterize the mechanism of transport of this form of iron, we measured binding of 55Fe-labeled ferrous ascorbate to rat liver plasma membrane vesicles under varying conditions. Binding of 5 μmol/L iron by both basolateral and canalicular membranes was time-dependent and linear for the first 5 sec. Initial rate of binding of ferrous ascorbate to basolateral membrane vesicles was temperature dependent and increased by calcium but, in contrast to the perfused rat liver, was not inhibited by other divalent cations. Binding velocities by basolateral membrane vesicles were saturable at increasing iron concentration (Km = 33 μmol/L, Vmax = 16 pmol/mg protein/sec). Ferrous iron binding by canalicular membrane vesicles was also temperature dependent, but initial association rates were not saturable over the concentration range studied (2 to 20 μmol/L).
We conclude that nontransferrin-bound iron associates with basolateral liver plasma membrane vesicles by a saturable mechanism sensitive to temperature and calcium and consistent with a membrane carrier. Other divalent cations do not inhibit membrane association but may compete for a subsequent cytosolic binding site. (Hepatology 1990;12:498-504).
Hepatitis C-associated hepatocellular carcinoma
Authors: Hasan Fuad , Jeffers Lennox J. , De Medina Maria , Reddy Rajender K. , Parker Talley , Schiff Eugene R. , Houghton Michael , Choo Quilim , Kuo George 
Published: March 2007

In the United States, a large percentage of patients with hepatocellular carcinoma are serologically negative for hepatitis B. We conducted a retrospective study to determine the prevalence of hepatitis C antibody in the sera of 59 patients with hepatocellular carcinoma who were HBsAg-negative and had no evidence of alcoholic liver disease, primary biiary cirrhosis, autoimmune hepatitis, hemochromatosis or α1-antitrypsin deficiency. Twenty patients (34%) were hepatitis C antibody-positive and hepatitis B core antibody-negative. All twenty patients had underlying cirrhosis, and seven (35%) had histories of transfusions. Eleven (19%) additional patients were also hepatitis C antibody-positive but were hepatitis B core antibody-positive as well. Twenty-one (36%) patients were both hepatitis C antibody- and hepatitis B core antibody-negative and seven (12%) were hepatitis C antibody-negative but hepatitis B core antibody-positive.
The prevalence of hepatitis C antibody was also determined among three other population groups serving as controls and found to be 14% in 28 HbsAg-positive patients with hepatocellular carcinoma, 44% in 76 patients with cryptogenic cirrhosis and 0.5% in 200 consecutive volunteer blood donors.
We conclude that hepatitis C antibody is prevalent among patients with hepatocellular carcinoma and may therefore be a common causative agent of this disease. A significant number of patients with and without cirrhosis, negative for hepatitis C antibody and hepatitis B core antibody, remain without a discernible cause for this malignancy. Perhaps a second-or third-generation test will detect hepatitis C antibody in some of these patients. (Hepatology 1990;12:589-591).
Diagnostic value of brush cytology in the diagnosis of bile duct carcinoma: A study in 65 patients with bile duct strictures
Authors: Rabinovitz Mordechai , Zajko Albert B. , Hassanein Tarek , Shetty Balu , Bron Klaus M. , Schade Robert R. , Gavaler Judith S. , Block Geoffrey , van Thiel David H. , Dekker Andrew 
Published: March 2007

Malignant strictures of the extrahepatic bile ducts are difficult to distinguish from benign strictures, particularly in patients with primary sclerosing cholangitis. Because attempts at diagnosing small cancers with fine-needle aspiration biopsy are not possible in the absence of an associated mass lesion and because the sensitivity of exfoliative biliary cytology is controversial, brush cytology has been used as a potential means of establishing a specific diagnosis of bile duct carcinoma. Herein we report our experience with this technique when performed on 65 patients over a 5-yr period. Each had at least one brushing. Thirty-seven were found to have bile duct carcinoma and 28 were found to have benign strictures. Of these 37, the first brushing was positive for malignancy in 15 (40%), whereas four (11%) had cells suspected but not diagnostic of malignancy. Thirteen patients with bile duct carcinoma whose initial brushings were negative for malignancy had second brushings. Of these, five (38%) had malignant cells, whereas three (24%) yielded suspicious cells. Three of the eight whose first two brushings were negative for malignancy were found to have malignant cells on the third brushing. In contrast, of the 28 patients with benign strictures, malignant cells were never found. However, in two patients, suspicious cells were reported with the first but not the second brushing. A single negative or suspicious cytological finding decreased the probability of bile duct carcinoma to 43%. Two and three sequential negative tests reduced the probability to 32% and 0%, respectively. When suspicious cytological findings were excluded from the negative results, the probability of having bile duct carcinoma was further reduced to 41%, 20% and 0%, respectively.
Using these results, we conclude that (a) a single cytological brushing of a bile duct stricture has a low yield, (b) the sensitivity of the test increases with repeated attempts, (c) the probability of having bile duct carcinoma after three sequential negative cytological brushings is very low (<6%) and (d) these data provide evidence for the usefulness of percutaneous transhepatic cholangiography and bile duct cytological findings in establishing a diagnosis of bile duct cancer. (HEPATOLOGY 1990;12:747-752).
Prognostic factors of hepatocellular carcinoma in the west: A multivariate analysis in 206 patients
Authors: Calvet Xavier , Bruix Jordi , Ginés Pere , Bru Concepció , Sole Manel , Vilana Ramón , Rodés Joan 
Published: March 2007

To investigate the prognostic factors in Western patients with hepatocellular carcinoma, 206 patients with confirmed diagnoses of hepatocellular carcinoma were studied in terms of survival. All patients were diagnosed between 1983 and 1987. A multivariate survival analysis (Cox regression model) using clinical, biochemical, ultrasonographical and pathological data obtained at diagnosis disclosed that bilirubin (p = 0.0001), ascites (p = 0.0001), toxic syndrome (defined by the presence of weight loss > 10% premorbid weight, malaise and anorexia) (p = 0.009), blood urea nitrogen (p = 0.025), tumor size (p = 0.001), γ-glutamyltranspeptidase (p = 0.0006), age (p = 0.0005), serum sodium (p = 0.003) and presence of metastases (p = 0.002) were independent predictors of survival. According to the contribution of each of these factors to the final model, a prognostic index was constructed allowing division of patients in different groups according to their relative risk of death: RRD = EXP (Age × 0.03 + Ascites × 0.8281 + BUN × 0.0137 + Serum sodium × (− 0.0538) + γ-Glutamyltranspeptidase × 0.0019 + Bilirubin × 0.0734 + Tumor size × 0.33 + Toxic syndrome × 0.4965 + Metastases × 0.55).
These results facilitate the stratification of hepatocellular carcinoma patients to design and evaluate future controlled trials. (HEPATOLOGY 1990;12:753-760).
A study of the inhibition of adrenaline-induced vasoconstriction in the isolated perfused liver of rabbit
Authors: Martínková Jiřina , Bulas Josef , Krejčí Vladimír , Hartman Miroslav , Tilšer Ivan , Hůlek Petr 
Published: March 2007

We have studied the action of a series of vasoactive and antispasmodic agents on the intrahepatic vasoconstriction induced by adrenaline in the isolated perfused liver of rabbits. The arterial and portal venous resistance, oxygen consumption, liver weight and bile flow were investigated. The drugs used were as follows: nonspecific α-adrenergic antagonists (DH-ergocristine, dibenamine, phenoxybenzamine), vasodilators with a direct miscellaneous action (theophylline, papaverine, dipyridamole, glucagon, Aiu-cor by Instituto Gentilli, Italy [inosine, ATP, IPI, UTP]) and antispasmodics (piperylone, tropenziline, noraminophenazone).
Adrenaline increased arterial and portal venous resistance followed by a diminution of oxygen consumption, liver weight and bile flow. α-Adrenergic antagonists inhibited the effects of adrenaline on portal venous resistance and oxygen consumption and especially the effects on hepatic arterial resistance. The most potent agent was phenoxybenzamine.
In contrast to α-adrenoceptor blockade, the effects of other vasoactive agents were without a sustained influence on hepatic arterial resistance (excepting those of glucagon and dipyridamole). Some of them were effective as antagonists on responses in the portal venous bed (papaverine, Aiu-cor). Moreover, there were drugs exerting an enhancement of the vasoconstrictor responses of hepatic artery to low concentrations of adrenaline with no effect on the portal venous bed (piperylone, tropenziline). Theophylline and noraminophenazone exerted no effect either on the arterial or portal venous bed.
No vasodilator agent antagonized the changes of the bile flow after adrenaline administration. (HEPATOLOGY 1990;12:1157-1165).
Involvement of tumor necrosis factor-α in development of hepatic injury in galactosamine-sensitized mice
Authors: Hishinuma Ieharu , Nagakawa Jun-Ichi , Hirota Kazuo , Miyamoto Kaname , Tsukidate Kazuo , Yamanaka Takashi , Katayama Kou-Ichi , Yamatsu Isao 
Published: March 2007

Intravenous injection of lipopolysaccharide and D-galactosamine, at doses of 0.2 μg/kg and 800 mg/kg, respectively, elicited massive hepatic necrosis within 24 hr in C3H/HeN mice. The plasma L-alanine aminotransferase (ALT, E.C. 2.6.1.2) or L-aspartate aminotransferase (AST, E.C. 2.6.1.1) activities at this point reached more than 2,000 IU/L. However, overt hepatic injury as evaluated by the plasma aminotransferase activities did not develop in mice in which only lipopolysaccharide or only D-galactosamine was injected. No tumor necrosis factor—like activities could be detected in the plasma of galactosamine- and lipopolysaccharide-injected mice as determined by the assay of cytotoxicity to highly tumor necrosis factor—sensitive L-P3 cells through the experimental period of 24 hr. However, passive immunization against mouse tumor necrosis factor—α with polyvalent rabbit anti-mouse tumor necrosis factor—α antiserum, which was able to neutralize the cytotoxic effects of recombinant mouse tumor necrosis factor—α on L-P3 cells, could protect the mice from the development of hepatic injury in a dose-dependent manner. Simultaneous injection of recombinant human tumor necrosis factor—α, instead of lipopolysaccharide, with 800 mg/kg of D-galactosamine in lipopolysaccharide-resistant C3H/HeJ mice sensitized the animals more than one thousand-fold to the development of hepatic injury. The livers appeared to be morphologically similar to those of galactosamine- and lipopolysaccharide-injected C3H/HeN mice.
These results suggest that endogenous tumor necrosis factor—α participates in the pathogenesis of lipopolysaccharide-elicited hepatic injury, and that tumor necrosis factor plays a crucial role in the development of liver necrosis in galactosamine-sensitized mice. (HEPATOLOGY 1990;12:1187-1191).
A biphasic pattern of anti-pre-s responses in acute hepatitis B virus infection
Authors: Budkowska Agata , Dubreuil Pascal , Maillard Patrick , Poynard Thierry , Pillot Jacques 
Published: March 2007

The clinical relevance of the immune response to the translation products of the pre-S1 and pre-S2 regions of hepatitis B virus was examined by testing sequential serum samples from 17 patients with acute self-limited hepatitis B and from two patients in whom chronic liver disease developed. Anti-pre-S antibodies were determined by enzyme immunoassays based on the inhibition of binding of monoclonal antibodies to epitopes in the pre-S1 and pre-S2 sequence.
In acute, self-limited infection, anti-pre-S antibodies appeared in a biphasic pattern. The early antibodies were detected at the time of clinical signs of acute disease when HBsAg and often HBeAg were present, but hepatitis B virus DNA was no longer detectable in serum. Anti-pre-S levels then fell, but subsequently reappeared as the late antibody during the recovery phase, after development of anti-HBe, but before anti-HBs. Anti-pre-S responses were detected in 15 of 17 patients who recovered (88.2%) and in both patients with acute hepatitis B virus infection evolving to chronic liver disease.
Although the early antibodies to pre-S1 and pre-S2 proteins appeared at the time of decreasing levels of infectious virus in serum in cases of self-limited infection, these antibodies also were transiently or continuously present with high levels of serum hepatitis B virus DNA in patients in whom chronic hepatitis B infection developed. Thus the anti-pre-S response in acute hepatitis is not a prognostic marker for clinical resolution. Mechanisms other than a lack of humoral anti-pre-S responses must be responsible for the failure to eliminate virus in acute hepatitis B evolving into chronic infection. (HEPATOLOGY 1990;12:1271-1277).
Normalization of ventilation/perfusion relationships after liver transplantation in patients with decompensated cirrhosis: Evidence for a hepatopulmonary syndrome
Authors: Eriksson Ljusk Siw , Söderman Charlotte , Ericzon Bo-Göran , Eleborg Lennart , Wahren John , Hedenstierna Göran 
Published: March 2007

To examine the effect of liver transplantation on the respiratory and cardiovascular functions, ventilation/perfusion relationships were determined by multiple inert gas elimination technique in six patients with end-stage liver disease 1 to 19 mo before and 2 to 6 mo after liver transplantation. Cardiac output and pulmonary vascular pressures were measured after catheterization of the pulmonary artery. All patients had normal spirometry and chest x-ray films before transplantation.
PaO2 before transplantation was 78.8 ± 7.4 mm Hg (range = 51.8 to 102.8 mm Hg). All patients had perfusion of poorly ventilated lung regions (low ventilation/perfusion relationships) varying from 3% to 19% of cardiac output (mean = 8.5% ± 2.4% of cardiac output) and two patients had intrapulmonary shunting (3% and 20% of cardiac output). Measured and calculated PaI2 agreed closely, indicating absence of pulmonary diffusion abnormality, as well as of extrapulmonary shunting. After transplantation, PaO2 normalized in all patients, and both shunting and low ventilation/perfusion relationships disappeared. Cardiac output decreased from 9.1 ± 1.4 to 6.6 ± 0.5 L/min (p < 0.05), and the pulmonary vascular resistance increased from 0.69 ± 0.14 to 1.64 ± 0.43 mm Hg/L/min (p < 0.05). The systemic vascular resistance also increased (before = 8.7 ± 1.0; after = 15.3 ± 1.1 mm Hg/L/min; p < 0.001).
Normalization of respiratory and cardiovascular alterations, after liver transplantation, in patients with end-stage liver disease indicates that these changes have a direct functional relationship to the diseased liver. It is hypothesized that this is part of a “hepatopulmonary syndrome,” which in similarity to the hepatorenal syndrome disappears with improved liver function. (HEPATOLOGY 1990;12:1350-1357).