摘要:

ABSTRACT—Adenomatous hyperplasia (AH), a hyperplastic parenchymal nodule, is detected most often through radiological and pathological observations in chronic advanced liver disease. AH can be classified into two categories: ordinary type or macroregenerative nodule (MRN) type I, and atypical type or MRN type II. Characteristically, both types contain portal tracts with portal veins and biliary elements. Ordinary AH may represent a large regenerative nodule with limited growth potential. Atypical AH shows slightly cellular and structural atypia, altered phenotypic expression, and increased proliferative activity compared to the surrounding liver. Histologic differentiation of atypical AH from well‐differentiated hepatocellular carcinoma (HCC) is controversial, and generally accepted diagnostic criteria are still lacking. Atypical AH occasionally contains overt malignant foci. Histological observations and portography show that nodules of AH are supplied by portal venous blood. While AH nodules appear to be hypoperfused according to arteriographic studies, atypical AH contains small arterial branches which are abundant in contrast to the surrounding liver. The data obtained so far indicate that atypical AH may be a hepatocellular neoplasm which belongs nosologically to a gray area of neoplasm, in which overt HCC is likely to develop. It is clinically recommended that atypical AH is treated as “malignant” because of the occasional inclusion of HCC foci. For its treatment, percutaneous ethanol injection is becoming

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00597.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

ABSTRACT—The expression of intercellular adhesion molecule‐1 (ICAM‐1) on the hepatocyte membrane was studied in 27 patients with chronic hepatitis B and C (CHB, CHC) by immunostaining using a monoclonal antibody. ICAM‐1 was expressed focally in a honeycomb‐like pattern by hepatocytes in livers of 26/27 patients. The degree of ICAM‐1 expression was closely related to the ALT level and the histological grade of liver damage. Abundant cytotoxic T cells (CD8 +, CD11b –) were found in ICAM‐1‐positive areas of the liver. Zones of focal necrosis contained both ICAM‐1‐positive hepatocytes and cytotoxic T cells. The expression of ICAM‐1 was decreased in 4/6 CHB patients after interferon‐α therapy. No relationship between the degree of hepatocyte ICAM‐1 expression and viral replication markers (DNA polymerase activity and the presence of HBcAg in the liver) was observed in patients with CHB. In addition, no positive correlation was found between the distribution of ICAM‐1‐positive hepatocytes and HBcAg‐positive hepatocytes. These results suggest that ICAM‐1 may play an important role in the pathogenesis of hepatocellular injury mediated

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00598.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

ABSTRACT—Seven patients with decompensated posthepatitis B cirrhosis were treated with low doses of interferon alpha. The initial plasma level of HBV‐DNA ranged from 3.0 to 189.3 pg/ml, and that of ALT from 37 to 156 IU/1. Liver biopsies demonstrated ongoing piecemeal necrosis. In sera of all but one patient, HBV‐DNA became undetectable by hybridisation techniques within 10 to 28 weeks. Plasma HBeAg became negative in four and HBe‐antibodies positive in three patients. Serum transaminase levels showed a marked initial rise 3 to 13 weeks after onset of therapy; they dropped to normal values later in all except one patient. Therapy was initiated at 1 MU (million units) three times a week for 2 weeks and was increased to 2.5 MU for 16 weeks. Later, this dosage was raised to 5 MU three times a week in some patients. Complications included variceal haemorrhage, aggravation of ascites or of encephalopathy, development of pneumonia, recurrence of spontaneous bacterial peritonitis or of gastric ulcer bleeding. One year after stopping the therapy, three patients are well and without any feature of liver decompensation. Three patients died before they could undergo a liver transplantation. In one patient treatment was interrupted because of marked exacerbation of liver cell necrosis. It thus seems possible to suppress HBeAg and HBV‐DNA in patients with decompensated cirrhosis. This is important to prepare them for possible liver transplantation. Interferon should be initiated at low doses and the patients be very carefully monitored. Prophylactic therapy for bacterial peritonitis and for variceal haemorrhage is

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00599.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

ABSTRACT—Although it has been established that liver failure is associated with arterial hypocapnia and alkalaemia (i.e., respiratory alkalosis), the influence of liver failure on mixed venous acid‐base status has not yet been studied. Thus, arterial and mixed venous acid‐base status were simultaneously measured in controls and in a large series of patients with cirrhosis. Grade B patients (n = 28) or Grade C patients (n = 21) had significantly lower arterial and mixed venous carbon dioxide tensions than controls (n = 29). Grade B or Grade C patients also had significantly higher arterial, mixed venous pH, and lower mixed venous bicarbonate concentrations than controls. Among Grade A patients (n = 27), those with the lowest Pugh's score (i.e., equal to five) had significantly lower mixed venous carbon dioxide tension than controls. The other arterial and mixed venous acid‐base values did not differ significantly between Grade A patients with the lowest Pugh's score and controls. Grade A patients with a Pugh's score equal to six and Grade B patients had similar acid‐base disorders. No significant differences were found between groups concerning the anion gap and plasma chloride concentrations. In conclusion, this study shows that in Grade B or C patients, respiratory alkalosis was responsible for mixed venous hypocapnia, alkalaemia and hypobicar‐bonataemia. In addition, in Grade A patients with the lowest Pugh's score (equal to five), analysis of arterial and mixed venous blood revealed that mixed venous hypocapnia was the sole anomaly of the acid‐base status. This last finding suggests that mixed venous hypocapnia might be an early event preceding the onset of arteri

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00600.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

ABSTRACT—Partial hepatectomy (PH) and a single intravenous injection of zymosan were used to provoke expansion of the Kupffer cell population in rat liver. The number of Kupffer cells per unit of area of liver increased after both stimulations. During these growth phases the number of binding sites for galactose‐exposing ligands was studied on Kupffer cell plasma membranes. Both partial hepatectomy and zymosan stimulation affected the binding of lactosylated bovine serum albumin conjugated to gold particles (LacBSA‐Au5). The reduction observed depended on the time after the PH or zymosan injection studied. Low levels of binding sites were found at 24 h from PH and 5 days after zymosan stimulation and represented only 1/4 or 1/10 of the binding sites expressed on the cell surface of Kupffer cells from normal adult rats. In addition, in both experimental situations we observed that the clustered distribution of gold particles typical of adult Kupffer cell was ch

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00601.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

ABSTRACT—We examined the oxygen content in the hepatic arterial, hepatic venous and portal venous blood to evaluate the oxygen supply to the liver and hepatic oxygen extraction in cirrhosis. The arterial‐portal venous difference of the oxygen content was within the normal range in cirrhosis patients, although the oxygen content of the hepatic artery and portal vein was lower than in the control patients. The hepatic venous oxygen content was normal in the cirrhosis patients. The oxygen tension and saturation were always higher in the splenic vein than in the other branches of the portal system. Oxygen was supplied chiefly by the hepatic artery, and arterial oxygen extraction was normal in cirrhosis. In addition, there was no change in arterial extraction during oxygen inhalation by cirrhosis patients. Portal venous oxygen extraction was decreased in cirrhosis and was increased by oxygen inhalation. These findings indicate the autoregulation of hepatic oxygen through a mutual relationship between the hepatic arterial and the portovenous oxygen sup

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00602.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

ABSTRACT—The histologic significance of various changes in the bile ductal structures as observed by cytokeratin immunoperoxidase assay was studied in 122 patients with alcoholic liver disease (ALD) as a part of a large Veterans Administration Cooperative Study on alcoholic hepatitis. Four types of morphologic changes in the biliary structures were observed: 1) proliferation of interlobular bile ducts in the portal tracts; 2) marginal bile ductular proliferation at the periphery of the portal tracts; 3) appearance of bile duct type cells (“oval cells”) in the liver parenchyma; and 4) metaplasia of bile duct epithelium to cells resembling hepatocytes. These bile ductal changes correlated strongly with liver fibrosis (p = 0.0003; 0.0003; 0.05; 0.0035, for 1, 2, 3, and 4, respectively), cirrhosis (p<0.0001 for all four parameters), portal inflammation (p<0.0001 for 1, 2, and 4; p = 0.0024 for “oval cells“), and with overall histologic severity scores (p<0.0001; p = 0.0001; p = 0.0017; p = 0.0005, respectively). However, these changes did not correlate significantly with fatty change, parenchymal degeneration and necrosis, cellular infiltrate or Kupffer cell hyperplasia, suggesting that they are probably not the direct consequences of liver cell necrosis. Periportal piecemeal necrosis correlated significantly with both portal bile duct (p = 0.0041) and marginal (p = 0.0078) bile ductular proliferation. Among all these changes, only marginal bile ductular proliferation correlated significantly with Mallory bodies present both in the hepatocytes (p = 0.05) and the bile ducts (p = 0.01). Both marginal bile ductular proliferation and “oval cells” correlated significantly with clinical severity of the liver disease as determined by high serum bilirubin and prolonged prothrombin time (Maddrey's discriminant function). This study suggests that: 1) a variety of important morphologic changes occur in the bile ductal structures in ALD, particularly when fibrosis and cirrhosis develop; 2) “oval cells” and bile duct metaplasia are frequent in ALD and appear to be significantly related to the development of fibrosis and cirrhosis; 3) bile ductules are an integral component of piecemeal necrosis in ALD; 4) some of the bile ductal changes may influence the clinical outcome of

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00603.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

ABSTRACT—The effect of corticosteroid pretreatment on interferon alfa treatment of chronic non‐A, non‐B or C hepatitis was evaluated in an open, randomized, controlled study. Normalization of the serum alanine aminotransferase level, which suggested complete response, was recorded in 14 (56%) of 25 patients at the end of a 6‐month treatment with 3 million units of interferon alfa three times weekly alone. Prednisolone withdrawal followed by the same interferon alfa treatment resulted in complete response in 14 (61%) of another 23 patients. Both of these rates are significantly higher than the spontaneous ALT normalization rate of 9% observed in 2 of 22 patients during the same period (p<0.01). ALT normalized within 2 months of interferon therapy in most (89%) of the complete responders. Of the patients pretreated with prednisolone, 43% showed a “rebound” following prednisolone withdrawal and 89% of the patients with “rebound” responded to subsequent interferon therapy. The cumulative probability of sustained remission in patients with and without prednisolone pretreatment in a 24‐month period of follow‐up after the end of therapy was 79% and 30%, respectively (p<0.05). Clinical relapse mostly (85%) occurred within 3 months after the end of therapy. No obvious factor could be identified as a predictor of response or relapse. The results of this study suggest that prednisolone withdrawal tends to enhance the durability of the beneficial effects of interferon alfa therapy in patients with chronic non‐A,

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00604.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00605.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0106-9543    

DOI:10.1111/j.1600-0676.1993.tb00606.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY