摘要:

AbstractIn a population‐based survey, 39 (0.90%) of 4,496 Saudi Arabian children (ages 1 to 10) were positive for antibody to hepatitis C virus. No significant difference was seen between the prevalence rate in males (0.9%) and females (0.8%) or between urban (0.7%) and rural dwellers (1.0%). A significant variation of rates (0% to 5.7%) was seen from one region to another. The Gizan population, noted for hyperendemic hepatitis B virus infection, had the highest prevalence of antibody to hepatitis C virus despite its cultural and socioeconomic similarities to other regions. In some regions of Saudi Arabia the prevalence of antibody to hepatitis C virus among children was 0% despite endemic rates for both hepatitis B virus and hepatitis A virus infections.An inverse relationship between age and antibody to hepatitis C virus positivity was noted, suggesting an early acquisition of infection in the population studied. Although the overall prevalence of antibody to hepatitis C virus in Saudi children appears low, endemic foci exist where transmission of infection appears to occur early in childhood. The significance of this characteristic for the incidence of chronic sequelae of hepatitis C virus infection needs further evaluation. (HEPATOLOGY 1991;14:215–2

ISSN:0270-9139    

DOI:10.1002/hep.1840140202

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractA variant of hepatitis B virus has been described recently in HBsAg+Mediterranean patients who lack HBeAg and who have an unusual and severe form of chronic hepatitis. This variant is unable to produce HBeAg because of the presence of a novel translational stop codon at the end of the precore region of the genome. By direct sequencing of DNA, generated by the polymerase chain reaction, we have evaluated the association between infection with this variant and the fulminant course of hepatitis B. Eighteen patients with fulminant hepatitis B were studied. Of the 15 cases from whose serum viral DNA could be sequenced, the variant was found in the admission sera of 8 of 9 HBeAg—patients but in none of 6 HBeAg+patients who had fulminant hepatitis B. Patients harboring the variant progressed more rapidly into hepatic encephalopathy, but those infected with the variant strain alone had a greater likelihood of survival than those infected with the normal strain or a mixture. The mutant strain may emerge spontaneously during fulminant hepatitis as occurs in chronic hepatitis B infection during seroconversion from HBeAg to antibody. Alternately, and perhaps less commonly, patients may be infected with the variantab initio. (HEPATOLOGY 1991;14:219–2

ISSN:0270-9139    

DOI:10.1002/hep.1840140203

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractT lymphocyte—mediated cytolytic immune reactions are considered a major cause of hepatocyte injury in chronic viral and autoimmune hepatitis. To further investigate local immune responses, we studied the expression of lymphocyte antigens and cell‐cell interaction molecules known to be involved in effector‐target cell interactions by light and electron microscopy in liver biopsy specimens from patients with chronic viral and autoimmune hepatitis.CD8+lymphocytes were found to be the predominant population of cells in the inflammatory infiltrate in chronic hepatitis B and non‐A, non‐B hepatitis. In contrast, CD4+cells constituted a comparably higher proportion of cells and were more numerous than CD8+cells in chronic autoimmune hepatitis. In both viral and autoimmune hepatitis, a substantial portion of lymphocytes expressed activation antigens such as T11/3 (CD2R) and IL‐2‐R (CD25). Lymphocyte function—associated antigen‐3 (CD58), which mediates lymphocyte adhesion and activation and is the natural ligand of the CD2/T11 lymphocyte surface receptor, could be demonstrated on endothelial cells and hepatocytes. Hepatocellular lymphocyte function—associated antigen‐3 expression in chronic hepatitis showed membranous and cytoplasmic staining of hepatocytes and had a positive correlation with the degree of inflammatory activity.These results suggest that effector‐target interactions between hepatocytes and lymphocytes mediated by the lymphocyte function—associated antigen‐3/CD2 pathway play a role in chronic inflammatory liver disease. Possible functional consequences of this interaction include enhancement of antigen‐specific immune reactions and antigen‐independent mechanisms of T cell activation, which may contribute considerably to the degree of inflammatory activity and tissue damage in chronic hepatiti

ISSN:0270-9139    

DOI:10.1002/hep.1840140204

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractIt has been hypothesized that the magnitude of proximal sodium reabsorption affects the response to aldosterone antagonists in nonazotemic cirrhotic patients with ascites. To verify this hypothesis, we evaluated intrarenal sodium handling by lithium clearance in 51 nonazotemic ascitic cirrhotic patients and in 23 controls who were maintained on the same low‐sodium diet (80 mmol/day). Seven of 51 cirrhotic patients underwent spontaneous diuresis, whereas 44 required diuretic treatment. Treatment was started with spironolactone at a dose of 150 mg once daily. The dose was increased to 300 mg and then to 500 mg once daily if no response ensued. Cirrhotic patients who did not experience ascites mobilization with 500 mg spironolactone were then treated with a combined diuretic regimen that included spironolactone at a fixed dose (500 mg once daily) and furosemide at an initial dose of 50 mg once daily. The dose was increased to 100, 150 and 200 mg once daily if no response was noticed. Response to diuretic treatment was defined as body weight loss greater than 700 gm every 3 days until ascites became clinically undetectable. Nonresponders (43%) to spironolactone showed lower sodium fractional excretion (0.34% ± 0.28% vs. 0.80% ± 0.50%; p<0.001) because of a lower fractional sodium delivery to the distal tubule (18.2% ± 5.8% vs. 23.4% ± 7.2%; p<0.025) than responders. Moreover, nonresponders showed lower distal sodium reabsorption, both in absolute terms (2,360 ± 723 μEq/min vs. 3,221 ± 960 μEq/min; p<0.01) and as a percentage of filtered sodium load (17.5% ± 5.7% vs. 23.1% ± 7.6%; p<0.01) despite higher values of plasma aldosterone (524 ± 542 pg/ml vs. 136 ± 213 pg/ml; p<0.025).We conclude that unresponsiveness to adequate doses of spironolactone in nonazotemic ascitic cirrhotic patients is related to a pathophysiological condition in which the role of aldosterone in renal sodium retention is limited by markedly enhanced proximal sodium reabsorption. (HEPATOLOGY 199

ISSN:0270-9139    

DOI:10.1002/hep.1840140205

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractCirculating catecholamines are increased in cirrhosis with portal hypertension, and increase further after propranolol. In 23 cirrhotic patients, plasma norepinephrine and epinephrine were determined in an artery, the azygos vein, the right renal vein and a hepatic vein before and after an oral 80‐mg dose of propranolol. Baseline azygos and renal venous norepinephrine levels were significantly higher than arterial norepinephrine levels (+ 20%, p<0.005; and + 28%, p<0.001, respectively). Hepatic venous norepinephrine and all venous epinephrine values were below the arterial values (all p<0.05). After propranolol intake, arterial norepinephrine and epinephrine increased (+ 16%, p<0.01; and + 93%, p<0.001, respectively). Significant increases in norepinephrine and epinephrine were found in azygos and renal veins (all p<0.01), whereas hepatic venous norepinephrine and epinephrine remained unchanged. Azygos and hepatic blood flow decreased after propranolol intake (−27%, p<0.05; and − 16%, p<0.01, respectively). Azygos spillover of norepinephrine (an estimate of locally released norepinephrine delivered to the circulation) and clearance of epinephrine remained unaltered. Hepatointestinal clearance showed no significant change for norepinephrine, but showed a borderline‐significant decrease for epinephrine (−23%, p = 0.08). Our results show a net production of norepinephrine in the prehepatic splanchnic area drained through superior portalsystemic collaterals and in the kidneys. The increase in circulating catecholamines after propranolol intake is probably due to a combination of further enhancement of sympathetic activity and a decrease in catecholamine degradation. (HEPATOLOGY 1991;14

ISSN:0270-9139    

DOI:10.1002/hep.1840140206

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractPooled sera collected from cirrhotic patients was fractionated by affinity chromatography with a fibronectin receptor monoclonal antibody against the β‐subunit of fibronectin receptor. Eluates were assayed using Western immunoblotting. The relative mobility of the protein reactive with fibronectin receptor antibody was nearly identical to that of the β‐subunit of fibronectin receptor, confirming that fibronectin receptor is present in human serum. Serum levels of the β‐subunit of fibronectin receptor were analyzed by sandwich enzyme‐linked immunosorbent assay in patients with various liver diseases. The serum level of fibronectin receptor (μg/ml) was significantly higher in patients with chronic hepatitis (inactive, 2.59 ± 0.04; active, 3.45 ± 0.13), cirrhosis (4.77 ± 0.30), alcoholic liver disease (2.96 ± 0.16) and hepatocellular carcinoma (4.71 ± 0.49) than in normal subjects (2.11 ± 0.08). Strong positive correlation was observed between serum levels of fibronectin receptor and histological findings, particularly in the degree of hepatic fibrosis. Immunohistochemical studies with fibronectin receptor antibody revealed that the β‐subunit of fibronectin receptor was present on the plasma membrane of hepatocytes and sinusoidal lining cells in the normal liver and was increased in fibrotic areas and on the plasma membrane of hepatocytes and sinusoidal lining cells of fibrotic liver. The serum level of fibronectin receptor in patients with chronic liver diseases may therefore be a useful marker of hepatic fibrosis. (HEPATOL

ISSN:0270-9139    

DOI:10.1002/hep.1840140207

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractPrevious studies have shown that antithrombin III levels are low in fulminant hepatic failure, and heparin kinetics are abnormal, making control of heparinization difficult during hemodialysis of these patients who are at risk of bleeding. In this study, we have performed a controlled, randomized trial of antithrombin III supplementation on heparin activity, occurrence of bleeding and the platelet count and activation during hemodialysis in 24 patients with fulminant hepatic failure. The treated group of 12 patients was given 3,000 units of antithrombin III before hemodialysis. Antithrombin III supplementation was shown to normalize antithrombin III levels during hemodialysis (prelevels: 0.22 ± 0.03 U/ml S.E.; at 1 hr 0.99 ± 0.06 U/ml; p<0.001; control prelevels: 0.24 ± 0.03 U/ml; at 1 hr 0.23 ± 0.04 U/ml). Total heparin usage was significantly decreased by antithrombin III supplementation (median 5,200 U; range = 2,005 to 13,000) as compared with the control group (median 10,200 U; range = 5,000 to 16,500; p<0.005). Blood heparin level (antifactor Xa activity) after the initial bolus was significantly greater in the antithrombin III—supplemented subjects (0.40 ± 0.07 U/ml compared with 0.22 ± 0.05 U/ml in the control group; p<0.05). The significant reduction in platelet count observed in the control patients (18% ± 6% at 1 hr; p<0.05) did not occur in antithrombin III patients (6% ± 4% at 1 hr), which was reflected by a lower release of the platelet‐specific protein β‐thromboglobulin. Two of 12 patients in both groups showed minor bleeding around vascular access sites during the first hemodialysis. Over the course of the study, no significant difference was seen in the frequency of bleeding from vascular access sites, gastrointestinal tract or other locations.Thus in a controlled study, supplementation of antithrombin III markedly reduced the amount of heparin required during hemodialysis of patients with fulminant hepatic failure and also reduced platelet losses. Antithrombin III supplementation may be of benefit in hemodialysis, continuous arteriovenous hemofiltration or other invasive techniques requiring anticoagulation in these patients at particular risk of bleeding. (HEPATOLOGY 19

ISSN:0270-9139    

DOI:10.1002/hep.1840140208

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractThe incidence and severity of osteopenic bone disease in primary sclerosing cholangitis is poorly defined. Clinical, biochemical and radiographic assessment and bone mineral density measurements of the lumbar spine were carried out in two groups of patients. Group 1 consisted of 30 patients with advanced primary sclerosing cholangitis; group 2 consisted of 18 patients with newly diagnosed primary sclerosing cholangitis. Only one patient had bone pain. All patients were normocalcemic; two had elevated serum parathormone levels. Fourteen patients (47%) from group 1 but no patients from group 2 had low serum 25‐hydroxyvitamin D levels. Mean bone mineral density was significantly reduced in group 1 patients (0.97 ± 0.04 gm/cm2) compared with age‐matched and sex‐matched controls (1.25 ± 0.01 gm/cm2, p<0.0001), and in 15 patients (50%) bone mineral density was below the fracture threshold (0.98 gm/cm2). The bone mineral density in group 2 was not significantly different from controls, and no patient was below the fracture threshold. In neither group did bone mineral density correlate with serum bilirubin, 25‐hydroxyvitamin D, fecal fat excretion, previous drug therapy or the presence of chronic ulcerative colitis. Histomorphometrical examination of bone from four group 1 patients showed increased bone resorption, reduced bone formation, moderate‐to‐severe osteopenia and no osteomalacia. In conclusion, severe osteopenic bone disease is common in advanced primary sclerosing cholangitis and, like that seen in other cholestatis diseases, is consistent with osteoporosis. (HEPATOLOGY 199

ISSN:0270-9139    

DOI:10.1002/hep.1840140209

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractA multivariate analysis of data from 90 patients with unresectable hepatocellular carcinoma was performed using Cox's regression model to identify factors possibly affecting their prognoses. Thirty‐one patients underwent arterial anticancer chemotherapy, and the remaining 59 patients received transcatheter arterial embolization with anticancer agents. Four of 27 variables tested for all the patients (i.e., encapsulation [p<0.05], gross appearance of hepatocellular carcinoma [p<0.01], clinical stage [p<0.01] and therapy [p<0.01]) were found to be prognostically significant. Five of 27 variables tested were prognostically significant for the transcatheter arterial embolization group; they were an extension rate of hepatocellular carcinoma (p<0.01), encapsulation (p<0.01), α‐fetoprotein (p<0.01), prothrombin time (p<0.01) and serum sodium (p<0.01). Regression equations were used to describe a prognostic index. A prognostic index was defined as the regression equation derived from the results of a total of 90 patients; PI‐1 = eY, where PI‐1 = prognostic index 1 Y = 1.549 (gross appearance of hepatocellular carcinoma −1.344) + 0.778 (encapsulation − 1.622) + 0.818 (clinical stage − 1.800) + 1.760 (therapy − 1.344) and prognostic index 2, the regression equation derived from the results of the transcatheter arterial embolization group of patients; PI‐2 = eY, where PI‐2 = prognostic index 2 Y = 1.210 (extension rate of hepatocellular carcinoma − 1.576) + 1.179 (encapsulation − 1.475) + 0.0001277 (α‐fetoprotein − 1420.792) −0.039 (prothrombin time − 72.237) − 0.214(serum sodium − 138.427). According to the prognostic index, the patients were divided into two groups (i.e., those with the good prognoses and those with bad prognoses). According to prognostic index 1, the prognosis of the patient who did not undergo transcatheter arterial embolization therapy was 5.8 times poorer than that of the patient who underwent transcatheter arterial embolization. One‐year survival rates of the former and the latter were 66% and 9.4%, respectively. According to prognostic index 2, the prognosis of the patient whose extension rate of hepatocellular carcinoma was greater than 60% of the entire liver was 38 times poorer than that of the patient whose extension rate of hepatocellular carcinoma was less than 20% of the entire liver. This study demonstrated that prognostic indexes can be used to predict the survival time of a group of patients with unresectable hepatocellular carcinoma and that prognostic indexes can be used to predict those who have better prognosis in the transcatheter arterial embolizat

ISSN:0270-9139    

DOI:10.1002/hep.1840140210

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY

摘要:

AbstractTransforming growth factor‐β1was localized by means of immunohistochemical reaction in liver biopsy specimens taken from patients having different chronic liver diseases with extending fibrosis. Two polyclonal antibodies that were produced in rabbits were directed against the amino terminal of transforming growth factor‐β1.Staining by anti‐CC(1–30) was primarily extracellular and located in the portal and periportal fibrotic areas of all seven cases with chronic active hepatitis. No staining was noted in the four chronic persistent cases studied. A strong reaction was seen with the antibody in nine of the ten cirrhotic samples, whereas it was negative in one inactive cirrhosis case and in all five cases with normal liver histological findings. No positive staining could be detected by the anti‐LC(1–30) in any of the liver tissues.Detection of transforming growth factor‐β1in active liver diseases at the site of fibrosis suggests that transforming growth factor‐β1might have a role in the process and progression of fibrosis during the development of the disease. (HEPATOLO

ISSN:0270-9139    

DOI:10.1002/hep.1840140211

出版商:W.B. Saunders    

年代:1991

数据来源: WILEY