Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether the response of serum alanine aminotransferase (ALT) to recombinant alpha-interferon was related to the presence or absence of antibodies to hepatitis C virus (anti-HCV) in patients with chronic non-A,non-B hepatitis. A group of 65 patients with chronic non-A, non-B hepatitis was studied. The source of contamination was blood transfusion or administration of blood products in 32, intravenous drug addiction in 14 and unknown in 19. The patients received 1, 3 or 5 MU of recombinant alpha-interferon, three times a week, for 6 months. A complete response was defined as normal ALT by the end of recombinant alpha-interferon treatment. Sera collected before treatment were tested for anti-HCV with an enzyme immunoassay. The overall percentage of anti-HCV positive patients in the study group was 75%. There was no difference between the anti-HCV positive and the anti-HCV negative patients before the treatment with respect to age, sex ratio, source of contamination, serum albumin, prothrombin, bilirubin, ALT or prevalence of cirrhosis. In the anti-HCV positive and the anti-HCV negative groups, there was no difference in the proportion of patients receiving the 1, 3 or 5 MU dosage. The percentage of patients with complete response was not different in anti-HCV positive patients (48%) and in anti-HCV negative patients (50%). There was also no difference in the kinetics of the decrease of mean serum ALT levels between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is the response to recombinant alpha interferon related to the presence of antibodies to hepatitis C virus in patients with chronic non-A, non-B hepatitis? 164 37

We evaluated the proapolipoprotein A-I (proapo A-I)-converting activity to clarify the pathogenesis of the high proapo A-I/apo A-I ratio in the high-density lipoprotein (HDL) from patients with acute hepatitis and liver cirrhosis. The serum proapo A-I-converting activities were measured using 3H-labeled proapo A-I. 3H-labeled proapo A-I was purified from the media of cultured Hep G2 cells by immunoaffinity chromatography. The serum proapo A-I-converting activities were found to be significantly reduced in the patient with liver cirrhosis (140 +/- 53 dpm/ml per h) or acute hepatitis (140 +/- 48 dpm/ml per h) compared to normal subjects (315 +/- 32 dpm/ml per h). Serum proapo A-I-converting activity has a positive correlation with liver function tests such as serum albumin, choline esterase activity, ICG clearance and inverse correlation with proapo A-I/apo A-I ratio in HDL. These results suggest that the high proapo A-I/apo A-I ratio is due to the decreased proapo A-I-converting activity, and that the liver plays a significant role in the conversion of proapo A-I to apo A-I.
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PMID:Decreased proapolipoprotein A-I processing in liver disease: evidence for hepatic participation in proapolipoprotein A-I conversion. 212 92

The prognostic value of plasma prekallikrein activity, prothrombin time, and serum albumin with regard to survival in chronic liver insufficiency was evaluated in 21 consecutive patients. Twenty patients had liver cirrhosis, and one patient had malignant liver disease (hepatocellular carcinoma). Eight patients died between 4 and 43 days after the time of blood sampling. These patients had a prekallikrein value less than 0.42. There were no overlapping prekallikrein values between patients who died and patients who survived (overlap index 0; p less than 0.001). Overlap index for prothrombin time was 0.35 (p less than 0.02), and for serum albumin 0.34 (p less than 0.02). In conclusion, plasma prekallikrein seems to indicate whether death is imminent in patients with liver insufficiency due to cirrhosis. Longitudinal studies of prekallikrein activity in different subgroups of patients with chronic and acute liver disease are recommended.
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PMID:Plasma prekallikrein as a prognostic indicator in chronic liver insufficiency. 215 45

Arterial ketone body ratio (AKBR) were examined in 114 cases of hepato-biliary tract diseases. AKBR of the normal control was 1.47 +/- 0.38, while it remained less than 0.7 in liver cirrhosis, hepatocellular carcinoma (HCC), alcoholic liver diseases and malignant biliary tract obstruction. AKBR correlated well with serum albumin and cholinesterase. Thirty five cases of HCC were treated with transcatheter arterial embolization (TAE), 20 cases with gelatin sponge and 15 cases without gelatin sponge. In cases with gelatin sponge AKBR decreased significantly immediately after TAE and recovered gradually during 24 hours. Without gelatin sponge AKBR decreased slightly and remained unchanged until 24 hours later. Concerning the prognosis after TAE, AKBR recovered well in cases with good prognosis, while in poor prognosis AKBR progressively decreased to below 0.3. In experimental TAE with gelatin sponge using rabbit VX2-induced liver tumor, AKBR decreased significantly. In fatal rabbit group after TAE, AKBR decreased progressively. Plasma endotoxin was also measured in TAE with experimental rabbit, AKBR and endotoxin showed reverse correlation. From these results it was suggested that the measurement of AKBR is very useful for the evaluation of efficacy and prognosis of TAE in primary liver cancer.
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PMID:[Changes in arterial ketone body ratio after transcatheter arterial embolization for hepatocellular carcinoma-clinical and experimental studies]. 217 Jul 13

We investigated the distribution of portal blood flow per kilogram of body weight (PBF/BW) in 112 healthy volunteers and 90 patients with liver cirrhosis using an ultrasonic Doppler duplex system. The PBF/BW in healthy volunteers showed a log-normal distribution, while the distribution was irregular and showed two peaks in patients with cirrhosis. This irregular distribution was thought to reflect their complex physiopathological state. We next analyzed the relationship between PBF/BW and the data from hepatic function tests (serum albumin, total bilirubin, indocyanine green 15-min retention rate, and indocyanine green plasma disappearance rate) in 48 patients with liver cirrhosis. The patients were divided into four groups according to their portal blood flow: group A with a hepatofugal or stagnant portal blood flow, group B with a hepatopetal PBF/BW of less than 12 ml/min/kg, group C with a hepatopetal PBF/BW of 12 or more but less than 20 ml/min/kg, and group D with a hepatopetal PBF/BW of 20 ml/min/kg or more. Among patients with cirrhosis, group A showed the worst results in hepatic function tests, group D the second worst, and group C the best. The effective hepatic blood flow was thought to have decreased because of the development of extrahepatic portosystemic shunts in the patients in groups A and B, whereas it decreased because of the development of intrahepatic shunts in patients in group D. The results of hepatic function tests deteriorated as a consequence of the decrease in the effective hepatic blood flow.
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PMID:Hepatic function and portal hemodynamics in patients with liver cirrhosis. 220 1

Dexamethasone (DXM), one of the strong synthetic glucocorticoids, has been used widely for therapeutic purposes and for evaluation of the hypothalamic-pituitary-adrenal axis. However, information concerning the plasma concentrations of DXM and its metabolism in various liver diseases is limited. In this study, plasma DXM levels were examined in patients with chronic inactive hepatitis (CH), patients with liver cirrhosis (LC) and normal subjects (NR) after oral administration of one milligram DXM. Plasma DXM levels were measured directly in plasma extract, using reliable and sensitive radioimmunoassay (RIA). The antiserum was obtained by immunizing rabbits with DXM-3-oxime-bovine serum albumin conjugate. Standard curves for DXM were obtained over the range 10-5000 pg. The cross reactivity of endogenous steroids with DXM antiserum was less than 0.1%. In the group of NR, the peak of plasma DXM was 20.9 +/- 2.9 ng/ml within 1.3 +/- 0.4 hours after administration. Half time of its disappearance was 3.3 +/- 1.1 hours, and plasma DXM disappeared in 24 hours, remaining less than 1 ng/ml. In patients with CH and those with LC, the peak levels of DXM were 10.8 +/- 1.0 ng/ml and 10.5 +/- 0.5 ng/ml, respectively, and those values were significantly lower than those of NR. Half time of DXM disappearance in patients with CH and in those with LC were 6.2 +/- 0.6 and 6.3 +/- 0.6 hours, respectively, significantly prolonged compared with that of NR. Although DXM metabolism was impaired in CH as well as in LC, the retention rate of indocyanine green (ICG) at 15 minutes in CH was found within the normal range, 10.0 +/- 1.1%, respectively. These results might suggest that the impaired DXM metabolism in patients with chronic liver disease may be affected not only by the decreased hepatic blood flow but also by some other factors.
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PMID:[Radioimmunoassay for dexamethasone and its plasma levels after oral administration in patients with liver disease]. 220 23

A thickened gallbladder wall is often seen with ultrasound in alcoholic cirrhosis. Hypoalbuminaemia is thought to be the cause since there is a strong association between bowel wall thickening and low serum albumin. To determine the role of portal hypertension in producing gallbladder wall thickening we studied 40 consecutive stable patients-37 with cirrhosis and three with portal hypertension due to primary biliary cirrhosis. Ultrasound assessment of the gallbladder wall was made after an overnight fast using a Technicare autosector. Wall thickness 4 mm or greater was considered abnormal. Twenty-seven patients had a thickened gallbladder wall and all had evidence of portal hypertension. Hypoalbuminaemia was not an important factor since it was only present in six cases with thickened walls. In two cases reduction in portal pressure with oral propranolol was associated with a decrease in gallbladder wall thickness. These results suggest that portal hypertension, not hypoalbuminaemia, is the dominant factor causing gallbladder wall thickening in cirrhosis. Ultrasound demonstration of gallbladder wall thickening in chronic liver disease should suggest the presence of portal hypertension.
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PMID:Gallbladder wall thickening (congestive cholecystopathy) in chronic liver disease: a sign of portal hypertension. 226 60

We have developed a new liver scanning agent (Ga-68 human serum albumin microspheres) in a convenient kit for use in positron emission computed tomography (PET). In this study, this scanning agent was evaluated for clinical usefulness as a function test for the reticuloendothelial system. A dose of 5 micrograms/kg (1-2 mCi) of Ga-68 microspheres was injected intravenously to 25 patients, 11 with chronic hepatitis and 14 with liver cirrhosis, and 5 normal volunteers for PET imaging of the liver and spleen using HEADTONE-III (SET 120W). The volumes of the liver and the spleen and the uptakes of Ga-68 microspheres were calculated as an index of the reticuloendothelial system function. In liver cirrhosis the liver volume estimated by PET was decreased and the spleen volume was increased. Both the liver uptake rate and differential absorption ratio (DAR) of the radioactivity were decreased corresponding with the degree of chronic liver disease. The spleen uptake rate was increased with progression of chronic liver diseases, but there was no difference in DAR between normal volunteers and patients with chronic liver disease. it was concluded that PET using Ga-68 microspheres is useful in the evaluation of the function of the reticuloendothelial system.
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PMID:[Estimation of the reticuloendothelial function by positron emission computed tomography (PET) study in chronic liver disease]. 232 35

Data from 73 asymptomatic patients with primary biliary cirrhosis were analyzed to determine clinical course and long-term survival. Of these, 44 entered a D-penicillamine treatment trial; 29 qualified but chose not to participate. Median follow-up was 7.6 yr (range, 2.8-12.2 yr). Liver biopsy at the initial visit showed advanced disease (fibrosis, cirrhosis) in 61% of the patients. During prospective clinical follow-up, which was available for 37 of the 44 study patients, one or more symptoms of liver disease developed in 33 (89%); esophageal varices were found in 15 (41%), and histologic progression to cirrhosis was found in 20 (67%) of the 30 precirrhotic patients. Significant (p less than 0.01) biochemical progression was reflected by a decrease in mean serum albumin concentrations and an increase in mean serum bilirubin levels in 32 patients followed for 4-6 yr. Survival data were available for all 73 patients; 17 died (11 secondary to liver failure), and 1 underwent liver transplantation. These patients had a 4-fold increase in mortality rate (p less than 0.001) compared with the U.S. population matched for age, race, and sex.
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PMID:Diminished survival in asymptomatic primary biliary cirrhosis. A prospective study. 233 3

The purpose of this paper is to provide a histopathologic basis for abnormalities in immune-complex clearance in liver disease. Fc receptors in CCl4-induced liver cirrhosis in rats were studied by applying peroxidase-antiperoxidase immunoglobulin G complex as a ligand to the frozen sections. Intravenous injection of bovine serum albumin-antibovine serum albumin complexes or colloidal carbon was combined with histological staining for endogenous peroxidase, fibronectin, laminin, or a lectin, Bandeiraea simplicifolia agglutinin I. In the cirrhotic process, sinusoidal Fc receptors showed a weakened reactivity to the ligand with focal absence, and the length of the Fc receptor-positive portion of the sinusoids in unit area decreased to about 50% of the normal value in the advanced cirrhosis. Fibronectin and the lectin showed the presence of sinusoids where Fc receptors were absent. The endothelium in Fc receptor-negative areas did not take up either immune complexes or carbon, and Kupffer cells were absent in these areas. A disturbed immune-complex metabolism was thus suggested to occur in association with the defect of sinusoidal Fc receptors in liver cirrhosis. These abnormalities appeared to not be directly related to perisinusoidal laminin deposition, i.e., capillarization of the sinusoid.
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PMID:Defect of sinusoidal Fc receptors and immune complex uptake in CCl4-induced liver cirrhosis in rats. 234 26


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