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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One dimensional profile scans with a whole body counter are refocused with a linear space invariant filter in the frequency domain, 'Hanning' window and inverse system transfer function. Artifacts are eliminated in a way that a clinically applicable method is developed. Topographic information is achieved with the highly energetic nuclide 82bromide. The bromide space (extracellular volume) in patients with liver cirrhosis (n = 9) compared to normal subjects (n = 10) is increased most in the upper abdominal thoracic region.
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PMID:Evaluation of one dimensional profile scans with a whole body counter--82bromide space in liver cirrhosis: concise communication. 11 92

Extracellular water (EWC; 82-bromide), total body water (TBW; 3-THO), intracellular water (ICW = TBW-ECW), plasma volume (PV; 51-Cr), and total body potassium (TBK; 40-K) were studied in patients with cirrhosis of the liver (n = 12) and in controls (n = 12). ECW (39%), TBW (28%), ICW (19%), and PV (24%) increased, TBK (28%) however, decreased in cirrhosis. The results indicate that it is less the lean body mass, but rather the intracellular potassium concentration that is lowered (cirrhosis: 84 +/- 21 mmol/l ICW; controls: 115 +/- 23 mmol/l ICW). Decreased potassium per cell (mmol) and increased intracellular water are discussed as possible reasons for this. The correlation between TBK (%) and serum potassium (mmol/l) was found to be r = 0.56 (p less than 0.002). Correlations between the biochemical parameters gamma-globulins, cholin esterase, serum sodium and serum albumin (g/l PV) and characteristic fluid disturbances in cirrhosis are highly significant whereas albumin (g/kg bodyweight) was the same in both groups. We can support the 'overflow theory' of ascites formation.
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PMID:Total body water, extracellular water, plasma volume, and total body potassium in cirrhosis of the liver. 49 99

To investigate the influence of body composition on leucine metabolism, leucine turnover and oxidation were measured in six patients with stable biopsy-proven cirrhosis and in six age- and gender-matched controls using [1-14C]leucine tracer. Fat-free body mass and body cell mass were estimated from quantified measurements of H2(18)O and bromide dilution. Although there were no differences in body weight, body surface area, body mass index, or fat-free body mass between study groups, body cell mass was decreased in cirrhotic patients (37.6 +/- 0.1 vs. 46.4 +/- 1.8 kg; P less than 0.05). Leucine turnover did not significantly differ between groups in absolute values or when corrected for body weight or fat free body mass. However, cirrhotic patients had accelerated leucine turnover based on body cell mass (171.3 +/- 8.2 vs. 143 +/- 7.6 mumol.kg-1.h-1; P less than 0.03). Plasma leucine levels were decreased in cirrhosis (76.9 +/- 9.7 vs. 117.9 +/- 8.1 mumol/L; P less than 0.001) and correlated with an expanded extracellular water compartment (r = -0.91; P less than 0.001) and leucine oxidation (r = 0.91; P less than 0.01) in the cirrhotic patients but not in the control subjects. These data indicate that body composition and fluid compartments are important factors influencing leucine metabolism in cirrhosis and should be considered in future studies.
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PMID:Body cell mass and leucine metabolism in cirrhosis. 155 38

Using H2[18O] tracer isotope dilution and corrected bromide space as standard reference techniques, we determined total body water and extracellular water in cirrhotic patients with (four men and four women) and without (seven men and six women) ascites and compared them with a normal control group (eight men and six women). These results were then compared with calculations of total body and extracellular water determined by the bioelectrical impedance analysis technique. According to H2[18(O)] dilution, total body water was similar in cirrhotic patients without ascites and in controls (60.8% +/- 2.1% vs. 60.3% +/- 1.4% body wt), but was increased in patients with ascites (69.7% +/- 1.2% body wt; p less than 0.002). Correlation was excellent between the H2[18(O)] dilution and bioelectrical impedance measurements of total body water in controls and cirrhotic patients without ascites (r = 0.98; p less than 0.0001). However, this correlation was poor in cirrhotic patients with ascites (r = 0.17; not significant). According to the bromide space, extracellular water (expressed as a percentage of total body water) was increased in cirrhotic patients with (57.8% +/- 1.8%; p less than 0.001) and without (44.0% +/- 1.2%; p less than 0.001) ascites compared with controls (36.6% +/- 1.0%). A poor correlation (r = 0.41; p less than 0.13) was seen for extracellular water measurements between the bromide space method and the bioelectrical impedance method, which failed to detect the differences among the three groups observed with the bromide space technique. Furthermore, bioelectrical impedance failed to detect any change in total body or extracellular water after paracentesis, with a degree of inaccuracy that increased linearly as the amount of ascitic fluid removed increased (r = 0.97; p less than 0.001). All these intergroup comparisons remained the same, whether the analysis was of both men and women combined or for each gender individually. However, we saw differences between men and women in the control group and cirrhotic group without ascites. These results demonstrate that abnormalities in water homeostasis and compartmentalization between intracellular (the difference between total body and extracellular water fluid) and extracellular water may exist in cirrhosis whether or not fluid accumulation is clinically evident. These data further indicate that alterations in the metabolically active body cell mass (as represented by intracellular water) in cirrhosis may occur independently of total body water and calculated fat-free body mass. In addition, gender is an important variable to control for in studies of this type.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Measurements of total body and extracellular water in cirrhotic patients with and without ascites. 195 61

A rat model was used to determine whether the metabolism of halothane is changed in the presence of cirrhosis and whether exacerbation of liver dysfunction is correlated with such a change. Cirrhosis was produced by gavaging enzyme-induced male Wistar rats with carbon tetrachloride in corn oil once weekly for 12 weeks. Control rats received corn oil only. After a 3-week period without treatment, blood and urine were collected from each rat for determination of background levels of inorganic fluoride, bromide, and trifluoroacetic acid (halothane metabolites) and for assessment of liver function. Rats were then anesthetized with 1.05% halothane in 50% oxygen for 3 h. Following anesthesia, serial blood and urine samples were taken to monitor halothane metabolism and liver function. No differences were observed between cirrhotic and non-cirrhotic rats in serum levels and urinary excretion of halothane metabolites. However, serum levels of SGOT and SGPT were significantly increased about 1.5-fold in the noncirrhotic group and about 2.5-fold in the cirrhotic group after anesthesia. The increased levels observed in the cirrhotic group were significantly greater than in the noncirrhotic group. The results imply that the exacerbation of liver dysfunction after halothane anesthesia is most likely related to an indirect effect, such as change in liver blood flow, rather than to toxic metabolites.
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PMID:Halothane metabolism in cirrhotic rats. 367 65

In a prospective randomized controlled clinical trial, prevention of hemorrhage from oesophageal varices by repeated peri- and intravariceal injections of 20 ml Aethoxysclerol 1% were compared with medical management alone. The study involved 126 patients with cirrhosis and recent variceal bleeding confirmed by endoscopy. Injection sclerotherapy was carried out using a fiberoptic gastroscope under 10-20 mg intravenous diazepam and 20 mg hyoscin -N-butyl-bromide. Injections were given at monthly intervals. During the first five sessions the agent was given by perivariceal injections followed by five sessions with intravariceal injections. After the 10 months of injection therapy the patients were followed up for 16 months. During the perivariceal injection period 37% of the patients in the sclerotherapy group had further bleeding compared with 39% of the control group. During intravariceal injections 12% of the sclerotherapy group and 38% of the control group had further bleeding (p less than 0.05). During the follow-up of 16 months after sclerotherapy, 16% of the sclerotherapy group and 56% of the control group had further bleeding (p less than 0.05), 35% of the sclerotherapy group and 61% of the control group died in these 26 months of investigation (p less than 0.05). Intravariceal injection sclerotherapy significantly decreased the incidence of further bleeding and mortality in patients with cirrhosis and oesophageal varices. Perivariceal injections did not appear to be effective.
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PMID:[Prospective controlled study of para- and intravariceal sclerosing therapy of esophageal varices]. 637 85

Glyceraldehyde-3-phosphate dehydrogenase (G3PDH) is often used as a control gene for mRNA expression, however it has been proposed to be overexpressed in all hepatocellular carcinomas (HCC). Equal amounts of tumor and paired normal (T/N) RNA, based on OD260/280 nm, were compared using ethidium bromide staining, poly-T probing, gene-specific dot blot and Northern blots using control probes G3PDH, actin and histone H4. Using mRNA blots 13/20 surgical HCC pairs did not overexpress G3PDH. Those 7/20 intact samples which did appear to overexpress G3PDH on Northern blot could not be detected by poly-T probing of dot blots. The apparent overexpression was not specific for the control gene G3PDH nor for the malignancy HCC. It may represent partial mRNA degradation, or the presence of as yet unknown substances which interfere with absorption at 260/280 nm. We advise caution in selecting human T/N pairs for differential gene expression studies. For HCC, no clinicopathological variables, including cirrhosis, predicted whether a T/N sample pair was likely to be balanced or not.
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PMID:Glyceraldehyde-3-phosphate dehydrogenase mRNA expression in hepatocellular carcinoma. 947 11

The metabolic fate of leucine's first and second carbon may be different depending on the tissue in which leucine is metabolized, as well as the prevailing hormonal milieu of that tissue. However, previous studies of leucine kinetics in humans have used only leucine labeled (as tracer) at the first carbon position. Because cirrhosis is associated with factors (such as insulin resistance and altered fuel substrate utilization) that may influence how leucine is degraded, the kinetics of leucine's first and second carbon using a simultaneous infusion of [1-14C] leucine and [2-13C] leucine were studied in the postabsorptive state and during an amino acid infusion in 6 stable cirrhotic patients and 6 matched controls. The data were normalized for different body compartments that were quantified from the dilution of H2 [180] and bromide. The body cell mass, but not body weight or fat-free body mass, was decreased in cirrhosis (P < .001). In response to the amino acid infusion, total leucine appearance from proteolysis and leucine's incorporation into protein increased significantly in both groups, but were higher in cirrhotic patients. Endogenous protein breakdown decreased in normals but remained unchanged in cirrhosis. These alterations in leucine metabolism became more prominent when data were expressed based on the body cell mass rather than on body weight. The oxidation of leucine's first carbon (C1) was decreased in cirrhosis, but the oxidation of leucine's second carbon (C2) did not differ between groups during both the postabsorptive period and the amino acid infusion, while nonoxidative leucine degradation [the difference between the oxidation of leucine's (C1) and (C2)] was also decreased in cirrhosis. In addition, there was a positive correlation between nonoxidative leucine degradation (which represents leucine incorporation into fat), and the respiratory quotient obtained from indirect calorimetry (r = .87; P < .001). These data suggest that the extent of leucine carbon oxidation is dependent on whether fat or carbohydrate is the prevailing fuel substrate. In addition, cirrhotic patients have decreased nonoxidative leucine degradation and are unable to suppress endogenous protein breakdown normally in response to amino acid administration. These abnormalities may contribute to the diminished fat stores and body cell mass commonly observed in cirrhosis.
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PMID:Defective nonoxidative leucine degradation and endogenous leucine flux in cirrhosis during an amino acid infusion. 979 22

We studied DNA damages (single-strand breaks and alkali-labile sites) in peripheral blood lymphocytes from patients with chronic viral hepatitis and cirrhosis of mixed etiology. The structure of DNA was estimated fluorometrically by changes in the intensity of ethidium bromide fluorescence. Monoinfection with hepatitis B and C viruses was not accompanied by considerable changes in DNA structure in peripheral blood lymphocytes from patients with chronic diseases. The incidence of DNA damages in lymphocytes increased in patients with hepatitis G virus and TTV monoinfection. This is probably related to replication of these viruses in nucleated blood cells. Our results suggest that hepatitis C virus potentiates damaging effect of hepatitis G virus on DNA in lymphocytes.
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PMID:DNA structure in peripheral blood lymphocytes from patients with chronic viral liver damages. 1212 57

1. Liver fibrosis is the compensatory state of cirrhosis. In the long asymptomatic period, it is imperative to select a proper dosing regimen for drugs that are applicable to hepatic fibrosis. Otherwise, progressive deterioration to uncompensated cirrhosis may occur. The present study explored the characteristics of drug metabolism in fibrotic liver. 2. A rat precision-cut fibrotic liver slice (PCFLS) technique was established and the metabolism of verapamil was studied employing this technique. A rat hepatic fibrosis model was successfully induced integrating complex factors that included a high-fat diet, alcohol and CCl4. The PCFLS were incubated under different conditions and lactate dehydrogenase leakage, glutathione S-transferase activity and 3[4,5-dimethythiazole-2-yl]-2,5-diphenyltetrazolium bromide reduction were used as indices to assess PCFLS viability. Activities of phase I and phase II metabolizing enzymes were monitored following treatment with cytochrome P450 (CYP) inducers. Normal and fibrotic liver slices were incubated individually with 10 micromol/L verapamil. The concentration of verapamil in the medium was determined by high-performance liquid chromatography and intrinsic clearance (Cl(int)) was calculated on the basis of the concentration-time curve. 3. The results showed that the PCFLS viability remained steady throughout the 6 h of culture when the thickness of slices was 300 microm and pH of the medium was 7.0; CYP inducers (phenobarbital and ethanol) enhanced CYP2E1, CYP3A1/2 and uridine diphosphate-glucuronate transferase (UDPGT) activities, respectively, in a time-dependent manner. The Cl(int) (microL/min per mg) values differed significantly between normal (9.7 +/- 1.8) and fibrotic (5.6 +/- 1.4) liver slices (P < 0.01). 4. These results suggested that the PCFLS could remain viable for 2-6 h under appropriate conditions. The stability and inducibility of drug-metabolizing enzymes of PCFLS were also demonstrated. Furthermore, the metabolic rate of verapamil in PCFLS was decreased. These findings add further support to the use of PCFLS as a tool to study drug metabolism and to guide clinical medication.
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PMID:Establishment of rat precision-cut fibrotic liver slice technique and its application in verapamil metabolism. 1743 8


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