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

1. Resting energy expenditure and the metabolic responses to adrenaline (infusion rate: 0.03 micrograms min-1 kg-1 fat-free mass for 1 h) were investigated in 25 patients with liver cirrhosis. The patient group was heterogeneous and varied with respect to the aetiology of cirrhosis, the clinical condition (i.e. Child A or B), the nutritional status and the degree of hyperinsulinaemia. 2. When compared with 10 healthy control subjects the basal plasma adrenaline and noradrenaline concentrations were both increased in cirrhosis and remained elevated during adrenaline infusion (+39% and +31%, respectively; P < 0.05). Concomitantly, the peripheral plasma insulin concentration and the molar C-peptide/insulin ratio were increased in liver cirrhosis (+96% and +30%, respectively; P < 0.05). Hyperinsulinaemia was more pronounced in patients with ethanol-induced liver cirrhosis. 3. When expressed per kg fat-free mass, resting energy expenditure was enhanced in liver cirrhosis (+21%; P < 0.05) and was more pronounced (i.e. resting energy expenditures of +35% to +49% above estimated values) in patients with ethanol-induced cirrhosis, at advanced stages of the disease and in association with decreased body cell mass. 4. Infusion of adrenaline increased heart rate, O2 consumption and the plasma concentrations of glucose, lactate, free fatty acids, glycerol and 3-hydroxybutyrate, and similar transient increases and subsequent decreases in the respiratory quotient were observed in both groups. However, the lipolytic, ketogenic and thermic responses were reduced in cirrhotic patients. Reduced metabolic responses were more pronounced in hyperinsulinaemic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Resting energy expenditure and the thermic effect of adrenaline in patients with liver cirrhosis. 132 35

Gamma-aminobutyric acidA/benzodiazepine receptor binding sites and the N-methyl-D-aspartate subclass of glutamate receptor sites were assessed in synaptic plasma membrane homogenates of cerebral cortex tissue obtained at autopsy from cirrhotic and noncirrhotic alcoholic patients and matched control subjects. The alcoholic patients consumed an average of greater than 80 g of ethanol/day, the control subjects less than 20 g/day. Postmortem delays up to approximately 100 h caused no significant loss of any of the binding sites; the patient and subject groups were closely matched for age. The affinities (KD) of the receptor sites did not differ between the patient and subject groups, nor between cortical regions. Using three different radioligands ([3H]muscimol, [3H]flunitrazepam, and [3H]diazepam), the gamma-aminobutyric acidA/benzodiazepine receptor complex was found to have greater density (Bmax) in superior frontal gyrus in alcoholic patients (which selectively shows morphological change in alcoholic patients), but was unchanged in motor cortex. Alcoholic patients with cirrhosis had much less pronounced changes. The density of the N-methyl-D-aspartate subclass of glutamate receptors, assessed with [3H]MK-801, did not vary across patient and subject groups.
 ...
PMID:Amino acid neurotransmitter receptor changes in cerebral cortex in alcoholism: effect of cirrhosis of the liver. 132 22

To assess the risk of developing liver cirrhosis associated with alcohol consumption, HBV and HCV infection markers, we carried out a case-control study involving 115 patients admitted to the medical departments of the general hospitals in the province of L'Aquila (Abruzzo, Italy) who received for the first time the diagnosis of liver cirrhosis, and 167 controls randomly selected among patients admitted to the same hospitals as the cases. Alcohol intake was measured in all 282 subjects using an already validated standardized questionnaire, and expressed as mean lifetime daily alcohol intake in grams. The mean lifetime daily alcohol intake showed a dose-dependent effect on the risk of cirrhosis: the relative risk significantly rose to 3.8 (95% CI: 2.0-7.3) for a mean daily intake of > or = 101 g alcohol; for HBsAg positivity the relative risk of cirrhosis was 23.0 (95% CI: 4.9-107.8) and for anti-HCV positivity it was 8.7 (95% CI: 4.3-17.6). After applying a multiple logistic regression analysis in a multivariate model including mean lifetime alcohol intake and anti-HCV status, both variables were significantly associated with the risk of cirrhosis (relative risks = 5.3-95% CI: 2.3-12.2 and 9.9-95% CI: 4.4-22.0, respectively). The combination of these two variables was found to fit an additive--but not multiplicative--model relative to the risk of cirrhosis: furthermore, the interaction of the anti-HCV status with the presence or absence of cirrhosis did not result in a significant source of variability for the mean lifetime daily alcohol intake.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Interaction between alcohol consumption and positivity for antibodies to hepatitis C virus on the risk of liver cirrhosis: a case-control study. Provincial Group for the Study of Chronic Liver Disease. 133 Jun 73

Forty-six patients with cirrhosis and 75 biopsy-proved hepatocellular carcinoma (HCC) nodules underwent percutaneous ethanol injection (PEI) regardless of number (up to five) and size (mean diameter, 3.6 cm) of tumoral lesions and clinical severity of cirrhosis (11 patients in Child's class C were included). Ethanol was injected under sonographic guidance through 20 to 22 gauge needles so as to obtain homogeneous hyperechogenicity of lesions. A total of 271 PEI sessions were carried out, delivering 2 to 14 ml per session. All nodules but one decreased in size, and seven were no longer appreciable on sonography. Recurrence was detected in two patients. The 3 year survival rate of all cases was 86%. Child's classes A and B patients fared better (3 yr survival 100%); 2 year survival of subjects with HCC < or = 3 cm was 92%. Multifocality did not affect survival. Most patients experienced mild pain at the site of injection, but only two major complications were encountered: partial chemical thrombosis of the left portal vein and cholangitis. Both cases were managed conservatively. In conclusion, PEI seems to offer a safe and valuable tool for therapy of HCC, especially in patients with good functional liver reserve and small (< or = 3 cm) tumors.
 ...
PMID:Percutaneous ethanol injection under sonographic guidance of hepatocellular carcinoma in compensated and decompensated cirrhotic patients. 133 95

From April 1978 through December 1989, a total of 17 patients with unresectable hepatocellular carcinoma (HCC) were treated with radiation therapy alone or radiation therapy in conjunction with percutaneous ethanol injection (PEI), transarterial infusion chemotherapy (TAI), or transarterial embolization (TAE) at the National Medical Center Hospital. The median survival of all patients was 13.8 months. The survival values determined at 1, 2, and 3 years were 58.8%, 26.1%, and 9.8%, respectively. Only the pretreatment liver function affected the survival value. Between patients who did not have liver cirrhosis (LC) as well as those who had LC of Child's class A and patients who had LC of Child's class B or C, the differences observed in the 1-year survival value and the median duration of survival were statistically significant (P < 0.05). The serum cholinesterase (ChE) level seemed to be a good indicator of liver function during the radiation therapy. A field size of 150 cm2 and a total dose of 5000 cGy (TDF 82) seemed to be well tolerated by patients who did not have LC and those who had LC of Child's class A. The field size determined whether patients with poor liver function such as LC of Child's class B or C would develop severe hepatic deterioration after undergoing radiation therapy.
 ...
PMID:Radiation therapy in patients with unresectable hepatocellular carcinoma. 133 96

Of the 692 patients with hepatocellular carcinoma (HCC) who were admitted to our hospital between 1976 and 1990, 60 (8.8%) had small HCC with a maximal diameter of below 2 cm. The outcome of these 60 cases was analyzed after they had been divided into 4 groups based on the therapeutic method used: operation group (17 cases), percutaneous ethanol injection therapy (PEIT) group (20 cases), transcatheter arterial embolization (TAE) group (13 cases), and oral anticancer drug therapy (per os) group (10 cases). The 1-, 2-, 3-, 4-, and 5-year survival values obtained for the operation group (100%, 87.5%, 87.5%, 87.5%, and 87.5%, respectively) were significantly higher than those found for the per os group (P < 0.01). The best therapeutic results were achieved in the operation group. Although the follow-up period for the PEIT group was short, the 2-year survival of this group was nearly equal to that of the operation group. Whereas the duration of survival tended to increase in inverse proportion to the severity of the underlying liver cirrhosis, the survival values did not differ between solitary and multiple tumors or among the different histological grades of HCC. In this series, 20 patients died; 9 deaths (45.0%) were due to progressive disease and 3 deaths (15.0%) were attributed to hepatic failure. Because the operation group included many patients who displayed relatively good liver function, we cannot rule out the possibility that their excellent outcome may have been associated with this background factor. Therefore, further prospective investigation is necessary to compare the efficacy of various therapies in patient groups with a homogeneous background.
 ...
PMID:Treatment of small hepatocellular carcinoma. 133 4

The present paper is devoted to overview the basic concepts of ethanol-induced hepatic injury and therapeutic modalities by which alcoholic liver disease can be alleviated. The role of alcohol dehydrogenase of both hepatic and gastric origin as well as the importance of the number one metabolite acetaldehyde are discussed, furthermore the effects of microsomal ethanol oxidizing system are also described. The features of the major clinicopathological consequences of alcohol abuse fatty liver, alcoholic hepatitis are briefly outlined, and the basic pathogenetic mechanisms that lead to cirrhosis--cell necrosis, regeneration and fibroplasia--are shown. The understanding of the pathophysiology of alcohol-induced liver injury may improve the therapy with drugs and nutritional factors, and allow successful prevention through the early recognition of heavy drinkers before their social or medical disintegration. In the management of alcoholic liver diseases, among the true hepatoprotective agents a naturally occurring flavonoid silymarin and an active methyl-donor metabolite S-adenosyl-L-methionine seem to be promising. An antifibrotic treatment with colchicine might also be of importance. Further prospective, well-designed, controlled clinical trials are still warranted to evaluate real efficacy of these drugs. The hepatic consequences of alcohol abuse may be treatable, however, prevention would be the true resolution of the major global health problem of alcoholism.
 ...
PMID:Pathogenesis and management of alcoholic liver injury. 134

Parotid saliva samples from 24 alcoholic subjects without evidence of cirrhosis were analyzed for changes in flow rate, composition, and epidermal growth factor (EGF) secretion. Mean (+/- SE) stimulated parotid saliva flow rate (ml/min/gland) was significantly (p less than 0.01) lower in alcoholic subjects than in matched control subjects. Reduction in parotid saliva flow rate was associated with significant (p less than 0.05) decrease in total protein and amylase secretion in this group of patients. In addition, secretion of immunoreactive EGF, a specific salivary protein, was also markedly reduced (p less than 0.05) in alcoholic patients. None of the parotid saliva samples from the alcoholic subjects had detectable bioactivity of EGF in saliva. These data suggest that chronic alcohol ingestion is associated with significant changes in parotid saliva secretion and its composition, which may perpetuate and compound ethanol-induced injury to the upper gastrointestinal tract.
 ...
PMID:Ethanol and human saliva: effect of chronic alcoholism on flow rate, composition, and epidermal growth factor. 137 39

We recently found that polyunsaturated lecithin prevents ethanol from causing cirrhosis in the baboon. Because transformation of lipocytes to transitional cells plays a key role in hepatic fibrogenesis in vivo, and because this process in alcohol-fed baboons was found to be attenuated by polyunsaturated lecithin, we focused on lipocytes to study the mechanism of the protective effect. Rat lipocytes cultured on plastic undergo spontaneous activation, accompanied by expression of alpha-smooth muscle actin isoform and production of substantial amounts of type I collagen. The latter was further increased on incubation with acetaldehyde. This in vitro model was used here to study how acetaldehyde-mediated collagen production and accumulation can be turned off. Addition of polyunsaturated lecithin (10 mumols/L) was found to prevent the acetaldehyde-induced increase in collagen accumulation by 83% (p less than 0.001). By contrast, a saturated phospholipid (10 mumols/L dilauroyl phosphatidylcholine), a monounsaturated one (10 mumols/L linoleoyl-palmitoyl phosphatidylcholine) or linoleic acid (20 mumols/L bound to albumin) had no such effect. Incorporation of [3H]proline into collagen and the expression of alpha-1 (I) procollagen mRNA were increased by acetaldehyde; the latter was not significantly affected by polyunsaturated lecithin. Polyunsaturated lecithin increased lipocyte collagenase activity by 100% (p less than 0.001), whereas dilauroyl phosphatidylcholine, linoleoyl-palmitoyl phosphatidylcholine and linoleic acid had no such action. We concluded that (a) polyunsaturated lecithin selectively prevents the acetaldehyde-induced increase in collagen accumulation in lipocyte cultures, whereas other phospholipids or linoleate have no such effect; and (b) polyunsaturated lecithin does not modify the acetaldehyde-mediated increase in alpha-1 (I) procollagen mRNA, but it increases collagenase activity, suggesting that the protective effect exerted by polyunsaturated lecithin against alcohol induced fibrosis in vivo is due at least in part to stimulation of collagenase activity, which may prevent excess collagen accumulation by offsetting increased collagen production.
 ...
PMID:Polyunsaturated lecithin prevents acetaldehyde-mediated hepatic collagen accumulation by stimulating collagenase activity in cultured lipocytes. 137 80

The relationship of pretreatment serum ferritin and hepatic iron concentration to body iron removed by venesections was evaluated in 33 patients with genetic hemochromatosis. The median values of the three variables considered were 1,950 micrograms/L (range = 255 to 10,000), 1,175 micrograms/100 mg dry weight (range = 270 to 4,310) and 10 gm (range = 2 to 41), respectively. At basal liver biopsy 18 patients had cirrhosis, 6 patients had fibrosis and 9 patients had a normal pattern; siderosis was degree 3 in 6 patients and degree 4 in 27 patients. The results of fitting a polynomial regression of second degree showed that the curve of serum ferritin on iron removed was a straight line (R2 = 0.79, with a significant coefficient of linearity, p less than 0.01, and a nonsignificant coefficient of curvature), whereas that of hepatic iron concentration on iron removed showed a curvature (R2 = 0.62, with significant coefficient of linearity and curvature, p less than 0.01) and reached a plateau. The sigmoid model fit the curve of hepatic iron concentration on iron removed (R2 = 0.61), which suggested a saturation of hepatic iron storage capability; the asymptote corresponded to a hepatic iron concentration of about 2,000 micrograms/100 mg. In alcoholic patients (17 cases) the location of the sigmoid was greater than in nonalcoholic patients. Our results suggest that iron deposition occurs in the liver before other organs are involved and that with massive iron overload hepatic deposits reach saturation, after which hepatic iron concentration does not always reflect the amount of total stores. Alcohol consumption could slow the saturation of hepatic iron deposits.
 ...
PMID:Saturability of hepatic iron deposits in genetic hemochromatosis. 139 2


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>