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)

Two groups of patients were selected according to their plasma levels of alpha-1-antitrypsin deficiency from among 58 patients with a chronic bronchopathy. Group I had normal plasma levels of alpha-1-antytrypsin; group II had plasma values lower than normal. The pathologic conditions associated with chronic bronchopathies were studied in both groups and so were the gasometric characteristics of the same. Chronic bronchopathies in subjects belonging to group II showed a clear tendency to present normal levels of pCO2 and hydrogen ions possibly related to a greater bronchial impairment in these patients. Independently of the genetic characteristics of plasma alpha-1-antitrypsin deficiency, its general levels are the real indication of its possible etiopathogenic action. Patients with recurrent plasma alpha-1-antitrypsin deficiency, its general levels are the real indication of its possible etiopathogenic action. Patients with recurrent plasma alpha-1-antitrypsin deficiency are more susceptible to bacterial infections, liver cirrhosis, diabetes, and allergic states. All this would be related to the protective effect of this protein fraction, and its reduction according to the most recognized theories would decrease the resistance of hepatic and pancreatic cells.
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PMID:[Diseases associated with chronic bronchopathies and plasma alpha-1-antitrypsin deficiency (author's transl)]. 31 92

The mechanisms by which excess alcohol directly damages the liver cells have been elucidated by studies in the baboon, which have shown that inability of the liver's enzyme systems to cope with hydrogen and fat overloads is far more significant in the progression to cirrhosis than any indirect effects of malnutrition. With the appearance of mitochondrial deformation, the process may have reached the stage of irreversibility.
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PMID:The metabolic basis of alcohol's toxicity. 83 93

Patients with liver cirrhosis develop marked abnormalities in small bowel motility and high plasma glucagon levels. Disturbances in small intestinal motor activity could be related to hyperglucagonemia. To investigate the relationship between fasting plasma glucagon levels and changes in small bowel motility in patients with liver cirrhosis, eighteen cirrhotic patients and ten controls were studied. Plasma glucagon was measured by RIA. Mouth to cecum transit time was estimated by lactulose hydrogen breath test. Fasting small bowel motility was investigated by means of intraluminal manometry. Plasma glucagon levels were significantly higher in patients with cirrhosis (61 +/- 5 pmol/l) than in controls (32 +/- 3 pmol/l); p < 0.01. In patients with liver disease, plasma glucagon levels were not significantly correlated to mouth to cecum transit time (r: -0.32), duration of migrating motor complex (r: -0.24), nor to the frequency of multiple clustered contractions (r: -0.26). The degree of small bowel dysmotility is not related to plasma glucagon levels in patients with hepatic cirrhosis. These results do not support the hypothesis that hyperglucagonemia plays an important pathogenic role in the abnormalities of gut motility in cirrhosis.
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PMID:[Are disturbances of small intestinal motility associated with hyperglucagonemia in patients with liver cirrhosis?]. 134 Sep 93

Gastric emptying, mouth-to-cecum transit, and whole-gut transit of a solid-liquid meal were measured in 46 chronic alcoholics and in 30 control subjects by using scintigraphic techniques, hydrogen breath test, and stool markers. In the alcoholics various parameters such as ethanol consumption, gastrointestinal symptoms, and alcoholic neuropathy were determined and related to gastrointestinal transit times. Although there was no significant overall difference of gastric emptying, abnormally delayed gastric emptying was detected in 23.9% of the alcoholics but no control subject (P less than 0.005). Mouth-to-cecum transit was significantly prolonged in the alcoholics (P less than 0.001) with 14 alcoholics (37.8%) disclosing delayed mouth-to-cecum transit. No significant differences between both groups were detected concerning whole gut transit. In the alcoholics there was a significant correlation of dyspeptic symptoms with delayed gastric emptying (P less than 0.006), and alcoholics with diarrhea had an accelerated mouth-to-cecum transit as compared to those without diarrhea (P less than 0.05). Neither the presence of autonomic or peripheral neuropathy nor the presence of liver cirrhosis or ascites was significantly related to gastrointestinal transit times. However, the daily ethanol ingestion significantly correlated with gastric emptying (P less than 0.005). It is concluded, therefore, that in chronic alcoholics the small intestine and the stomach are most likely to be affected by gastrointestinal transit disorders and that these transit abnormalities are potentially related to toxic damage of gastrointestinal smooth muscle.
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PMID:Gastrointestinal transit of solid-liquid meal in chronic alcoholics. 207 Jul 5

In this study, the author intended to examine the validity of the inhaled hydrogen gas clearance method (i-H2) for determination of the hepatic blood flow (HBF), and also to show some applicabilities of the method in experimental animals and patients with liver diseases. Simultaneous determinations of HBF by i-H2 and electromagnetic flowmetry in rabbits revealed an excellent correlation between the values obtained by the two methods. Moreover, HBF in rabbits measured by i-H2 varied in parallel with that by thermocouple flowmetry or laser Doppler velocimetry after administration of norepinephrine, propranolol or glucagon. In carbon tetrachloride-treated rats, HBF measured by i-H2 correlated better with the severity of damage in the sinusoidal structure than the severity of hepatic cell injury or the serum levels of transaminases. HBF as determined by i-H2 was significantly decreased in acute hepatitis (AH), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis (LC) and fatty liver. Reduced HBF in AH returned to normal during recovery of the disease. The ratio of HBF in tumor/normal tissue was greater than 1.0 for hepatocellular carcinoma in contrast to the ratio of less than 1.0 for metastatic liver carcinoma. Propranolol caused a decrease in HBF by 31%, and vasopressin by 39% in patients with CIH or LC. In contrast, glucagon induced its increase by 65%, 35% and 17%, respectively, in patients with CIH, AH and LC.
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PMID:[Measurement of hepatic blood flow by the hydrogen gas clearance method. Experimental and clinical observations]. 236 96

5 patients with primary biliary cirrhosis (PBC), 9 patients with compensated hepatic cirrhosis of different etiology and 12 control persons were tested for renal acidification after peroral CaCl2 administration and urine Na2SO4 and pCO2 infusion as well as the gradient between partial urine pressure and blood pressure after NaHCO3 application. Distal renal tubular acidosis (DRTA) was diagnosed in one patient with PBC, latent DRTA in other 2 patients with PBC. Not even one patient's acidification disorder was eliminated through an increased sodium application to the acidification site after Na2SO4 application. After NaHCO3 application, the gradient between the CO2 partial pressure in the urine and blood in both patients with PBC was, however, latent, DRTA normal. After pH gradient elimination in patients with PBC and DRTA, the hydrogen iont secretion is thus comparable with the control persons. Based on this study, the authors believe that the gradient type of DRTA is characteristic of primary biliary cirrhosis.
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PMID:[Distal renal tubular acidosis in primary biliary cirrhosis]. 239 87

A new solid phase enzyme-linked immunosorbent assay (ELISA) was developed for the quantitation of human Factor VII antigen (F VII Ag), using a monospecific rabbit anti-F VII antiserum. Anti-F VII F(ab')2 fragments were adsorbed to polystyrene plates. The binding of serial dilutions of control or test plasma, containing F VII, was detected by incubation with peroxidase-labeled anti- FV II IgG followed by the addition of hydrogen peroxyde and O-phenylenediamine. This ELISA is specific, sensitive (detection limit: 0.05%) and accurate (coefficient of variation: 1.5-4% for within- and 1.6-9% for between-assays). F VII coagulant activity (F VII C) and F VII C) and F VII Ag were determined in large populations of controls and patients. In normal plasma (n = 38), F VII Ag ranged from 83 to 117% and the correlation coefficient between F VII Ag and F VII C was 0.94. In patients with severe (F VII C inf. 1%) congenital F VII deficiency (n = 5), F VII Ag was undetectable in two cases (inf. 0.05%) and markedly reduced (0.35 to 5.6%) in the three other cases. In patients with liver cirrhosis (n = 15), F VII Ag ranged from 21% to 59% and was in good correlation with F VII C (r = 0.84). In dicoumarol treated patients (n = 15), the levels of F VII Ag ranged from 51% to 79% and a poor correlation (r = 0.52) with F VII C was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An enzyme immunoassay (ELISA) for the quantitation of human factor VII. 243 28

In a clinical study (1.1.1986-28.2.1988) the oro-cecal transit time of lactulose was studied in 45 patients with liver cirrhosis of different etiologies by hydrogen breath test. The results were compared to the transit time of 16 healthy volunteers. The oro-cecal transit time of patients with alcoholic cirrhosis (means = 154 +/- 29 min.) was significantly increased (P less than or equal to 0.001) while non alcoholic cirrhosis (means = 99 +/- 34 min.) did not differ from the control group (means = 98 +/- 16 min.) As an explanation of the increased oro-cecal transit time an alcoholic autonomic neuropathy (- greater than n. vagus) is discussed.
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PMID:[Effect of chronic alcohol drinking and liver cirrhosis on oro-cecal transit time (H2 breath test)]. 255 75

Phosphorus-31 magnetic resonance (MR) spectroscopy was performed on the liver of patients with alcoholic hepatitis (n = 10), alcoholic cirrhosis (n = 9), and viral hepatitis B (n = 3) and on healthy control subjects (n = 21). A hydrogen-1 MR image-guided localization technique (ISIS) was used to acquire P-31 spectra selectively from a volume of interest within the liver. Spectra were analyzed to yield absolute molar concentrations of hepatic phosphomonoesters, phosphodiesters, inorganic phosphate, and adenosine triphosphate. It was found that (a) hepatic metabolite ratios in alcoholic liver disease were not significantly different from those in healthy subjects, (b) absolute hepatic metabolite concentrations were decreased by 25%-46% in alcoholic hepatitis and 13%-50% in alcoholic cirrhosis compared with those in healthy subjects, and (c) hepatic intracellular pH was 7.4 in healthy subjects, more acidic in alcoholic cirrhosis, and more alkaline in alcoholic hepatitis. The findings indicate that hepatic metabolite ratios are not a sensitive measure of alcoholic liver disease, that quantitative P-31 MR spectroscopy is able to noninvasively show metabolic changes associated with alcoholic liver disease, and that alcoholic hepatitis and cirrhosis may be distinguished by means of hepatic intracellular pH measured with MR spectroscopy.
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PMID:Alcoholic liver disease: quantitative image-guided P-31 MR spectroscopy. 279 71

Neutrophil functions of phagocytosis and intracellular killing of bacteria were examined in 40 patients with alcoholic cirrhosis of whom 18 had a superimposed acute alcoholic hepatitis. In 65% of these, defective neutrophil phagocytosis was demonstrable, and in 62.5% there was a defect of intracellular killing of either Staphylococcus aureus or Escherichia coli. Studies of the patients' serum failed to reveal inhibitors of neutrophil function. Additional assays of superoxide (O2-) and hydrogen peroxide production, hexose monophosphate shunt activity, degranulation and cellular levels of granule enzymes and glutathione revealed that these neutrophil defects are caused by both reduced production of superoxide and defects of degranulation. The hydrogen peroxide/superoxide molar ratio was raised in patients' neutrophils, and the strong inverse correlation found between the value of this ratio and intracellular levels of reduced glutathione would be consistent with the hypothesis that the neutrophils from patients with cirrhosis are unable to detoxify hydrogen peroxide effectively and that this is a result of reduced levels of glutathione in the cells. The consequent increase in oxidant stress, both intra- and extracellularly, may be the cause of phagocytic and degranulation defects. The reduced responses of patients' neutrophils may be caused by previous exposure of the cells to activating stimuli in circulation, as evidenced by depleted intracellular levels of granule enzymes and glutathione. Neutrophils from the patients with a superimposed acute alcoholic hepatitis had depressed phagocytosis in the early stages of incubation but, on the whole, neutrophils from these patients had a greater capacity for ingestion and killing of bacteria than neutrophils from patients with cirrhosis alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormalities of neutrophil phagocytosis, intracellular killing and metabolic activity in alcoholic cirrhosis and hepatitis. 300 18


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