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

Following some remarks on the hyposomolar-hyponatraemic syndrome and on the formation of free water, the possible aetiopathogenetic mechanisms of hyponatraemia in ascitogenous cirrhosis of the liver and in particular the role of ADH are considered. 3 cases out of 18 suffering from ascitic phase cirrhosis in whom inability to produce free water was accompanied by conserved urinary excretion of sodium are reported. One explanation might be the intervention of ADH or of an antidiuretic substance.
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PMID:[The hyposmolar-hyponatremic syndrome in hepatic cirrhosis. Possible role of ADH]. 43 39

The kinetics of extracellular water (82Br) and total body water (THO) in controls and patients with liver cirrhosis are studied. Analysis of the plasma activity of the radionuclides as a function of time shows that distribution volumes and kinetics can be described by a linear open three-compartment model and that the volumes are of about equal size. Measuring is carried out in the central compartment in which the radionuclides are injected as a bolus. In cirrhotic patients equilibration into a third compartment is attained about four times slower than in controls. Elimination is reduced by about the same factor. Reduced diffusion and effective blood flow in the cirrhotic patients are discussed as possible reasons for the differences.
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PMID:[Kinetics of whole-body water and bromide space in patients with liver cirrhosis (author's transl)]. 43 11

The metabolism of amphetamine was studied in three groups of mice, including normal mice (N), mice given chronic doses of phenobarbital via their drinking water (PB), and mice exposed to carbon tetrachloride vapors daily during the course of chronic phenobarbital consumption (PB/CCl4). Renal and hepatic tissue from animals of each group were examined by electron microscopy. Mice in the PB/CCl4 group demonstrated the classical symptoms of carbon tetrachloride-induced hepatic cirrhosis, and structural damage to the kidney. The PB group presented a normal renal pathology, but ultrastructural changes including swollen mitochondria and dilation of the endoplasmic reticulum were evident in the hepatocytes. The N, PB and PB/CCl4 mice excreted 84.5, 61.5 and 72.3 percent respectively of a dose of 14C-amphetamine sulfate in the 0-72 hour urine. Seven major urinary metabolites were detected in the normal group, 4 in PB group, and 3 in the PB/CCl4 group. Unchanged amphetamine, rho-hydroxyamphetamine and benzoic acid were tentatively identified by combined techniques of gas chromatography and thin-layer chromatography with autoradiography.
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PMID:Amphetamine metabolism in mice exposed chronically to phenobarbital and to phenobarbital with carbon tetrachloride. 44 95

The acid-base and hydroelectrolyte balance were evaluated in 116 patients with cirrhosis of the liver divided (a posteriori) into subjects without ascites, those with tractable ascites, and those with intractable ascites. Alterations were much earlier and more frequent in the pre-ascitic stage. A fall in arterial blood O2 tension also proved a poor prognostic factor. The water load test and 24-hr determination of natriuria best reflected the clinical picture and should thus act as pointers to the correct planning of treatment.
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PMID:[Changes in acid-base equilibrium and water-electrolyte balance in hepatic cirrhosis]. 45 Feb 95

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.
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PMID:[The physiopathology of ascites]. 46 62

Estimates were made of the arsenic concentration in liver specimens from nine patients having idiopathic portal hypertension (IP), and in four livers these were found to be significantly higher than those in patients with cirrhosis and in control subjects. The splenovenogram revealed extensive portosystemic collateral circulation. Corrected sinusoidal pressure and blood flow studies showed higher levels in four patients than in normal subjects. Microscopic examination of liver tissues revealed periportal fibrosis. The higher hepatic arsenic levels that were found were due to the inadvertent drinking of water contaminated with arsenic, adulterated opium, and indigenous medicines. A history of opium intake was not forthcoming but two patients had drunk water contaminated with arsenic and two others had taken bhasams (Ayurvedic medicines prepared by repeated oxidation of ores). Though the aetiology of idiopathic portal hypertension is not known, it is possible that arsenic intake may be one of the factors.
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PMID:Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India. 46 68

1. In a group of patients with cirrhosis who showed a wide range of values for the rate of renal sodium excretion, the latter was found to be inversely related to both the plasma concentration and rate of renal excretion of aldosterone. However, for a given sodium excretion the values for aldosterone were significantly lower in the patients than for a group of healthy control subjects. These findings suggest either an increased renal tubular sensitivity to aldosterone or the participation of other factors in the pathogenesis of the sodium retention. 2. Based on measurements of the rate of urine flow and the clearances of free water and inulin during a maximal water diuresis, the fractional reabsorption of sodium by the 'proximal', 'diluting segment' and 'distal' segments of the nephron was estimated. For patients retaining sodium the enhanced reabsorption occurred at both proximal and distal sites, the latter being quantitatively more important. There was no significantly enhanced sodium reabsorption in the diluting segment.
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PMID:Renal sodium retention in cirrhosis: relation to aldosterone and nephron site. 47 99

1. The mineralocorticoid 9 alpha-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an 'escape' from its sodium-retaining effects was observed, the other five continuing to retain sodium. 2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the 'effective' extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. The findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume. 3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.
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PMID:Studies on mineralocorticoid 'escape' in cirrhosis. 47 24

After summing up existing theories about the origins and development of functional hepatic encephalopathy, the authors report on the effects of six-hour intravenous infusions of ornithine alphaketoglutarate (60 g dissolved in 500 ml distilled water), administered to 10 patients with ethylic hepatic cirrhosis in conjunction with a normal protein intake (70 g/day). Arterial blood ammonemia, venous blood aminoacidemia and the insulin/glucagon ratio did not vary during or after infusion. This method of treatment therefore seems to meet the protein requirements of these undernourished patients.
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PMID:Effects of ornithine alphaketoglutarate on blood insulin, glucagon and aminoacids in alcoholic cirrhosis. 48 88

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


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