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

The renal regulation of sodium is intertwined with the extracellular fluid volume (ECFV). Most adjustments in sodium elimination in man are accomplished via alterations in tubular reabsorption. The latter is sensitive to change in ECFV. An expanded ECFV results in less reabsorption and more excretion of sodium, and a contracted ECFV has the converse effect. There are direct and indirect mechanisms whereby ECFV influences sodium reabsorption. Patients with nephrotic syndrome, heart failure, and cirrhosis "behave" physiologically as normal individuals with a contracted ECFV. Water balance is normally determined by intake and losses in sweat which is always hypoosmotic to plasma, by evaporation from skin and lungs, and through renal excretion. The major factors that determine the ability to concentrate the urine are (1) the establishment of a concentrated environment around the collecting ducts, and (2) the elaboration and effects on the kidney of antidiuretic hormone. The evaluation of a patient with abnormalities of sodium and water rests initially and largely on clinical information. The clinical setting provides clues to anticipating, preventing, and interpreting distortions of body sodium and water. The laboratory can detect an abnormality, confirm or refute clinical assessment, and assist in the quantitative aspects of treatment and its efficacy.
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PMID:Sodium and water: an overview. 96 14

"Refractory" ascites was drained off by combinations of antialdosterone (spironolactone, canrenone) and pseudoantialdosterone (triamterene, amiloride) drugs inducing as high sodium excretion as 100 mEq per day in two patients with liver cirrhosis kept on a 9 mEq Na diet. Potentiation of the natriuretic effects of the two types of antikaliuretic drugs occurred by real synergism rather than addition. Although natriuretic acitivity showed a typical dose-related pattern, potassium excretion was unpredictable. Significant increase in potassium excretion (reversal of the suppression) occurred when 300 mg triamterene was combined with 200 mg canrenone in one of the two patients and when the dose of spironolactone or canrenone was increased from 200 mg to 600 mg within the combinations with 300 mg triamterene or 20 mg amiloride in the other. Parallel increase in sodium and potassium excretions might be caused by a proximal tubular effect or by inhibition of potassium reabsorption along with sodium in Henle's loop. The vasopressin (DDAVP) refractory distorsion of the relationship between osmolal clearance and free water reabsorpton (induced by pseudo-antialdosterone agents and potentiated by antialdosterone drugs) observed in all the 6 cases of the present patient material favoured the "loop hypothesis".
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PMID:Reversal of the suppressed potassium excretion during treatment with combinations of antikaliuretic drugs (spironolactone, canrenone, triamterene, amiloride) in patients with liver cirrhosis. 100 53

Rats have been treated for 6 weeks with thioacetamide (0.1% in drinking water). The biochemical changes in liver microsomal metabolism of estradiol which are similar to those observed in human liver cirrhosis become already apparent after one week of treatment. These are diminishment of hepatic microsomal cytochromes P-450 and b5, comparable decrease of 2-hydroxylation and increase of formation of estrone from estradiol. The alterations of estrogen metabolism are reversible within two weeks after ending thioacetamide treatment. These data correspond to the already well established histological response of rat liver to thioacetamide, and its reversibility.
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PMID:[Time course of thioacetamide-induced changes in estrogen metabolism in the rat liver]. 100 99

In 12 patients with cirrhosis of the liver, determination of the liver volume by ultrasonic scanning and of the galactose elimination capacity (GE) were made before and after portal decompression surgery. The liver volume decreased significantly, with a median decrease of 402 ml (psmaller than 0.01). Also the GE decreased, but relatively less than the liver volume, so that the calculated GE per unit liver volume increased, with a median increase of 5 mg per minute times 100 ml liver volume (psmaller than 0.005). The decrease in liver volume following portal decompression is assumed to be due in part to reduction of liver blood volume, in part to loss of tissue water and fat, and probably to some loss of parenchyma, accounting for a reduction of the GE.
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PMID:Liver volume estimated by ultrasonic scanning before and after portal decompression surgery. 107 88

3 patients with hepatic cirrhosis and ascites underwent increased diuresis on six occasions, closely related to episodes of gastrointestinal bleeding. In each instance the increased urine volume was preceded by a sharp increase in blood urea nitrogen, presumably due to absorption of nitrogenous compounds from the gastrointestinal tract, suggesting a mechanism of osmotic diuresis. In each case there was a signigicant increase in serum sodium and osmolality, related to the greater-water-than-sodium diuresis induced by urea, which was promptly reversed by the administration of water or isotonic solution. Clinically this syndrome may be defined as the association of hypernatremia and hyperosmolality due to osmotic diuresis from urea appearing in a cirrhotic patient with ascites and gastrointestinal bleeding.
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PMID:Hypernatremia following gastrointestinal bleeding in cirrhosis with ascites. 107 10

Bumetanide2 is a new diuretic with a rapid onset and short duration of action. It is advocated for the treatment of oedema of cardiac origin; that associated with cirrhosis of the liver and renal diseases, including the nephrotic syndrome oedema of pregnancy and in pulmonary oedema. Bumetanide produces a pattern of water and electrolyte excretion closely resembling that of frusemide although it differs structurally from frusemide and other diuretics. 1 mg of bumetanide produces a diuretic effect similar to that evoked by 40 to 60 mg of frusemide. Short-and long-term studies in oedema of varying aetiology have shown bumetanide to be an effective diuretic. Because it is chemically different from existing diuretics, bumetanide may be helpful in oedema resistant to other drugs. It is well tolerated, but like other natriuretics it causes hypericaemia and may cause hypokalaemia during long-term administration.
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PMID:Bumetanide: A preliminary report of its pharmacological properties and therapeutic efficacy in oedema. 112 4

We bring up to date our series of direct measurements of portal flow and pressure in patients with cirrhosis of the liver. In 153 patients the portal flow averaged 447 plus or minus 350 ml. Hg per minute and the portal pressure 28.5 plus or minus 4 mm. Hg (approximately 387 mm. H2O). Both quantities compare favorably with our previous measurements in smaller groups of patients. In 80 of our patients we had also measurements of pressure on the hepatic and splanchnic sides of a clamp occluding the portal vein. Nine of these patients had an hepatic occluded portal pressure higher than either or both the free portal pressure and the splanchnic occluded portal pressure. Of these nine patients with reversed pressure differences, two had stagnant portal flow and the remaining seven had forward flow into the liver measuring from 80 to 1,116 ml. Hg per minute.
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PMID:The hemodynamics of portal hypertension revisited: determinants and significance of occluded portal pressures. 112 90

In 10 patients with hepatic cirrhosis of various etiology both the insorption and the volume of distribution of tritiated water are determined. Indicator for the velocity of insorption is the time interval between the oral application of 200 mu-Ci THO distributed in 100 ml tap water and the appearance of a peak concentration of the isotope in the serum. In comparison with normal controls the insorption of THO is protracted in patients with hepatic cirrhosis from 37.0 plus or minus 4.4 min (S.E.) to a mean of 69.0 plus or minus 29.6 min. Individually the "insorption time" can be quite normal. The prolongation of the process of insorption is independent of the apparent volume of distribution of THO or of the etiology of hepatic cirrhosis. In the early phases of the insorption which are characterized by the main increase of the radioactivity in serum there is no difference between patients with hepatic cirrhosis and normal controls. Although an alteration of body fluid metabolism can not be excluded as a source of the prolonged equilibration, it is suggested that changes of the intestinal blood flow, of the tissue pressure and of the colloidosmotic pressure are due to a disturbance of the insorption of tritiated water in patients with hepatic cirrhosis.
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PMID:[Insorption of tritiated water in hepatic cirrhosis (author's transl)]. 113 22

Zinc deficiency is a concomitant of both alcoholism and cirrhosis, as indicated by plasma and tissue measurements in man. The intracellular sites of zinc distribution, the site-specific nature of alcohol/cirrhosis-related depletion, and the alcohol exposure-zinc depletion time function have not been reported. Spague-Dawley rats (16) at 5 to 6 weeks were given normal chow and 20 per cent ethanol as sole water source. Control animals (14) had tap water. In rats killed at 2, 5, 9, and 14 weeks, zinc levels were measured by atomic absorption spectroscopy in plasma (p); muscle tissue (MT), cell sap (MCS) cell sap-free (MCSF), and mitochondria (MM); liver tissue (LT), cell sap (MCS), cell sap-free fraction (LCSF), And mitochondria (LM). Control zinc levels were stable in all tissues over the 14-week study; p = 108, plus or minus 10 mug per 100 ml., MT = 125 plus or minus 18, MCS = 30.3 plus or minus 3, MCSF = 70 plus or minus 6, MM = 209 plus or minus 17, LT = 198 plus or minus 29, LCS = 125 plus or minus 11.0, LCSF = 79.5 plus or minus 11.2, and LM = 291 plus or minus 30 mug per gram of dry tissue. Ethanol-fed rats showed marked decrease in all liver zinc fractions from the earliest (2 weeks) time, with the greatest depletion in LM to 35 per cent of control. MT and p zinc showed monotonic gradual declines at the rate of 3 per cent per week, becoming statistically different from control at 9 weeks in both tissues. Normal weight gain occurred in control animals: alcohol rats gained 52 per cent of control to 5 weeks, and showed no subsequent gain, weighing 62 per cent of control levels at 14 weeks. Liver mitochondria contain the highest zinc concentration, and are most rapidly depleted. MT and p declines follow hepatic zinc loss.
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PMID:Distribution of zinc in skeletal muscle and liver tissue in normal and dietary controlled alcoholic rats. 117 Feb 68

Spontaneous hyponatremia in cirrhosis with ascites is generally considered to be due to an impaired renal ability to excrete free water, to be a contraindication of diuretics, and to be a bad prognostic sign. These concepts are reviewed in this paper. 55 cirrhotics with ascites were divided into three groups. Group I consisted of 13 patients with hyponatremia and very low free-water clearance CH2O, 0.07 +/- 0.26 ml/min). These patients also had poor renal function: low inulin clearance (CINU, 40.6 +/- 25.9 ml/min) and paraaminohippurate clearance (CPAH, 383 +/- 275 ml/min). Group II consisted of 8 patients who also had hyponatremia. CH2O, CINU, and CPAH in these patients were fairly high: 5.85 +/- 1.53 ml/min, 85.7 +/- 26.2 ml/min, and 651 +/- 294 ml/min. These values are similar to those o7 +/- 4.27 ml/min, 94.7 +/- 33.1 ml/min, and 598 +/- 199 ml/min. Hyponatremia in Group I could be related to the impaired free-water clearance. The mechanism of hyponatremia in Group II patients is not clear. Patients with hyponatremia and low CINU and CPAH had a negative response to diuretics and a poor prognosis. Patients with hyponatremia but with relatively good renal function had a good prognosis, similar to Group III patients. They responded to diuretics with no worsening of their hyponatremia.
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PMID:Prognostic value of spontaneous hyponatremia in cirrhosis with ascites. 126 41


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