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

In a series of 68 cirrhotics subjected to portacaval anastomosis for digestive haemorrhage, alterations in the acid base balance, 3, 6, 12, 24 and 48 weeks after anastomosis, were examined. Following operation, an increase in the incidence of the usual acid base disturbances of liver cirrhosis is observed. Respiratory alkalosis increases with no direct relationship to teh postoperative increase in ammoniemia, the main stimulating agent of the resporatory centres. This is probably because the active fraction on the nerve cells is the non-ionized one only, freely diffusible through the haematoencephalic barrier, the plasma concentration of which is a function of blood pH. Postoperative metabolic alkalosis is secondary to the potassium and chloride depletion consequent on operative trauma, on the malnutrition syndrome and, in the case of potassium, on secondary hyperaldosteronism which, unlike what is observed in the other groups of cirrhotics, is uncorrected by anastomosis. After the shunt, metabolic acidosis may be the expression of an increase in lactates and pyruvates following on further liver function deterioration, and of a functional renal insufficiency which anastomosis makes more manifest.
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PMID:[Acid-base metabolism in patients with hepatic cirrhosis treated with portacaval anastomosis at various intervals after the operation]. 30 8

Bumetanide and frusemide were compared in a crossover study of 10 patients with cirrhosis and fluid overload. Patients received each drug for 3 months. Doses of bumetide varied from 1 mg on alternate days to 3 mg daily (mean 1.3 mg/day), and for frusemide from 40 mg on alternate days to 160 mg daily (mean 72 mg/day). Both drugs proved effective in controlling ascites and oedema, 9 out of the 10 patients showing a satisfactory response. Minor side-effects, hypokalaemia and hyperuricaemia were common with both agents, and hypomagnesaemia and metabolic alkalosis developed in some patients.
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PMID:Treatment of fluid retention in cirrhosis: a comparison of bumetanide and frusemide. 33 56

Acid-base status was determined in 86 patients with cirrhosis of the liver. Group I comprised 55 patients living more than 3 months after examination (stable). Another 18 stable patients with a surgical porta-caval shunt (p.c.a.) formed group II. Group III consisted of 12 terminal patients without p.c.a. examined within the last week of life. With respect to liver function group II was intermediate between I and III. The most common acid-base disturbance in group I was compensated respiratory alkalosis (20%) followed by compensated metabolic alkalosis (15%). 50% of group II presented compensated respiratory alkalosis. 85% of group III showed metabolic acidosis, which was compensated in only half of the patients. Respiratory alkalosis seemed more related to impairment of liver function than to portasystemic shunting. The genesis of the terminal metabolic acidosis was complex. Renal function was reduced in 92% of group III, and lactic acidosis was found in 36%. In this group hepatic function was most severely impaired, and 60% were hypotensive. These disturbances were not related to aetiology or treatment of the liver disease.
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PMID:Acid-base status in liver cirrhosis. Disturbances in stable, terminal and portal-caval shunted patients. 127 3

Diuretics have long been used to lower blood pressure in hypertensive patients or to control body fluid and electrolyte homeostasis in diseases such as congestive heart failure, chronic renal failure or cirrhosis. The initial response to diuretics is a negative sodium and fluid balance. The diuretic-induced loss of salt and water activates several hormonal systems such as vasopressin, the renin-angiotensin-aldosterone system or the sympathetic nervous system which tend to compensate for the changes in sodium and water balance. This neurohormonal response may have important clinical implications. Thus, the activation of the renin-angiotensin-aldosterone cascade appears to be partially responsible for the flat dose-blood pressure response curve of thiazides in hypertensive patients. It may also be responsible for the difference between responders and non-responders to diuretic therapy and for the development of side-effects such as hypokalaemia, metabolic alkalosis or hyponatraemia. There are several ways to prevent the undesirable consequences of the neurohormonal responses to diuretics. The first is to use low doses of these agents. It is also possible to combine them with agents that block the activity of the renin-angiotensin-aldosterone system such as ACE inhibitors or in combination with drugs that reduce aldosterone secretion such as calcium antagonists. The development of drugs able to enhance urinary sodium excretion and to reduce simultaneously the activity of the renin-angiotensin-aldosterone system may offer a new interesting alternative. This might perhaps be achieved in the future with the administration of neutral endopeptidase inhibitors which interfere with the enzymatic degradation of atrial natriuretic peptide.
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PMID:Neurohormonal consequences of diuretics in different cardiovascular syndromes. 136 43

Disorders of acid-base balance are frequently encountered in fulminant hepatic failure, liver cirrhosis and autoimmune liver diseases. The disorders per se except lactic acidosis rarely poses serious clinical problems. However metabolic alkalosis induced by administration of diuretics and hypokalemia in renal tubular acidosis are risk factors for hepatic encephalopathy.
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PMID:[Disorders of acid-base balance in liver disease]. 143 10

Eighty unselected cases of hyponatremia complicating liver cirrhosis were analysed. Of these cases, 20 had sodium levels less than 135 mmol/L, 48 less than or equal to 130 mmol/L and 12 less than or equal to 125 mmol/L. 5 cases developed acute hyponatremic syndrome after abdominal paracentesis and high-dose of diuretics. Of these 5 cases, 1 died and 4 recovered after immediate infusion of 3% sodium chloride (200-300 ml/d intravenously for 7-10 days). Both the crystal and colloid pressure of blood determined in 10 cases were less than normal. The sodium level of the ascitic fluid determined in 5 cases was higher than that of serum. Respiratory alkalosis complicated with metabolic alkalosis or acidosis were the main features of acid-base disorders. These might be due to alkalinizing agents therapy, infection and hepato-renal syndrome. Based on these clinical studies, it was shown that paracentesis and diuretics are the main causes of acute hyponatremic syndrome, so these measures should be taken carefully in patients with hyponatremic state previously, especially in patients with poor general, hepatic and renal conditions.
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PMID:[Hyponatremia in patients with ascites complicating liver cirrhosis]. 158 43

Despite a marked reduction of the urea cycle capacity, patients with well-compensated chronic liver disease excrete near-normal amounts of urea. Compensation of the urea cycle defect apparently occurs through the activation of liver glutaminase, as suggested by an inverse relationship between the in vitro ureagenic capacity and the flux through glutaminase in liver tissue from patients with a normal, fatty, or cirrhotic liver. In these patients, the flux through glutaminase, as determined in vitro, increases in parallel with the plasma bicarbonate level and plasma pH determined in vivo. In view of this and results from previous studies, the following hypothesis is suggested: The decrease of urea cycle enzyme activities in liver cirrhosis produces metabolic alkalosis due to an impaired bicarbonate elimination. Alkalosis in turn activates and stabilizes hepatic glutaminase and accordingly mitochondrial ammonia provision for carbamoylphosphate synthetase. This results in a compensatory stimulation of the urea cycle flux in the cirrhotic patient to near-normal rates, despite the marked reduction of urea cycle enzyme activity. Accordingly, alkalosis is an important driving force for urea synthesis in the cirrhotic patient. With respect to clinical medicine, attention must be paid to acid-base disturbances in the hyperammonemic patient.
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PMID:Metabolic alkalosis as driving force for urea synthesis in liver disease: pathogenetic model and therapeutic implications. 160 Mar 51

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.
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PMID:Hyperventilation with hypoproteinemia. 318 88

This chapter reviews the disturbances of the serum sodium and potassium concentrations, acid-base imbalances, and acute renal dysfunction that are seen frequently in alcoholic patients. The hyponatremia common in decompensated cirrhotics is caused by an impairment of renal free water clearance and concomitant water ingestion. Excessive proximal renal tubular sodium reabsorption and nonosmotic vasopressin release underlie the defect in renal water excretion in cirrhosis. Restriction of water intake is the principal therapeutic measure for hyponatremia. Hypokalemia is common in alcoholics but when observed does not always represent true potassium depletion. Although most cirrhotics have a diminished total body potassium content, intracellular potassium concentration is usually normal. In some patients gastrointestinal and renal potassium losses and nutritional potassium deficiency may cause true potassium depletion. Respiratory and metabolic alkalosis are the acid-base disturbances seen most frequently in alcoholics. Acidosis is relatively uncommon and is usually due to renal insufficiency, lactic acid or keto-acid accumulation. Toxin ingestion (methanol, ethylene glycol, or isopropanol) may also cause severe acidosis. Rhabdomyolysis, common in severe alcoholism, may produce various electrolyte disturbances and acute renal failure. The prognosis for recovery is good although temporary dialysis may be necessary.
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PMID:Disorders of the serum electrolytes, acid-base balance, and renal function in alcoholism. 370 21

It has been suggested that hepatic urea synthesis, which consumes HCO-3, plays an important role in acid-base homeostasis. This study measured urea synthesis rate (Ra urea) directly to assess its role in determining the acid-base status in patients with end-stage cirrhosis and after orthotopic liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]urea. Six healthy volunteers served as controls. Ra urea was 5.05 +/- 0.40 (SE) and 3.11 +/- 0.51 micromol. kg-1. min-1, respectively, in controls and patients with cirrhosis (P < 0. 05). Arterial base excess was 0.6 +/- 0.3 meq/l in controls and -1.1 +/- 1.3 meq/l in cirrhotic patients (not different). After OLT, Ra urea was 15.05 +/- 1.73 micromol. kg-1. min-1, which accompanied an arterial base excess of 7.0 +/- 0.3 meq/l (P < 0.001). We conclude that impaired Ra urea in cirrhotic patients does not produce metabolic alkalosis. Concurrent postoperative metabolic alkalosis and increased Ra urea indicate that the alkalosis is not caused by impaired Ra urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic alkalosis by augmenting Ra urea, thus increasing HCO-3 consumption and moderating the severity of metabolic alkalosis produced elsewhere.
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PMID:Effect of liver disease and transplantation on urea synthesis in humans: relationship to acid-base status. 1033 5


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