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)

Risk for renal insufficiency (RI) resulting from nonsteroidal anti-inflammatory drugs (NSAID) exists in cirrhosis with ascites, nephrotic syndrome, decompensated congestive heart failure, and chronic renal disease. We saw seven cases of NSAID RI that demonstrate important additional clinical risk factors. These include advanced age (mean, 76 years), use of diuretic drugs (6/7 patients), and evidence of renal vascular disease as suggested by long-standing hypertension, diabetes, or atherosclerotic cardiovascular disease (7/7 patients). Analysis of past case reports of NSAID RI also showed these features. Treatment of acute gouty arthritis was the most common precipitating event. Evolving NSAID RI was suggested by rising serum urea nitrogen, serum creatinine, and serum potassium levels, and body weight gain associated with low fractional excretion of sodium. We conclude that since NSAID RI is preventable and reversible, it is important to recognize and monitor the conditions of those patients at risk.
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PMID:Identification of risk for renal insufficiency from nonsteroidal anti-inflammatory drugs. 686 44

1. The metabolic effect of alpha-oxoisocaproate (4-methyl-2-oxovalerate) infusion was examined in six patients with cirrhosis and in nine healthy control subjects. The arterial concentrations of amino acids, urea, ammonia, insulin and catecholamines were determined in the basal state and during intravenous infusion of alpha-oxoisocaproate (300 mumol/min) for 150 min. The exchanges of amino acids and substrates across the splanchnic region, the brain and the leg were examined in the healthy subjects by a catheter technique. 2. Basal alpha-oxoisocaproate levels were similar in patients and control subjects. During infusion the concentrations of alpha-oxoisocaproate rose to 90-130 mumol/l; they were 20-35% lower in the patients. Arterial leucine concentration increased in both groups to 250-300 mumol/l. Valine and isoleucine concentraions decreased (50-60%) as did to a lesser extent the concentrations of aromatic amino acids and methionine. 3. Regional exchange of amino acids was not significantly influenced by alpha-oxoisocaproate infusion. Arterial urea concentration decreased (12%, P less than 0.05) and ammonia levels rose (15-25%, P less than 0.05) in both groups. In the patients both adrenaline (100%, P less than 0.001) and noradrenaline concentrations were elevated (350%, P less than 0.001) in the basal state; insulin levels were similar to those in control subjects. 4. It is concluded that alpha-oxoisocaproate is rapidly transaminated to leucine in patients with cirrhosis and in healthy control subjects. alpha-Oxoisocaproate infusion resembles leucine infusion in its influence on aromatic amino acid concentrations, but in addition it elicits increased ammonia levels and decreased urea formation.
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PMID:Intravenous infusion of alpha-oxoisocaproate: influence on amino acid and nitrogen metabolism in patients with liver cirrhosis. 706 Mar 35

Since urea and uric acid clearance are affected by the effective intravascular volume, we measured the fractional urea and uric acid excretion in cirrhosis. High urea and uric acid clearances were observed in 30 and 55 percent, respectively, of 20 consecutive cirrhotic patients with normal renal function. In seven patients with a high fractional uric acid excretion, 5 mg of isosorbide dinitrate every four hours for 24 hours induced a significant increase in the serum uric acid level (from 3.7 +/- 0.8 mg/dl to 4.4 +/- 0.8 mg/dl; less than 0.001) with a concomitant decrease in the fractional uric acid excretion (from 14.0 +/- 3.2 percent to 8.8 +/- 3.1 percent; less than 0.02). During the same test, the blood urea level increased from 3.3 +/- 1.1 mmol/liter to 4.1 +/- 1.2 mmol/liter (p less than 0.005) with a decrease in fractional excretion from 51 +/- 4.5 percent to 39 +/- 5 percent (p less than 0.001). The oral intake of sulfinpyrazone in six of these patients induced a normal uricosuric response. In two cirrhotic patients with ascites, 40 mg of furosemide associated with a 24-hour severe water restriction was also shown to normalize the high fractional excretion of both urea and uric acid. In nine patients with ascites, we observed a significant increase in blood urea and uric acid concentration despite the absence of change in creatinine clearance once ascites was removed by diuretics. On the basis of these findings, we believe that the high fractional excretion of both urea and uric acid frequently observed in cirrhosis is related to an increase in the effective vascular volume.
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PMID:High uric acid and urea clearance in cirrhosis secondary to increased "effective vascular volume". 712 59

The aims of this study were: 1. the assessment of the nitrogen balance (NB) in both compensated and encephalopathic cirrhotics, 2. the evaluation of the efficacy of a new therapeutic approach: amino acid solutions enriched with branched chain (BCAA) but poor in aromatic (AAA) amino acids. Solutions containing only BCAA were also employed: 42 cirrhotics were divided into the following groups: 1st group (26 cases), cirrhosis without hepatic encephalopathy (HE); 2nd group (16 cases), cirrhosis with HE. Six patients (23%) in the 1st group showed a positive NB at the beginning; 20 (77%) were negative; 18 of them were fed an oral diet (0.8 g protein/kg/day; 35 cal/kg/day) as a result of which they were brought into a positive NB within 5 days (from - 7.38 +/- 0.95 to + 3.67 +/- 0.46 g N/24 h). In two cases the diet failed to give a positive NB, so it was replaced by a BCAA enriched solution infusion (NB raised from - 1.0 +/- 5.4 g N/24 h). Patients in the 2nd group were put on total parenteral nutrition (TPN); two cases receiving glucose alone achieved a positive NB only when BCAA enriched solutions were added (from - 4.0 to + 3.0 g N/24 h). Four patients treated for 3 days with BCAA alone did not achieve a positive NB; in these cases likewise, BCAA enriched solutions were added in order to achieve a positive NB (from - 0.8 to + 4.2 g N/24 h); all 14 cases treated from the beginning with glucose + BCAA enriched solutions became positive, on average, within 5 days (from - 4.82 +/- 0.89 to + 3.15 +/- 0.61 g N/24 h). In addition to the NB, other parameters (blood ammonia, BCAA/AAA ratio, blood urea, electroencephalograms) and clinical symptoms were beneficially influenced by these solutions.
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PMID:Negative nitrogen balance in cirrhotics. (A correct therapeutic approach). 729 72

After reduction and splitting of disulfide linkages the fibrinmonomer and fibrin of 45 patients with histologically confirmed liver cirrhosis and 38 patients with chronic renal failure (serum creatinine greater than 5 mg%) were analysed by SDS-PAA electrophoresis. Furthermore the activity of factor XIII was measured immunologically. The results indicated no polymerization of alpha-chains of fibrin while gamma-dimers were formed regularly in 71% of patients with liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis and in 45% of patients with chronic renal failure. In liver cirrhosis the lack of alpha-polymerization correlated to the severity of the disease and to the decrease of factor XIII activity (no alpha-polymers formed when below 80% of normal). In renal failure this correlation was not demonstrable since in all cases the activity of factor XIII was within the normal range. After the addition of C14-labelled urea to normal plasma during clotting an incorporation of this tracer could be demonstrated by scintiscanner diamins like urea, forming in the course of renal failure, probably serve as the "wrong substrate" for the transaminidase factor XIII.
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PMID:Structure of fibrin and fibrinmonomer in renal and hepatic failure. 739 32

Twenty patients with cirrhosis and ascites but no renal failure were given piretanide, a new loop diuretic, in order to investigate its efficacy and to relate the diuretic response with the pretreatment plasma aldosterone concentration. Eleven patients responded to piretanide 12 mg/day (equivalent in potency to 80 mg furosemide); there was no response in nine patients. Both groups were similar with regard to liver function, plasma urea, serum creatinine, plasma electrolytes, urine volume, and urine potassium concentration. The basal urinary sodium excretion was significantly higher in those patients who responded (23.6 +/- 5.7 mmol/day vs. 4.3 +/- 1.42 mmol/day; P < 0.01) (M +/- SE). Plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were normal or only slightly increased in patients who responded to piretanide (PRA = 1.22 +/- 0.20 ng/ml/h; PAC = 12.25 +/- 2.20 ng/100 ml) and very high in patients who did not respond (PRA = 8.71 +/- 1.18 ng/ml/h; PAC = 84.6 +/- 16.2 ng/100 ml) (P < 0.001). Patients unresponsive to piretanide 12 mg/day also failed to respond when the dose was increased to 24 mg/day. However, the addition of spironolactone, 150 mg/day, to piretanide was followed in these patients by a marked increase in diuresis and natriuresis. These results strongly suggest that the pre-treatment level of aldosterone is an important factor influencing the response to loop diuretics in patients with non-azotaemic cirrhosis and ascites.
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PMID:Use of piretanide, a new loop diuretic, in cirrhosis with ascites: relationship between the diuretic response and the plasma aldosterone level. 743 5

Hepatic urea synthesis is the organism's main channel for the disposal of nitrogen and it may be an 'essential' liver function. In six control subjects and five patients with cirrhosis of the liver urea synthesis was studied during continuous infusion for six to 24 hours of about 3 mmol alpha-amino nitrogen/h X kg body weight. The urea synthesis rate was calculated in intervals of two hours as urinary excretion with correction for accumulation in the total body water and for hydrolysis of urea in the gut. The peripheral venous plasma alpha-amino nitrogen concentration increased from 3 to about 14 mmol/l and the urea nitrogen synthesis rate from 25 to about 215 mmol/h. In all cases the urea synthesis rate rose linearly with the alpha-amino concentration throughout the examined range. The slope of this linear relationship is an expression of the hepatic conversion of alpha-amino nitrogen to urea nitrogen ('functional hepatic nitrogen clearance'). The functional hepatic nitrogen clearance was 22.4 l/h in control subjects and 13.7 1/h (P < 0.025) in the patients with cirrhosis. It was correlated with quantitative measures of the liver function (the galactose elimination capacity, r = 0.84, and the clearance of antipyrine, 4 = 0.80). These observations, while confirming the abundant capacity of the urea synthesis system, imply that a given urea synthesis rate requires a higher alpha-amino level in patients with reduced liver function.
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PMID:Synthesis of urea after stimulation with amino acids: relation to liver function. 745 May 64

Caring for the problem drinker in the perioperative period is a challenging task. If alcohol abuse is suspected, a careful assessment is indicated before surgery is performed. Both the CAGE and SMAST questionnaires are good screening tools for alcoholism. Preoperative evaluation of alcohol-dependent patients should include a complete blood count, blood urea nitrogen, serum electrolyte levels, creatinine and glucose levels, liver function tests, coagulation studies, an electrocardiogram and a chest radiograph. Smoking cessation and aggressive postoperative respiratory care are especially important for alcoholic patients who have chronic obstructive pulmonary disease. Elective surgery should not be considered in patients with acute hepatitis or cirrhosis, since the operative mortality rate is quite high in these patients. Alcohol withdrawal is managed primarily with benzodiazepines, although clonidine and beta blockers may also be beneficial.
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PMID:Perioperative management of the alcohol-dependent patient. 748 20

Hepatorenal syndrome (HRS) is a functional renal failure occurring in advanced liver cirrhosis with ascites. It is due to renal cortical vasoconstriction resulting from complex hemodynamic disturbances related to cirrhosis and portal hypertension. There is no consistently effective therapy except for liver transplantation. We report a case of severe HRS in a patient with advanced liver cirrhosis and portal hypertension. Three sessions of hemodialysis were performed because of severe renal failure (serum urea 83 mg/dl, serum creatinine 6 mg/dl). Creation of an intrahepatic portosystemic shunt reduced the portocaval gradient from 18 to 7 mm Hg. Spectacular improvement of the renal function was observed soon after the procedure, with spontaneous recovery of diuresis and a return of serum urea and creatinine to baseline values. The patient unfortunately died 2 months later from adult respiratory distress syndrome post emergency surgery for a massive bleed related to a duodenal ulcer. Throughout this episode, the renal function remained stable. The postmortem examination showed histologically normal kidneys. We conclude that the intrahepatic portosystemic shunt can improve renal function in cirrhotic patients with HRS; it could be used in patients awaiting liver transplantation to reverse preoperative renal failure.
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PMID:Improvement of hepatorenal syndrome by transjugular intrahepatic portosystemic shunt. 761 Dec 21

beta-Blockers are widely used to prevent gastrointestinal hemorrhage in cirrhosis. The metabolic effects of treatment are scarcely studied: hepatic function reportedly does not change significantly, but beta-adrenoceptors have been reported to regulate protein and amino acid metabolism. We studied hepatic nitrogen metabolism in response to constant alanine infusion in seven patients with cirrhosis before and 7 to 10 days after treatment with oral propranolol (60 to 100 mg/d). Beta-blockade was effective: it decreased heart rate by 25%, abolished orthostatic tachycardia, and reduced portal blood flow by 20%. Alanine-stimulated urea nitrogen synthesis rate (UNSR) was higher in patients with propranolol treatment, without any difference in aminonitrogen concentration. The kinetics of hepatic conversion of amino acid nitrogen into urea--ie, functional hepatic nitrogen clearance (FHNC)--increased by 30%, from (mean +/- SD) 17.0 +/- 4.1 to 22.0 +/- 6.6 L/h (P < .01). Increased urea production during alanine infusion resulted in negative nitrogen exchange even at the peak of alpha-aminonitrogen concentration. Basal insulin level was only slightly reduced during propranolol treatment, whereas the insulin response to alanine was significantly blunted. No differences in glucagon and cortisol were demonstrated. Epinephrine and norepinephrine levels were high-normal and did not vary after treatment. Increased urea production and stimulation of hepatic nitrogen clearance during beta-blockade may be mediated by relative hypoinsulinemia or by direct involvement of beta-adrenoceptors in the control of nitrogen metabolism, possibly by regulation of amino acid uptake and release in peripheral tissues.
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PMID:Effects of beta-blockade on hepatic conversion of amino acid nitrogen and on urea synthesis in cirrhosis. 761 49


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