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)

On the basis of their own experience and data from the literature, the authors warn against the simultaneous administration of diuretic agents and non-steroidal antiinflammatory drugs. Apart from the drastic reduction in the natriuretic effects of some diuretics, this association may lead to acute non-oliguric renal failure in patients with one of the following predisposing factors: volemic depletion, effective circulating volume (cardiac insufficiency, liver cirrhosis), preexisting nephropathy (lupus erythematosus, chronic renal failure), or borderline renal function (geriatric patients, diabetics).
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PMID:[Non-steroid anti-inflammatory agents, diuretics and kidney function: a warning]. 662 43

Red blood cell and serum selenium concentrations were investigated to determine normal concentrations for our geographic area and if potential differences existed in patients with selected diagnoses (hepatic, renal, malignant, and chronic diseases). Selenium was quantified in samples of red blood cells, serum and urine by neutron activation analysis. The results were analyzed by comparing 1) pooled data from all ages for each disease with normal values, and 2) normal values with age-matched patients in each disease category. Decreases in red blood cell selenium concentrations (P less than 0.05) occurred in normal subjects over 60 years of age without concurrent significant decreases in serum selenium. Although differential results were noted in age-matched groups, overall results showed that decreased concentrations of selenium in both red cells and in serum occurred with alcoholic cirrhosis, malignancies, and chronic renal failure (P less than 0.025). Red blood cell selenium concentrations also were decreased in patients with stable chronic disease. Decreased serum selenium concentrations were positively correlated with albumin concentrations in patients with cirrhosis. There was no correlation between serum selenium and bilirubin concentrations in patients with liver disease or between serum selenium and creatinine concentrations in patients with chronic renal failure whose urinary excretion of selenium was far below control levels.
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PMID:Red blood cell and serum selenium concentrations as influenced by age and selected diseases. 665 58

We report the incidence of normal (50.4%), increased (46.7%), and decreased (2.9%) anion gap among hospitalized patients in a retrospective study. The mean and range of increased anion gaps were 25 and 19-28 mmol/L. Values exceeding 30 mmol/L were uncommon and may indicate either acidosis or laboratory error. The most common causes of the increased anion gap among patients were chronic renal failure, congestive heart failure, malignant neoplasm, and diabetes mellitus. Increased anion gap in this study may be due to excess acids along with decreases in sodium, chloride, and carbon dioxide. The mean and range of decreased anion gap were 6 and 3-8 mmol/L. Anion-gap values less than 3 mmol/L were uncommon (one of 500 cases), and a high incidence of such values may indicate laboratory error. Nephrotic syndrome, liver cirrhosis, intestinal obstruction, and severe hemorrhage were the common disorders associated with decreased anion gap, which resulted from hypoalbuminemia and hyponatremia. Although most patients with decreased anion gap had hypoalbuminemia, hypoalbuminemic patients did not necessarily have decreased anion gap.
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PMID:Value of the anion gap in clinical diagnosis and laboratory evaluation. 682 31

1 Bumetanide (1 mg) was given orally and intravenously to a group of patients with chronic renal failure (n = 6) and to another group with cirrhosis of the liver (n = 8). 2 The pharmacokinetics, using a two-compartment model, and the pharmacodynamics of the drug in these patients were compared with those previously obtained for normal subjects. 3 In the renal group serum bumetanide concentrations were higher than for the normal subjects and the terminal half-lives were significantly prolonged (P less than 0.001). A decreased whole body clearance was attributable to a low renal clearance of drug, the non-renal clearance being significantly increased (P less than 0.01). 4 For the patients with liver disease, serum bumetanide concentrations were higher than for the renal group, and the terminal half-lives were significantly further prolonged (P less than 0.001). Both non-renal and renal clearances were significantly reduced (P less than 0.001). 5 Absorption rates were not significantly altered in either group and the values of F (bioavailability) were 0.82 and 0.95 for the patients with renal disease and hepatic disease, respectively. 6 A poor pharmacodynamic response and a reduced bumetanide excretion rate were observed for the patients with chronic renal failure, whereas with hepatic disease normal bumetanide excretion rates were observed with an impaired diuretic response.
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PMID:The pharmacokinetics and pharmacodynamics of the diuretic bumetanide in hepatic and renal disease. 684 58

In 121 patients with either liver cirrhosis or chronic renal failure, abnormal values for the concentrations of two pancreatic enzymes in serum were a frequent finding. In renal insufficiency a decreased rate of enzyme elimination is the most likely cause of the above-normal values we observed for serum immunoreactive trypsin and pancreatic isoamylase activity. As for patients with liver cirrhosis, we believe that changes in entrance rates into the blood--i.e., an affected pancreas--is a likely explanation of the abnormally high values we often found for these serum enzymes.
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PMID:Immunoreactive trypsin and pancreatic isoamylase activity in serum of patients with chronic renal failure or hepatic cirrhosis. 697 16

Serum 3'monoiodothyronine (3'-T1) levels were estimated by means of a specific radioimmunoassay (RIA) preceded by an ethanol extraction. The recovery of 3'T1 was in mean (+/-SEM) 110 +/- 9%, and the lower detection limit was 23 pmol/l. Serum levels of 3'T1 in 34 euthyroid healthy subjects were (median (range)) 55 pmol/l (less than 23 - 168 pmol/l), in 13 hyperthyroid patients 133 pmol/l (70 - 265 pmol/l) (P less than 0.01) and in 13 hypothyroid patients less than 23 pmol/l (less than 23 - 68 pmol/l) (P less than 0.01). In 11 patients with chronic renal failure serum 3'-T1 levels were highly increased 285 pmol/l (115 - 1538 pmol/l) (P less than 0.01) and correlated inversely to creatinine clearance (R = -0.68, P less than 0.05). In patients with liver cirrhosis serum 3'-T1 levels were unaffected, whereas in 19 patients with endogenous depression studied before and after recovery from the depression serum levels decreased from 70 pmol/l (less than 23 - 248 pmol/l) to 30 pmol/l (less than 23 - 95 pmol/l) (P less than 0.01). Administration of propranolol 40 mg b.i.d. for 2 weeks did not affect serum 3'-T1 levels. The study shows that 3'-T1 is present in serum from euthyroid man and varies with thyroid function. Further, it is suggested that 3'-T1 in contrast to other iodothyronines primarily is eliminated by the kidneys.
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PMID:Serum 3'-monoiodothyronine levels in normal subjects and in patients with thyroid and non-thyroid disease. 727 5

The binding of three loop diuretics, piretanide, bumetanide and furosemide, to serum proteins from patients with liver cirrhosis or fulminant hepatitis was investigated using equilibrium dialysis. A good correlation was found between serum albumin concentration and the percentage of each unbound (free) loop diuretic in patients with liver disease. The binding data obtained from patients with liver cirrhosis was compared with that of patients with chronic renal failure. Calculations made according to the Sandberg-Rosenthal's formula revealed that the maximum binding concentration (nP) varied in some cases. These findings necessitated a detailed investigation into whether the increased percentage of each unbound loop diuretic in patients with liver disease is attributable not only to lowered serum albumin concentration but also to inhibition of the protein binding by some endogenous substances. Thus, similar experiments were performed using rats with experimental liver cirrhosis. The binding of the loop diuretics to serum proteins in cirrhotic rats differed greatly from the findings obtained from cirrhotic patients. The percentage of unbound loop diuretic was well correlated with serum albumin concentration but not with the concentration of serum bilirubin (an endogenous substance) in cirrhotic rats.
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PMID:Further investigations on the binding of loop diuretics to serum proteins from patients with liver disease. 732 87

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

Basal plasma concentrations of human pancreatic polypeptide (PP) were measured in 14 patients with chronic renal failure (CRF), 13 patients with cirrhosis of the liver, and age-matched controls. PP was significantly higher in patients with CRF than in controls (817 +/- 183 vs. 157 +/- 118 pg/ml; P < 0.005). The degree of PP elevation in patients with CRF correlated well with the degree of their renal insufficiency (r = 0.85; P < 0.001). Fractionation of plasma over Sephadex G-50 columns revealed comparable elution patterns in patients with CRF and in normal controls. Hemodialysis had no effect on the PP concentration. We also determined arterial venous PP concentration differences and plasma blood flow across the kidneys and liver in 13 patients with cirrhosis and arteriovenous differences across of the liver in 13 controls with normal hepatic and renal functions. The mean PP concentration was significantly higher in arterial plasma than in renal venous plasma (143 +/- 24 vs. 123 +/- 23 pg/ml; P < 0.025). Renal fractional extraction was 17.2 +/- 6.6%, and renal clearance of PP was 151 +/- 47 ml/min. No significant extraction of PP occurred across the liver. It is concluded that the kidneys, but not the liver, are important sites for the metabolism of PP and that elevated PP concentrations in patients with CRF may contribute to their uremic syndrome.
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PMID:Human pancreatic polypeptide in chronic renal failure and cirrhosis of the liver: role of kidneys and liver in pancreatic polypeptide metabolism. 741 May 34

Chronic liver disease as well as chronic renal failure are responsible for abnormal nutrient metabolism and high rates of undernutrition. Although surgery is frequently required in such patients, the perioperative nutritional management has not yet been extensively studied in these conditions. During chronic liver disease, preoperative nutritional status and postoperative outcome are correlated. However, nutritional status can only be considered as one out of several factors of the prognosis, including the grade of liver insufficiency and the type of surgical procedure. Thus, it is difficult to evaluate the real influence of undernutrition on postoperative outcome. Similarly, the usefulness of preoperative nutrition is not definitely demonstrated in this condition. The nutritional requirements of patients with liver cirrhosis are estimated to be protein 1g and 30-35 kcal.kg-1.d-1. The duration of nutritional supplementation before surgery may not exceed 10 days. Postoperative parenteral nutrition seems to be well tolerated during chronic liver disease. Although some data in the literature suggest that it may be of interest after liver transplantation, the efficacy of postoperative parenteral nutrition needs to be proven in larger series. In chronically uraemic patients, the effects of undernutrition on postoperative morbidity and mortality have been poorly studied. Infectious complications after renal transplantation are favoured by several factors, including immunosuppressive therapy and malnutrition. The efficacy as well as the tolerance of perioperative nutritional support in patients with chronic renal failure are poorly known. In haemodialysis patients, candidates for renal graft, the nutritional status is usually well preserved when the recommended nutritional needs are provided: proteins 1.2-1.4 g and 35-40 kcal.kg-1.d-1.
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PMID:[Role of hepatocellular insufficiency and kidney failure on nutritional management]. 748 26


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