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)

The serum protein patterns of 38 patients with alcoholic liver cirrhosis were studied and compared with those of 15 patients with cryptogenic cirrhosis and of 18 normal volunteers. Serum prealbumin and albumin were significantly lowered in alcoholic liver cirrhosis in comparison with the normals. In liver cirrhosis, the four acute phase reactants, alpha 1-antiproteinase, orosomucoid, and haptoglobin and caeruloplasmin, showed a pattern in serum, in which alpha 1-antiproteinase was increased, orosomucoid and haptoglobin were decreased, and caeruloplasmin was normal. Immunoglobulins G, A and M were significantly elevated. IgA was significantly more elevated in patients with alcoholic disease than in patients with cryptogenic cirrhosis. The construction of a surgical portal-systemic shunt resulted in a significant decrease in serum concentrations of the acute phase reactants, while prealbumin, albumin and immunoglobulins were unaffected.
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PMID:Serum proteins in liver cirrhosis: effects of shunt surgery. 245 Sep 57

The pharmacokinetics of etodolac, a new nonsteroidal anti-inflammatory drug, were compared in normal subjects, in patients with renal and hepatic disease, and in elderly patients. In 28 normal subjects, orally administered etodolac was rapidly absorbed. By 1.2 hours after ingestion of a 200 mg dose, the maximum serum concentration (Cmax) averaged 15.9 micrograms/ml, with more than 99% of the drug bound to serum protein. Clearance was primarily hepatic. The mean half-life (t1/2) was 6 to 7 hours. There were no apparent differences in Cmax, the time at which Cmax occurred (tmax), area under the serum concentration/time curve (AUC0-24), or t1/2 between groups of young men (n = 20), elderly men (n = 24), and elderly men with osteoarthritis (n = 20), after a single dose of etodolac or after 7 days of subchronic administration. Moreover there was no evidence of accumulation. There also were no differences in Cmax, tmax, AUC0-24 or t1/2 between groups of normal subjects (n = 10) and patients with mild-to-moderate renal impairment (n = 10). Patients with end-stage renal disease who were receiving chronic hemodialysis had the same mean serum concentration of free drug as normal subjects, even though mean serum levels of protein-bound etodolac were slightly lower than those in the normal subjects. The only significant (p less than 0.05) difference between patients with stable hepatic cirrhosis and normal, age-matched subjects was a slightly shorter tmax in the cirrhotic subjects (1.1 vs. 1.4 hours). These findings suggest that no alteration of etodolac dosage would be necessary in these high-risk groups.
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PMID:Profile of etodolac: pharmacokinetic evaluation in special populations. 252 81

The alpha 1-antitrypsin (AAT) or protease inhibitor (Pi) genetic polymorphism was studied in 144 white, 100 coloured, 104 Indian and 127 black (Northern Sotho) healthy individuals (controls), in the Pretoria area. Their Pi phenotype and gene frequency distributions are compared with world-wide data on other population groups. The severely deficient Pi phenotypes S, Z and SZ jointly attain frequencies of 0.3-0.4% in coloureds and whites; in blacks and Indians the corresponding frequencies are very much lower. The implication for preventive medicine and public health is that in South Africa the sequelae of Pi deficiencies such as cirrhosis of the liver and/or emphysema of the lung are of practical importance in whites and coloureds and much less so in blacks and Indians. In 176 white breast cancer patients studied, the Pi phenotype and gene frequency distributions were found to be similar to those of healthy controls (not statistically significant). Cohorts of other patients were also phenotyped because of their low alpha 1-globulin concentrations in routine serum protein electrophoresis and/or their specific disease condition (cirrhosis of the liver or emphysema of the lung) known to be associated with AAT deficiency. These results are discussed in terms of their significance for family follow-up, genetic counselling and a preventive service. The need to avoid atmospheric pollution, especially cigarette smoke, is emphasised as a major and cost-effective preventive measure.
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PMID:Alpha-1-antitrypsin genetic polymorphism in South Africa. 349 69

A transudative pleural effusion develops when the systemic factors influencing the formation or absorption of the pleural fluid are altered. The pleural surfaces are not involved by the primary pathologic process. The diagnosis of transudative effusion is simple to establish by examining the characteristics of the pleural fluid. Transudates have all of the following three characteristics: The ratio of the pleural fluid to the serum protein is less than 0.5. The ratio of the pleural fluid to the serum LDH is less than 0.6. The pleural fluid LDH is less than two thirds the upper limit of normal for the serum LDH. Among the conditions that produce transudative pleural effusion, congestive heart failure is by far the most common. Pulmonary embolism, cirrhosis of the liver with ascites, and the nephrotic syndrome are the other common causes. Management of transudative pleural effusions involves managing the primary disease. Refractory, massive effusions can be controlled by tetracycline pleurodesis.
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PMID:Transudative pleural effusions. 384 1

We report cirrhosis and alpha 1-antitrypsin deficiency in two patients over 50 years of age who had an initial diagnosis of cryptogenic cirrhosis. Serum alpha 1-antitrypsin levels were in the homozygous range and a liver biopsy demonstrated cirrhosis with periodic acid-Schiff-positive, diastase-resistant globules in both. Red intracytoplasmic inclusion globules seen on trichrome staining in the first patient, and a decreased alpha-1 fraction on serum protein electrophoresis in the second suggested the diagnosis. We propose that the diagnosis of alpha 1-antitrypsin deficiency be considered in all patients, regardless of age, and that trichrome staining be part of the routine histologic evaluation in all patients with cirrhosis of uncertain etiology.
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PMID:Alpha 1-antitrypsin deficiency presenting as cryptogenic cirrhosis in adults over 50. 390 38

The P-component of amyloid (SAP) is a normal serum protein. Recent studies have pointed to the liver as the site of synthesis of SAP. Moreover, we have recently demonstrated a close correlation between serum level of SAP and the degree of liver impairment in patients with acute hepatitis, chronic active hepatitis, and cirrhosis. In the present study we have investigated liver involvement and serum SAP level during measles infection. Up to 80% of patients with measles had evidence of hepatic dysfunction. Serum SAP level was markedly decreased in patients with measles and correlated with the presence of liver involvement. Taken together, this finding suggests that serum SAP level might be a useful and sensitive indicator of liver disease.
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PMID:Serum amyloid P-component as a marker of liver involvement in measles infection. 399 39

The protein binding of four non-depolarizing neuromuscular blocking drugs-tubocurarine, fazadinium, pancuronium and Org NC45-was measured, in serum from normal patients and from patients with cirrhosis of the liver, by an ultracentrifugation method. The fraction bound to serum protein in normal patients was 56% for tubocurarine, 51% for fazadinium, 29% for pancuronium and 30% for Org NC 45. In patients with cirrhosis, the protein binding of the four drugs was similar to that obtained in the normal patient.
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PMID:Binding of tubocurarine, fazadinium, pancuronium and Org NC 45 to serum proteins in normal man and in patients with cirrhosis. 612 60

The pharmacokinetics of cefoperazone were studied and compared in six normal subjects and six patients with severe liver disease. All subjects received a 2-g intravenous infusion of cefoperazone over 15 min. Significantly different results were noted between normal subjects and patients with cirrhosis (range [mean]) for the following: peak serum concentrations (203 to 345 [239] versus 82 to 206 [141] micrograms/ml; P less than 0.01); serum beta half-lives (1.0 to 1.8 [1.5] versus 2.3 to 9.9 [4.5] h; P less than 0.05); renal excretion (17 to 27 [21] versus 32 to 60 [50]%; P less than 0.01); and apparent volumes of distribution at steady state (4.1 to 7.8 [6.3] versus 12.7 to 23.8 [15.9] liters/1.73 m2; P less than 0.01). Lower peak serum levels in the patients with cirrhosis were probably related to an increased apparent volume of distribution secondary to ascites and to decreased serum protein binding of cefoperazone. Longer beta half-lives in the patients with cirrhosis were probably secondary to both decreased hepatic excretion caused by severe liver disease and to increased apparent volume of distribution. However, the longest beta half-life among the patients with cirrhosis was in a subject with a serum creatinine level of 2.1 mg/dl. We conclude that, although mild to moderate impairment of cefoperazone excretion occurs in patients with hepatic disease, adjustment of dosage may be necessary only with concomitant renal insufficiency.
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PMID:Cefoperazone pharmacokinetics in normal subjects and patients with cirrhosis. 622 91

alpha 1-Antitrypsin is a serum protein protease inhibitor. The homozygous deficiency state for alpha 1-antitrypsin is associated with the development of chronic obstructive lung disease and liver cirrhosis. Familial hypercholesterolemia is a genetic defect in which the nonhepatic tissues of affected persons are partially or completely deficient in cellular receptors for low-density lipoproteins, the major plasma cholesterol transport protein. Homozygotes and heterozygotes for familial hypercholesterolemia experience premature coronary artery disease. We have identified a young patient who manifested heterozygous deficiencies for both of these gene products. The occurrence of these defects in tandem has not been previously reported.
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PMID:Heterozygous defects in alpha 1-antitrypsin and low-density lipoprotein receptor. Simultaneous occurrence in a pediatric patient. 625 88

Single-dose ranitidine kinetics were studied in 10 patients with cirrhosis as proved by liver biopsy. All were clinically stable. After an overnight fast, ranitidine was given in a randomized crossover order as a bolus intravenous injection (50 mg) or was taken by mouth (150 mg). Terminal t1/2 was 2.7 +/- 0.4 hr after oral dosing and 2.9 +/- 0.4 hr after intravenous injection. Total plasma clearance was 470 +/- 170 ml/min and the steady-state volume of distribution was 1.2 +/- 0.2 l/kg. There was considerable intersubject variability in the ranitidine serum concentration-time profile after oral dosing. Systemic availability as assessed by AUC analysis was 58% +/- 11%. Not all of the dose could be recovered in the urine as unchanged ranitidine and its known metabolites after intravenous injection. At 0.5 microgram/ml the serum protein binding of ranitidine was 4.6% +/- 1.3%. It is concluded that disposition of ranitidine in these 10 stable subjects with cirrhosis was not significantly altered. The minor changes observed in some were as likely to be the result of secondary perturbations in physiologic status as to effects of cirrhosis on drug metabolism.
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PMID:Ranitidine disposition and systemic availability in hepatic cirrhosis. 632 87


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