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)

A sensitive, specific, and simple method for determining serum or urine arylesterase (EC 3.1.1.2) is described. The enzyme acts on phenyl acetate to release phenol, which produces a stable indophenol dye with 4-aminoantipyrine and potassium ferricyanide. Arylesterase, a thiol enzyme, is reactivated by 2-mercaptoethanol and by cysteine, but not by reduced glutathione. Calcium is indispensable to stabilize and to activate (Km = 0.85 mmol/L) the enzyme; complete protection is achieved at CaCl2 20 mmol/L. Magnesium acts as a weak (Ki = 116 mmol/L), lanthanum as a potent (Ki = 5 mumol/L) competitive inhibitor. The activity is measured in diluted sera at phenyl acetate 4.0 mmol/L (Km = 1.12 mmol/L), pH 7.8 and 25 degrees C. The normal range extends from 53 to 186 kU/L, and four isoenzymes are present in sera from healthy adults. Arylesterase decreases in hepatic disorders, especially in cirrhosis and carcinoma of the liver, with reduction of the penultimate fraction in polyacryalmide gel electrophoresis.
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PMID:Arylesterase in serum: elaboration and clinical application of a fixed-incubation method. 47 20

The pharmacokinetics of carfecillin (Carbenicillin-phenyl-ester) were studied in 10 healthy subjects, in 5 patients with hepatic cirrhosis and in 5 cases of renal insufficiency. In healthy subjects maximal carbenicillin serum levels attained by therapeutic doses were about 20 microgram/ml; concentrations in the urine surpassed 1000 mu/ml. The phenol moiety was detectable as free phenol in sera (less than 1 microgram/ml) and urine (less than 3 microgram/ml), but its major part was transformed to glucuronide and sulphate conjugates. Pharmacokinetics were not altered significantly by hepatic lesion. In renal insufficiency, serum levels of both carbenicillin and conjugated phenol were higher and their decrease delayed, while urine concentration was low. Carfecillin treatment was successful in 20 out of 30 patients with UTI.
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PMID:Pharmacokinetic and clinical studies with carfecillin. 63 72

Formation of endogenous toxins through protein metabolism and detoxification through liver are described. In chronic hepatic insufficiency (cirrhosis of the liver), with failure of liver metabolism, levels of endogenous toxins in plasma and tissue, i.e. ammonia, phenol-derivatives and free fatty acids, rise. Plasma levels of ammonia and free fatty acids are both dependent on the Krebs cycle. This interaction and mutual dependance was examined clinically through application of amino acids that lower plasma ammonia level. Di-L(+)ornithin-alpha-ketoglutaric acid was able to lower ammonia levels in patients with liver cirrhosis. The difference between pre- and postinfusion levels of ammonia was significant, this corresponds to the observations of other authors. In addition we found a fall in levels of free fatty acids, triglycerides, and cholesterol. This effect on fatmetabolism was also observed in patients with no evidence of incipient or manifest hepatic insufficiency. The biochemical basis and the clinical implications of these findings are discussed.
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PMID:[Influence of ornithin-alpha-ketoglutaric acid on fatmetabolism in patients with cirrhosis of the liver (author's transl)]. 93 1

A total of 508 patients had an non-decompression surgery for esophago-gastric varices in our department, from September 1979 to December 1991. These patients consisted of 387 cases of transthoracic esophageal transection with para-esophagogastric devascularization, 40 cases of transabdominal esophageal transection, and 81 cases of Hassab procedure. The original diseases were cirrhosis in 432 patients, IPH in 35, extrahepatic-portal occlusion in 24, primary biliary cirrhosis in 6, Budd-Chiari syndrome in 4, and others in 7. Operative mortality rate was 5.3%. By thoracic approach, esophageal varices completely disappeared. Postoperative cumulative variceal recurrence and bleeding rates at 10 years were 12% and 7%, although recurrence occurred more often than not in cases with hepatocellular carcinoma (HCC). Cumulative survival rates at 5, 10 years were 69%, 46% in liver cirrhosis without HCC. Present study confirmed that our non-decompression surgery is effective in controlling esophagogastric varices in long term of periods.
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PMID:[Results of non-decompression surgery for esophago-gastric varices--postoperative disappearance, recurrence, rebleeding rate of varices, and cumulative survival rate]. 147 Jan 35

Endoscopic esophageal variceal sclerotherapy was performed in 301 patients with portal hypertension (emergency, 72 and elective, 229) using 3% aqueous phenol as sclerosant. The cause of portal hypertension was cirrhosis of the liver in 189 patients (Child's class A-48, B-66, and C-75), extrahepatic portal venous obstruction (EHPVO) in 90, and non-cirrhotic portal fibrosis in 22 patients. In the emergency group, active bleeding was controlled in 87% of cases. Re-bleeding occurred in 101 of 290 (35%) surviving patients. Obliteration of varices was achieved in 228 (84%) patients, with a mean of 5.14 +/- 2.27 sclerotherapy sessions. Of 301 patients, 29 (9.6%) had an early in-hospital mortality (30.5% in emergency and 3% in elective group), with 16 deaths due to variceal bleeding. Of the remaining 272 patients, 40 (15%) died during follow-up, of which only 11 died of variceal bleeding. Complications, such as superficial ulcers, dysphagia, and strictures, were observed in 14%, 7% of emergency, and 3% of elective patients. None of the patients developed systemic toxicity. In conclusion, 3% aqueous phenol is an effective, safe, and economical sclerosant for esophageal variceal sclerotherapy.
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PMID:Endoscopic esophageal variceal sclerotherapy using 3% aqueous phenol. 156 12

We conducted a follow-up study to evaluate mortality among 14,861 workers employed in five facilities producing or using phenol and formaldehyde. More than 360,000 person-years of follow-up accrued. Mortality rates from all causes of death combined were similar to those in the general U.S. population. We observed excesses of cancer of the esophagus, cancer of the kidney, and Hodgkin's disease among workers exposed to phenol, but none of these excesses showed a dose-response relation with exposure to phenol. Excess lung cancer mortality (SMR = 1.2) showed no consistent pattern by any exposure index. Workers exposed to phenol had lower mortality ratios for cancer of the buccal cavity and pharynx, cancer of the stomach, cancer of the brain, arteriosclerotic heart disease, emphysema, disease of the digestive system, and cirrhosis of the liver. Of these, arteriosclerotic heart disease, emphysema, and cirrhosis of the liver were inversely related to duration of phenol exposure and to cumulative phenol exposure levels. Although these inverse associations may be due to chance or uncontrolled confounders, the ability of phenol to interfere with the generation of oxidants in experimental systems suggests that the pattern may have biologic plausibility.
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PMID:Mortality among industrial workers exposed to phenol. 205

We describe the simple and rapid enzyme immunoassay of protein C in human plasma with use of a Cobas Fara centrifugal analyzer. The antibody, labeled with horseradish peroxidase, is reacted with antigen (protein C) for 15 min. The peroxidase activity of the resulting antigen-antibody conjugate is measured at 500 nm for 5 min in the presence of excess H2O2, phenol, and 4-aminoantipyrine, as compared with that of free conjugates. Results are calculated from a stored standard curve and expressed as a percentage of the value determined for a pooled specimen of normal adult plasma. The standard curve is linear from 0% to 200%. The CV is generally less than 4% for different concentrations of protein C. In liver cirrhosis, hepatocellular carcinoma, therapy with warfarin, thrombosis, and disseminated intravascular coagulation, protein C concentrations are about 40-70% of normal. Results obtained with the present homogeneous enzyme immunoassay correlated well with those by enzyme-labeled immunosorbent assay (r = 0.97).
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PMID:Protein C in human plasma determined by homogeneous enzyme immunoassay with use of a centrifugal analyzer. 304 78

Acute and chronic liver damage was induced in rats by thioacetamide (TAA). Centrilobular liver cell damage associated with an accumulation of lipid droplets was produced by a single high dose (10 mg TAA/100 g b.m.). Liver fibrosis, micronodular and macronodular liver cirrhosis were induced by chronic TAA treatment (300 ml/l drinking water for 1.5, 3 or 6 months). Acute administration of TAA caused a significant decrease of hepatic phenol red excretion but no compensatory increase of its urinary excretion. In contrast, 24 h after bile duct ligation renal excretion of the dye increased by about 50%. After chronic exposure to TAA for three months hepatic phenol red excretion remained reduced and renal excretion raised significantly. This compensatory increase of urinary excreted phenol red amounts did not occur after 6 months of TAA treatment, probably as a result of additional nephrotoxicity of TAA. Two weeks after cessation of TAA exposure for 3 months, hepatic and renal phenol red excretion returned to normal. Bile flow per animal increased significantly after 3 months of TAA exposure. Apparently this is due to a reduced intrahepatic reabsorption of canalicular bile in TAA-damaged liver.
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PMID:Relation between renal and hepatic excretion of drugs: VII. Hepatic and renal excretion of phenol red in thioacetamide-induced acute and chronic liver damage. 338 66

Both cryptogenic liver cirrhosis and idiopathic portal hypertension without pathological findings of liver cirrhosis (IPH) are relatively common in Japan. To find differrence between IPH and cryptogenic liver cirrhosis of Japanese, we investigated human leukocyte antigen (HLA), familial clustering of liver diseases as well as prevalence of HBs antigen in 31 patients with IPH. The age of patients with IPH ranged between 6 and 67 years old (mean, 40 years). The ratio of female to male in patients with IPH was 3.1. The incidence of chronic liver diseases in the relatives of patients with cryptogenic liver cirrhosis was significantly high (29.1%), whereas that in the relatives of patients with IPH was not high (12.9%) as compared with hospitalized controls (8.9%). The phenotype frequencies of the specificities of HLA A and B loci in patients with IPH did not differ from those in healthy controls. And the incidence of HBs antigen and antibody in patient with IPH (3.2% and 20.7%, respectively) was similar to those in normal subjects in Japan. These findings suggest that IPH in Japan is a different clinical entity from cryptogenic liver cirrhosis and that HB virus may not be one of the main causes of IPH.
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PMID:Human leukocyte antigen (HLA) in patients with idiopathic portal hypertension (IPH). 746 6

Splenic sinuses in idiopathic portal hypertension (IPH; 8 patients), liver cirrhosis (LC; 14 patients) and in regenerating autotransplanted spleens from 25 rats were compared with each other by scanning electron microscopy (SEM) and immunohistochemistry using antibodies against proliferating cell nuclear antigen (PCNA). Spleens obtained from six patients with gastric carcinoma and from five untreated adult rats were examined as controls. SEM of the sinuses showed that in IPH endothelial cells became irregular in shape, and the interendothelial slits of sinuses were irregularly enlarged. Sinus endothelial processes traversing the sinusal lumen were also found. The same changes were observed in the proliferating sinuses during regeneration of splenic tissue after autotransplantation in rats, but disappeared when the regeneration was completed. Irregular endothelial cells were few in LC. PCNA-positive sinus endothelial cells were increased in number in IPH as compared with those in LC; the mean number of PCNA-positive ones per cm2 was 45.4 in IPH and 8.2 in LC. It was suggested that, from SEM observation of sinus endothelial cells and counting PCNA-positive sinus endothelial cells, the sinuses of the spleen in IPH consist of proliferating endothelial cells or are in the state of increased proliferation. In conclusion, splenomegaly in IPH was presumed to be caused by proliferation of sinus endothelial cells, and by the increased splenic blood flow in the irregularly widened interendothelial slits of the sinuses.
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PMID:Structural characteristic of splenic sinuses in idiopathic portal hypertension. 854 36


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