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 group of 207 consecutive patients admitted for decompensated liver cirrhosis of different etiologies (alcoholic, HBsAg-associated and cryptogenic), was studied in order to assess the independent long-term (up to 5 years) prognostic value of 13 clinical, biochemical and etiological factors. These were analyzed by the Cox Regression Model using a step-wise backward procedure. The final model included bilirubin (p = 0.003), HBsAg (p = 0.006), encephalopathy (p = 0.010) and a factor comprising urea and albumin (p less than 0.001). The model was validated by a split-sample testing technique and may be used to predict survival in decompensated cirrhosis. A comparison with Child-Pugh's score in terms of survival prediction was carried out and was favorable to our model. We conclude that this model can be useful for predicting short and long-term survival in the three most common types of liver cirrhosis and that the additional overhead to calculate it seems justified in view of the large availability of microcomputers where simple programs can be run to perform this task and draw the predicted survival curves.
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PMID:[Prognostic factors and survival model for decompensated hepatic cirrhosis]. 176 12

Antithrombin III is an anticoagulant synthesized in the liver cells. The aim of this study was to estimate the serum level of antithrombin III in cirrhotics. Investigations were carried out in 32 patients with cirrhosis and in 20 healthy controls. Antithrombin III measured by radial immunodiffusion was found significantly lower (19.2 +/- 6.8 mg%) than in controls (28.0 +/- +/- 5.2 mg%) (p less than 0.01). The level of antithrombin III is positively correlated with pseudo-cholinesterase and, less significantly with blood albumin. Therefore decreased antithrombin III reflects liver cell disfunction in cirrhosis and its decrease may predispose to thrombotic events which occur sporadically in cirrhosis.
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PMID:The significance of low antithrombin III levels in cirrhosis. 178 43

The value of the aminoterminal procollagen-III-peptide (P-III-P) in predicting death or survival was evaluated in a group of 43 patients with proven postnecrotic or alcoholic cirrhosis. Patients were followed-up prospectively for 2 years. The prognostic value of P-III-P was compared with the Child classification, fasting and postprandial serum bile acids, and standard laboratory tests such as bilirubin, prothrombin index, pseudocholinesterase, albumin, GOT, GPT, gamma-GT, and clinical findings such as ascites, encephalopathy (assessed with the number connection test = NCT), and nutritional status. Between patients who died and those who survived the following 2 years, there were significant differences in the following parameters at the time of inclusion in the study: encephalopathy judged by NCT (p = 0.001), serum albumin (p = 0.0012), postprandial serum bile acids (p = 0.0024), fasting serum bile acids (p = 0.0025), pseudocholinesterase (p = 0.0044), GOT (p = 0.015), bilirubin (p = 0.016), and prothrombin index (p = 0.01). None of the other parameters investigated, including SP-III-P (p = 0.46), revealed any statistically significant differences between patients who died and survivors. The prognostic significance of laboratory tests and recorded clinical findings was evaluated, either alone or in combination with life-table analysis using the Cox model. SP-III-P, alone or in combination with other parameters, failed to improve prediction of mortality in patients with cirrhosis. In comparison to the Child classification (p = 0.0004) the combination of NCT and postprandial serum bile acids showed a similar ability (p = 0.0003) to predict patient survival.
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PMID:Predictive value of serum procollagen-III-peptide for the survival of patients with cirrhosis. 180 22

The aim of our study is to prove whether the development of the low-T3-syndrome in patients with liver cirrhosis is associated with their prognosis. For this purpose we determined the peripheral thyroid hormone levels in 28 patients with liver cirrhosis. For prognosis assessment we calculated the Prognostic Index (PI) on the basis of Cox's regression model as recently described by us. Calculating this index we used 11 parameters: liver morphology, consciousness, spider naevi, PCV, thrombocytes, gamma-GT, cholesterol, albumin, Quick's value, IgA, and potassium. It is demonstrated that there is an inverse correlation between T3-serum levels and PI (p = 0.03). An association could not be detected neither between reverse T3 and PI nor between T3 and rT3. On the other hand basal TSH was also inversely associated with PI. Thus, the low T3-serum levels did not induce a rise of basal TSH in cirrhotics. Moreover, the mean serum-T3-concentration differed significantly from that of 6 decreased patients and from that of the surviving (p = 0.00076). It seems to be true that low T3-serum levels are a very sensitive parameter for prognosis prediction in patients with liver cirrhosis.
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PMID:Development of the low-T3-syndrome and prognosis assessment in patients with liver cirrhosis. 181 59

Forty-four patients aged between 12 and 64 years comprising 16 hepatitis (group 1); 12 cirrhosis (group 2); 16 primary liver cell carcinoma (group 3) and 18 normal controls were studied. In hepatitis, plasma total cholesterol and total cholesterol/phospholipid ratio were significantly reduced, while the changes in red cell cholesterol and phospholipid and plasma phospholipid were not. The blood glucose was significantly reduced. The plasma total cholesterol/phospholipid ratio was positively correlated with the plasma total bilirubin. In cirrhosis patients, red cell total cholesterol and ratio to phospholipid were significantly increased and the plasma cholesterol reduced with no significant changes in red cell and plasma phospholipids. The plasma total cholesterol/phospholipid ratio was reduced while the corresponding ratio in red cells was increased. Both total cholesterol and the ratio to phospholipid in red cells were negatively correlated with albumin and positively correlated with the plasma total bilirubin. In primary liver cell carcinoma, the plasma and red cholesterol and their ratio in the red cell were significantly increased while the ratio in plasma was not. The serum albumin levels were reduced while the liver enzymes and total bilirubin were raised in all patient groups. Our results suggest a possible relationship between liver function and cholesterol deposition in red cells in liver disease.
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PMID:Erythrocyte and plasma lipids in liver diseases. 184 97

We performed a functional respiratory examination which consisted of arterial gasometry, spirometry, diffusion capacity to CO2, alveolo-arterial gradient of O2 and pulmonary volumes to 8 patients with cirrhosis diagnosed by clinical history, laboratory exams, abdominal ultrasound and histology. Our results showed a slight obstructive pattern of peripheric airways (FMM: 88.87 +/- 8.7%) in the spirometry, no difference in arterial gases at upright and recumbent position was observed, with low values of apO2 (75.51 +/- 1.16 upright and 75.87 +/- 2.16 mmHg recumbent) without statistic significance. The gradient G(Aa) O2 increased to (30.89 +/- 1.06 mmHg). Besides there was a diffusion abnormality with a DLCO2/VA of (71.87 +/- 6.05%). Breathing 100% O2, did not change the gradient which allows us to postulate the existence of an abnormality of gaseous interchange due to shunts. We found no relationship between albumin levels and DLCO2/VO neither with pO2 in upright position; there was a relationship at recumbent position between the hepatic disorder and the arterial desaturation. We concluded that there is no significant hypoxia even with position changes, there is increase of G (Aa) O2 by shunt type disorders and that this is probably related with albumin levels.
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PMID:[Liver cirrhosis: pulmonary function]. 184 58

Portosystemic shunt fraction estimation using transcolonic iodine-123-iodoamphetamine (IMP) has been previously validated relative to portal vein macroaggregated albumin injections using an experimental model of cirrhosis. Transcolonic technetium-99m-pertechnetate (TcO4-) has been proposed as an alternative tracer to IMP to study portal circulation in cirrhotic patients. We compared shunt fraction estimates from paired transcolonic IMP and TcO4- studies performed on a group of dogs before and after common bile duct ligation surgery. Pertechnetate over-estimated shunt fraction in 6/7 postoperative studies relative to IMP. A good correlation between the two methods was demonstrated, however, the slope of the regression line was substantially less than 1.0 with TcO4- values reaching 100% at IMP shunt values of approximately 60%. This apparent inability to accurately assess high shunt flows may limit the quantitative aspects of TcO4- studies on patients with severe portosystemic shunting.
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PMID:Comparison of shunt fraction estimation using transcolonic iodine-123-iodoamphetamine and technetium-99m-pertechnetate in a group of dogs with experimentally-induced chronic biliary cirrhosis. 184 11

Iron is essential for life, but iron overload is toxic and potentially fatal. The liver is a major site of iron storage and is particularly susceptible to injury from iron overload, especially when (as in primary hemochromatosis) the iron accumulates in hepatocytes. Iron can be taken up by the liver in several forms and by several pathways including: (1) receptor-mediated endocytosis of diferric or monoferric transferrin or ferritin, (2) reduction and carrier-facilitated internalization of iron from transferrin without internalization of the protein moiety of transferrin, (3) electrogenic uptake of low molecular weight, non-protein bound forms of iron, and (4) uptake of heme from heme-albumin, heme-hemopexin, or hemoglobin-haptoglobin complexes. Normally, pathway 2 is probably the major one for uptake of iron by hepatocytes. Iron is stored in the liver in the cores of ferritin shells and as hemosiderin, an insoluble product derived from iron-rich ferritin. Iron in hepatocytes stimulates translation of ferritin mRNA and represses transcription of DNA for transferrin and transferrin receptors. The major pathologic effects of chronic hepatic iron overload are: (1) fibrosis and cirrhosis, (2) porphyria cutanea tarda, and (3) hepatocellular carcinoma. Although precise pathogenetic mechanisms remain unknown, iron probably produces these and other toxic effects by increasing oxidative stress and lysosomal lability. Vigorous efforts at diagnosis and treatment of iron overload are essential since the pathologic effects of iron are totally preventable by early vigorous iron removal and prevention of iron re-accumulation.
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PMID:Iron and the liver. 184 76

[Tc-99m] Galactosyl-neoglycoalbumin (TcNGA) is a synthetic radiolabeled ligand specific to the hepatocyte receptor, hepatic binding protein (HBP), a specific receptor to serum asialoglycoprotein. A TcNGA study was performed on 34 humans: normal volunteers (7) chronic hepatitis (6), hepatic cirrhosis (8), and hepatocellular carcinoma superimposed on cirrhosis (13). Heart and liver time activity curves were obtained following intravenous injection of TcNGA (5 mCi, 1.82 x 10(-9) mol/kg). HBP concentration ([HBP]) was calculated by curve-fitting techniques using the nonlinear three compartment model, which includes biomolecular reaction between HBP and TcNGA. [HBP] values were compared with conventional liver function tests. [HBP] had a good correlation with prothrombin time (n = 34, r = 0.694, p = 0.0001) thrombotest (n = 34, r = 0.692, p = 0.0001), hepaplastin test (n = 26, r = 0.787, p = 0.0001), albumin (n = 34, r = 0.712, p = 0.0001), cholinesterase (n = 34, r = 0.801, p = 0.0001), ICGR15 (n = 33, r = 0.761, p = 0.0001), KICG (n = 30, r = 0.709, p = 0.0001), ICG Rmax (n = 12, r = 0.735, p = 0.0064) and Child-Turcotte classification score (n = 34, r = 0.819, p = 0.0001). We concluded that excellent correlations of [HBP] to conventional liver function tests suggest that in vivo receptor measurement via TcNGA kinetic analysis is a sensitive and promising method in the estimation of hepatic functional reserve in patients with chronic liver disease.
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PMID:[In vivo measurement of hepatic binding protein in chronic liver disease--validation as a measure of hepatic functional reserve]. 185 Dec 38

Serum level of osteocalcin (OC) is believed to be a specific biochemical parameter of bone formation. Decreased serum OC has been reported in alcohol-intoxicated subjects, in patients with primary biliary cirrhosis and in patients with chronic alcoholic liver disease. The question was, whether lower OC level could be detected in patients with nonalcoholic and non-cholestatic chronic liver disease. The serum OC was measured by RIA developed in our laboratory. Results were compared to age and sex matched controls. Decreased OC level was found in 35 out of 47 (74%) patients with non-alcoholic and non-cholestatic liver disease as chronic persistent hepatitis, chronic active hepatitis, fatty liver and cirrhosis, in 21 out of 26 (80%) patients with alcoholic liver disease and in 8 out of 15 (53%) primary biliary cirrhosis. None of the patients had elevated value. There was no correlation between the decreased OC level and the duration or severity of the liver disease and the laboratory parameters as bilirubin, AST, ALT, alkaline phosphatase, albumin, prothrombin, and serum 25-OH-D3 vitamin level. Decreased OC was found also in the patients without cirrhosis. The possible causes are discussed. Relying upon these findings it is supposed that chronic liver disease by itself can influence the osteoblast activity also by some unknown mechanism.
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PMID:[Decreased serum osteocalcin level in non-alcoholic and alcoholic chronic liver diseases]. 185 6


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