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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). This contrasts with the conspicuous tendency of patients with Laennec's cirrhosis to retain salt and water. In an attempt to clarify this clinical observation, renal handling of sodium was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone in five patients with PBC. These PBC patients were compared with two control populations: five edema-free patients with Laennec's cirrhosis and nine healthy volunteers. The natriuretic and diuretic response to ECVE was significantly greater in the patients with PBC as compared with the two control groups. CH2O for given rates of urine flow were similar in PBC patients as compared with normal subjects. The data suggest that a supranormal rejection of sodium at the proximal tubule in response to ECVE underlies the exaggerated natriuresis of PBC. The augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this variety of cirrhosis.
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PMID:Exaggerated natriuretic response to volume expansion in patients with primary biliary cirrhosis. 60 57

Endogenous production of carbon monoxide (VCO), total and direct reacting serum bilirubin (TSB, DRB) were determined in 26 patients with liver cirrhosis and portal hypertension to evaluate the effect of various shunt operations on total heme catabolism. The material was divided into 3 groups. In group I, 11 patients not operated upon, mean VCO (+/- S.D.) was 18.4 +/- 6.0 micronmol/mmol total body heme per day (reference value 12.6 +/- 2.9). In group tii, 7 patients operated upon with subcutaneous transposition and a subtotal resection of the spleen, mean VCO (14.4 +/- 4.7) was not significantly raised. In group III, 8 patients operated upon with a modified distal splenorenal shunt, the highest mean VCO (26.1 +/- 9.0) was found. Mean TSB in the three groups was 34.8 +/- 29.2, 11.2 +/- 3.0, and 46.4 +/- 41.0 micronmol/l, respectively, and mean DRB 18.2 +/- 20.8, 3.7 +/- 1.0, and 26.8 +/- 34.1 micronmol/l, respectively. Estimated from preoperative laboratory values there was no difference in liver function between the three groups. The conclusion drawn is that heme catabolism, increased by 50% in liver cirrhosis complicated by portal hypertension probably due to a slight decrease in erythrocyte survival, tends to normalize after subcutaneous transposition and subtotal resection of the spleen. After spleno-renal shunting, on the other hand, a further increase in heme catabolism is seen. And so the increase in serum bilirubin often seen after the latter type of surgery is mainly related to a raised bilirubin production and not to a further decrease in liver function.
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PMID:Heme catabolism in liver cirrhosis with portal hypertension after shunt surgery. 88 32

In two groups of patients with liver cirrhosis and normal EEG (Group A) and with pathological EEG (Group B) it was possible to demonstrate a correlation between the severity grade of the EEG changes, the livertypical deviations of serum chemistry and alterations in cerebral oxidative metabolism. The metabolism of the brain showed a reduced oxygen consumption and carbon dioxide output in the patients with pathological EEG changes. All patients showed a raised glucose uptake, an increased lactate release, a raised ammonia uptake and glutamine output. These findings in patients with liver cirrhosis indicate a disturbance of the oxidative energy metabolism of the brain with secondary intensification of glycolysis. Pathological changes in the EEG only appear if the oxygen consumption of the brain is limited (as in the patients of Group B). These EEG changes have a poor prognosis in respect to life expectancy. With consideration of the data from animal experiments and the reported results of cerebral blood flow and oxydative metabolism in patients with liver cirrhosis it might be assumed that liver insufficiency with elevated serum ammonia results in a deranged oxydative cerebral metabolism which might explain hepatic encephalopathy.
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PMID:Comparative studies of the electroencephalogram and the cerebral oxidative metabolism in patients with liver cirrhosis. 120 68

Spontaneous hyponatremia in cirrhosis with ascites is generally considered to be due to an impaired renal ability to excrete free water, to be a contraindication of diuretics, and to be a bad prognostic sign. These concepts are reviewed in this paper. 55 cirrhotics with ascites were divided into three groups. Group I consisted of 13 patients with hyponatremia and very low free-water clearance CH2O, 0.07 +/- 0.26 ml/min). These patients also had poor renal function: low inulin clearance (CINU, 40.6 +/- 25.9 ml/min) and paraaminohippurate clearance (CPAH, 383 +/- 275 ml/min). Group II consisted of 8 patients who also had hyponatremia. CH2O, CINU, and CPAH in these patients were fairly high: 5.85 +/- 1.53 ml/min, 85.7 +/- 26.2 ml/min, and 651 +/- 294 ml/min. These values are similar to those o7 +/- 4.27 ml/min, 94.7 +/- 33.1 ml/min, and 598 +/- 199 ml/min. Hyponatremia in Group I could be related to the impaired free-water clearance. The mechanism of hyponatremia in Group II patients is not clear. Patients with hyponatremia and low CINU and CPAH had a negative response to diuretics and a poor prognosis. Patients with hyponatremia but with relatively good renal function had a good prognosis, similar to Group III patients. They responded to diuretics with no worsening of their hyponatremia.
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PMID:Prognostic value of spontaneous hyponatremia in cirrhosis with ascites. 126 41

After ingestion of galactose (10 g per m2) labeled with 14C or 13C, breath was collected from subjects at intervals for 4 hr followed by measurement of 14CO2 by liquid scintillation counting or of 13CO2 by mass spectrometry. Nine subjects without liver disease and 21 "cirrhotic" patients were tested with 14C; 8 control subjects and 4 patients with diagnosis of cirrhosis were tested with 13C. The mean rates of expiration of labeled CO2 by the patients with "cirrhosis" were one-third to one-half of mean normal rates during the first 90 min. The time of peak concentration of tracer CO2 for cirrhotic patients (150 to 180 min) was later than for normal subjects (90 to 120 min). There was distinctly greater separation between control and liver disease groups by test of 14CO2 radioactivity at 1 hr than by serum alkaline phosphatase, total bilirubin, and transaminase, but only slightly better separation than by serum albumin concentration (which was highly correlated with 14CO2 output). The [14C]galactose test is simpler than the standard intravenous galactose tolerance test, and , like the latter, appears superior to some other tests for recognition of cirrhosis. The use of 13C provides an example of a new direction for clinical application of this stable, nonradioactive nuclide.
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PMID:Test for alcoholic cirrhosis by conversion of [14C]- or [13C]galactose to expired CO2. 127 55

Tumor hemodynamics including arterial vascularity (AV) and portal perfusion (PP) were evaluated in histologically confirmed 55 hepatic nodules associated with cirrhosis using ultrasonographic (US) angiography during intraarterial carbon dioxide microbubbles injection and CT during arterial portography. Tumor hemodynamic patterns were classified into 6 types as follows: Type I (n = 10): PP (+), AV (hypo); Type I' (n = 2): PP (+), AV (iso); Type II (n = 5): PP (-), AV (hypo); Type III (n = 8): PP (-), AV (iso); Type IV (n = 25): PP (-), AV (hyper), Type V (n = 5): PP (partially +), AV (vascular spot in hypovascular). Eight nodules of Type I were diagnosed as benign nodules histologically including adenomatous hyperplasia (AH) (n = 6) and regenerative nodule (n = 2). Hundred percent (5/5) of Type II and 88% (7/8) of Type III nodules were well-differentiated HCC, in contrast to 8% (2/25) of Type IV nodules, typical HCCs. Fatty metamorphosis was observed in 75% (6/8) of Type III nodules, in contrast to 16% (4/25) of typical (classical) HCC nodules (Type IV). We concluded that at the malignant transformation from AH to HCC, reduction of portal blood flow in the nodule precedes the initiation of the increase of the arterial tumor vessel. Moreover, early stage HCC could exhibit hypovascular (Type I, II), isovascular (Type III), or vascular spot in hypovascular pattern (Type V) compared with a typical HCC (Type IV). It was also suggested that the more mature as a neoplasms the HCC becomes, the more the arterial tumor vessel in the nodule increases and fatty metamorphosis of well-differentiated HCC is highly related with tumor hemodynamic condition, i.e., hypoperfusion state from both arterial and portal vessel.
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PMID:[Tumor hemodynamics in hepatic nodules associated with liver cirrhosis: relationship between cancer progression and tumor hemodynamic change]. 165 18

In 59 patients with liver cirrhosis (23 female, 36 male; aged between 30 and 73 years) the aminophenazone breath-test according to the Haustein-Schenker modification was performed. The results were related to morphological, clinical and haemodynamic criteria. In contrast to a control group, consisting of 8 women and 8 men aged between 23 and 27 years with healthy livers, the aminophenazone elimination proved to be heavily delayed (p less than 0.001). In consideration of the Havanna-classification the 14CO2-elimination was most heavily retarded in patients with portal cirrhosis, but compared with non-portal cirrhosis, the difference was below significance level. A significant dependence on the clinical degree of severity was found. The aminophenazone-elimination was frequently low in portal hypertension and considerably decreased after portocaval shunt with values below 200 DPM/mmol CO2/70 kg body weight. In some cases it could be demonstrated, that the test is not only of diagnostic relevance, but reflects the progression of cirrhosis.
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PMID:[Studies on diagnostic and prognostic validity of aminophenazone breath test in liver cirrhosis]. 181 53

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

The blood supplies of nodular lesions associated with liver cirrhosis were analyzed in vivo with various imaging modalities. The portal blood supply was evaluated with computed tomography (CT) during arterial portography (CTAP); the arterial blood supply was evaluated with hepatic angiography, CT angiography, CT following intraarterial injection of iodized oil, or ultrasound following intraarterial injection of carbon dioxide microbubbles. A total of 84 surgically confirmed hepatocellular carcinomas (HCCs) (less than or equal to 3 cm) and 25 areas of adenomatous hyperplasia (AH) were included in the study. At CTAP, a portal blood supply was seen in 96% of cases of AH and only 6% of HCCs (chi 2, P less than .005). In contrast, an arterial supply greater than that of the surrounding liver was verified in 94% of the HCCs and only 4% of the cases of AH (chi 2, P less than .005). The blood supply of areas of AH with atypical hepatocytes and the blood supply of well-differentiated HCCs (Edmondson grade 1) tended to be intermediate between that of AH without atypia and that of HCC that was Edmondson and Steiner grade 2 or greater. Evaluation of the blood supply of the nodular lesions associated with liver cirrhosis is considered to be useful in the differential diagnosis and treatment of early-stage HCC.
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PMID:Benign and malignant nodules in cirrhotic livers: distinction based on blood supply. 184 40

To clarify the involvement of atrial natriuretic peptide (ANP) in the pathogenesis of liver cirrhosis, we measured plasma ANP in patients with various stages of cirrhosis and in age-matched normal subjects. Urinary cyclic guanosine monophosphate (cGMP) was also measured as a marker of active biological ANP. In addition, effects of exogenous synthetic human ANP (0.5 micrograms/kg) on renal functions were examined in normal subjects and in cirrhotics without ascites or with mild ascites. Plasma ANP levels were not significantly different among these 3 groups. Urinary cGMP concentrations were significantly higher in both cirrhotics without ascites and cirrhotics with mild ascites, (340 pmol/ml, P less than 0.05 and 496 pmol/ml, P less than 0.01 respectively) than normal subjects (95 pmol/ml). In normal subjects, marked increases in urinary volume (UV), sodium excretion (UNaV), fraction excretion of sodium (FENa) and free water clearance (CH2O) were induced after ANP infusion, and significant recoveries were subsequently observed in these parameters. However, in cirrhotics, the responses to ANP infusion of UV, FENa and CH2O were far less dramatic. The response of UV, UNaV and FENa in cirrhotics with mild ascites was delayed compared to cirrhotics without ascites. These results suggest that the blunted natriuretic responsiveness to ANP is contributory to the pathogenesis of initial sodium retention in cirrhotics.
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PMID:Atrial natriuretic peptide in liver cirrhosis with mild ascites. 216 95


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