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PubMed1975

Serum antibody responses to an ascitic variant of rat hepatoma D23.

Antibody was detected by membrane immunofluorescence tests in sera of rats bearing an ascitic variant of a transplanted hepatoma, and in concentrated cell-free ascitic fluid. Ascites hepatoma cells were also shown to have immunoglobulin, possibly tumour specific antibody, bound to their surface. The kinetics of antibody responses to ascites hepatoma and hepatoma cells from solid tumours were compared: both tumour types gave positive reactions by the third day after implantation; antibody was present throughout subsequent tumour growth with the ascites whereas antibody was not detected after tumour became palpable in rats injected with hepatoma cells from solid tumour. Antibody responses to ascites tumour were investigated in rats bearing solid hepatoma tumour. Subcutaneous hepatoma did not influence the antibody response to ascites, but rats bearing intraperitoneal tumours showed a diminished serum antibody response to ascitic hepatoma.

Animals↗
PubMed2001

Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites.

The diagnosis of refractory ascites in cirrhotic patients carries a poor prognosis and liver transplantation should always be considered in this situation. Identification of patients who will not respond to diuretic therapy usually requires several weeks of observation during which a trial of diuretics is instituted using stepwise increases in dosage in order to classify ascites as refractory. In the present study we evaluated the effect of a single dose of 80 mg intravenous furosemide on urinary sodium excretion over 8 hours in cirrhotic patients with ascites responsive to diuretic treatment (group 1; n = 14) and patients with refractory ascites (group 2; n = 15). The test was performed after 3 days without diuretics and patients were on a 80 mEq sodium/day diet. Refractory ascites was defined by the absence of response after 3 months of high doses of diuretics (spironolactone 200 mg/d + furosemide 80 mg/d + metolazone 2.5 mg/d) and the need for repeated paracentesis. The two groups had similar degrees of liver and renal dysfunction as assessed by the Pugh score and creatinine clearance. The effects of furosemide on 8-hour natriuresis was much higher in patients with responsive ascites as compared with patients with refractory ascites (125 +/- 46 vs. 30 +/- 16 mEq; mean +/- SD; P <.0001). A natriuresis lower than 50 mEq/8 hours was observed in all group-2 patients as compared with none from group 1. The present study shows that patients with refractory ascites can be identified quickly and accurately by using this simple furosemide-induced natriuresis test, which could be very useful to select patients for liver transplantation.

Ascites↗
PubMed1997

Differential diagnosis of ascites.

The differential diagnosis of ascites often leads to confusion and an inability to exclude its multitude of causes in many patients. In this review, we outline the clinical features and laboratory investigations that usually elucidate the cause of ascites for the clinician in a simple and logical manner. Roughly 80-85% of cases of ascites are related to underlying chronic liver disease, but cardiac failure, tuberculosis, malignancy-related ascites and other less common causes should always be considered. Careful evaluation of the patient, including a clinical history, physical examination and diagnostic paracentesis should routinely be performed to determine the cause of ascites. Fluid should be sent for cell count and albumin along with simultaneous determination of serum albumin to determine the serum: ascites albumin gradient. This gradient allows classification of the cause of ascites into portal hypertension-related and nonrelated with a diagnostic accuracy of > or = 97%. The causes of ascites are individually discussed in relationship to their clinical features and to the laboratory investigations that are relevant in each situation.

Ascites↗
PubMed1991

Paracentesis with intravenous infusion of albumin as compared with peritoneovenous shunting in cirrhosis with refractory ascites.

BACKGROUND: There is no satisfactory treatment for refractory ascites in patients with cirrhosis. Both peritoneovenous shunts and paracentesis have been used, but there is uncertainty about their relative merits. METHODS: We studied 89 patients with cirrhosis and refractory ascites who were randomly assigned to receive either repeated large-volume paracentesis plus intravenous albumin or a LeVeen peritoneovenous shunt. Patients in the paracentesis group in whom recurrent tense ascites developed during follow-up were treated with paracentesis, and those in the peritoneovenous-shunt group with diuretic agents or by the insertion of a new shunt if there was shunt obstruction. RESULTS: During the first hospitalization, ascites was removed in all 41 patients in the paracentesis group and in 44 of the 48 patients in the peritoneovenous-shunt group. The mean (+/- SD) duration of hospitalization in the two groups was 11 +/- 5 and 19 +/- 9 days, respectively (P less than 0.01). There were no significant differences in the number of patients who had complications or died. During follow-up, 37 patients in each group were hospitalized again. In the paracentesis group, the number of rehospitalizations for any reason (174 vs. 97 in the peritoneovenous-shunt group) or for ascites (125 vs. 38) was significantly higher, and the median time to a first readmission for any reason (1 +/- 1 vs. 2 +/- 2 months) or for ascites (2 +/- 2 vs. 8 +/- 17 months) was significantly shorter than in the peritoneovenous-shunt group. The total times in the hospital during follow-up, however, were similar in the two groups (48 +/- 49 and 44 +/- 39 days, respectively). Three patients had obstructions of their peritoneovenous shunts during their first hospitalizations, and 15 patients had a total of 20 obstructions during follow-up. Survival was similar in both groups. CONCLUSIONS: The LeVeen shunt and paracentesis are equally effective in relieving refractory ascites. The former may provide better long-term control of ascites, but shunt occlusion is common and survival is not improved.

Albumins↗
PubMed2003

Lysophosphatidic acid (LPA) in malignant ascites stimulates motility of human pancreatic cancer cells through LPA1.

Cytokines and growth factors in malignant ascites are thought to modulate a variety of cellular activities of cancer cells and normal host cells. The motility of cancer cells is an especially important activity for invasion and metastasis. Here, we examined the components in ascites, which are responsible for cell motility, from patients and cancer cell-injected mice. Ascites remarkably stimulated the migration of pancreatic cancer cells. This response was inhibited or abolished by pertussis toxin, monoglyceride lipase, an enzyme hydrolyzing lysophosphatidic acid (LPA), and Ki16425 and VPC12249, antagonists for LPA receptors (LPA1 and LPA3), but not by an LPA3-selective antagonist. These agents also inhibited the response to LPA but not to the epidermal growth factor. In malignant ascites, LPA is present at a high level, which can explain the migration activity, and the fractionation study of ascites by lipid extraction and subsequent thin-layer chromatography indicated LPA as an active component. A significant level of LPA1 receptor mRNA is expressed in pancreatic cancer cells with high migration activity to ascites but not in cells with low migration activity. Small interfering RNA against LPA1 receptors specifically inhibited the receptor mRNA expression and abolished the migration response to ascites. These results suggest that LPA is a critical component of ascites for the motility of pancreatic cancer cells and LPA1 receptors may mediate this activity. LPA receptor antagonists including Ki16425 are potential therapeutic drugs against the migration and invasion of cancer cells.

Adult↗
PubMed2001

Therapeutic effects of viral vector-mediated antiangiogenic gene transfer in malignant ascites.

Malignant ascites is a common complication of advanced intraabdominal neoplasms for which standard treatments are suboptimal. Evidence suggests that tumor-mediated angiogenesis and enhanced vascular permeability in the peritoneal wall due to high levels of vascular endothelial growth factor play a fundamental role in the pathogenesis of malignant ascites. To explore the advantage of viral vector-mediated "targeted antiangiogenic therapy" in ascites formation, we constructed and administered adenoviral vectors encoding several different antiangiogenic proteins (angiostatin, endostatin, platelet factor 4, and a fusion protein between angiostatin and endostatin) alone or in combination intraperitoneally in mice with peritoneal carcinomatosis from breast cancer (TA3 cells) and ovarian cancer (SKOV-3 i.p. and ES-2 cell lines) to explore the potential of additive or synergistic activity. Our data demonstrated statistically significant downregulation of ascites formation, tumor growth, vascularity, and prolongation of animal survival after intraperitoneal treatment with antiangiogenic adenoviral vectors in three different ascites tumor models. Combined treatment proved to be more effective than treatment with one vector alone. Reduced ascites formation was accompanied by decreased microvascular density in the peritoneal wall and increased apoptosis of tumor cells after administration of antiangiogenic vectors in vivo. Of interest was the observation that AdPF4 caused a significant decrease in the level of VEGF secreted by tumor cells both in vitro and in TA3 ascites tumor-bearing animals in vivo. These data suggest that adenoviral vector-mediated delivery of genes encoding antiangiogenic proteins may represent a potentially new treatment modality for malignant ascites.

Adenoviridae↗
PubMed1993

High levels of tumor necrosis factor-alpha and interleukin-6 in the ascitic fluid of cirrhotic patients with spontaneous bacterial peritonitis.

We prospectively measured the concentrations of immunoreactive tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interleukin-6 (IL-6) in the serum and ascitic fluid of 14 alcoholic cirrhotic patients with spontaneous bacterial peritonitis (SBP) and 16 alcoholic cirrhotic patients with sterile ascitic fluid. TNF-alpha levels in ascitic fluid were significantly higher for the patients with SBP: 399.57 +/- 129.23 pg/mL vs. 35.76 +/- 5.57 pg/mL (P < .001). IL-6 levels in ascitic fluid were also significantly higher for the patients with SBP: 170,713 +/- 57,109 ng/mL vs. 5,414 +/- 973 ng/mL (P < .001). By contrast, serum levels of TNF-alpha and IL-6 were just slightly more elevated than normal values. The concentration of IL-1 in the ascitic fluid of all patients was elevated, but there was no difference between patients with SBP or sterile ascites in this respect. In the patients with SBP, levels of TNF-alpha and IL-6 in ascitic fluid decreased during the first 48 hours of antibiotic treatment. Our results suggest that measurements of TNF-alpha and IL-6 in ascitic fluid may become useful markers both for the diagnosis of SBP and for monitoring the treatment of cirrhotic patients.

Ascitic Fluid↗
PubMed1997

Prorenin and active renin concentrations in plasma and ascites during severe ovarian hyperstimulation syndrome.

The pathophysiology of ovarian hyperstimulation syndrome (OHSS) remains unclear. Several lines of evidence indicate that OHSS is associated with a stimulation of the renin-angiotensin system (RAS), but its functional significance as well as its role in the pathogenesis of the syndrome are not yet determined. OHSS is associated with high plasma and ascitic concentrations of total renin, renin activity (RA) and angiotensin II (Ang II). Their ovarian or renal origin is, however, still a matter of debate. To clarify these issues further, total renin, active renin, prorenin, RA and aldosterone were measured in plasma and ascites of nine patients who developed severe OHSS after in-vitro fertilization. Blood and ascites were sampled simultaneously during therapeutic paracentesis. Total renin and prorenin concentrations were significantly higher in the ascites (mean concentration +/- SE respectively of 5920 +/- 1430 mIU/l and 5250 +/- 1350 mIU/l) than in the plasma (respectively 3060 +/- 740 mIU/l and 2000 +/- 460 mIU/l) (P = 0.020 and 0.017 respectively). Conversely, active renin and RA concentrations tended to be lower, although not statistically significantly so in the ascites (respectively 670 +/- 190 mIU/l and 47 +/- 11 ng Ang I/ml/h) than in the plasma (respectively 1060 +/- 370 mIU/l and 75 +/- 21 ng Ang I/ml/h). Aldosterone concentrations were significantly higher in the serum (2609 +/- 374 pg/ml) than in the ascites (2025 +/- 347 pg/ml) (P = 0.015). The concentration gradient between plasma and ascites for total renin and prorenin supports the hypothesis of their ovarian origin in ascites and, to a large extent, in plasma, while it is likely that the high plasma active renin and RA concentrations reflect a peripheral activation of the RAS. In conclusion, the present findings are consistent with a marked stimulation of both ovarian and renal RAS during OHSS.

Adult↗
PubMed1975

Proteases during the growth of Ehrlich ascites tumor. II. The kallikrein-kinin system.

Ascitic fluid and ascites tumor cells from Swiss mice bearing Ehrlich ascites tumor were assayed for components of the kallikrein-kinin system at various times during tumor growth. Changes in component levels were correlated with those in the plasma. Ascitic fluid contained an acetone-activated prekallikrein that increased in concentration during tumor growth and reached peak levels during the 7th-10th day post transplant. No free kinin activity was present in the ascitic fluid. During tumor growth, kininogen levels increased in parallel with prekallikrein levels. The ascitic fluid also contained a kinin-destroying activity that was initially high during the early phase of tumor growth. Tumor cell fractions, prepared by ultracentrifugal techniques, had no kinin-forming activity while possessing kinin-destroying activity that was localized in the soluble protoplasmic protein and nuclear fractions. The kinin-forming activity of the ascitic fluid resembled that of the plasma with respect to pH optima, kinetics of kinin formation, and effect of protease inhibitors. The kininase activity of both ascitic fluid and plasma differed from that of the tumor cell fractions.

Animals↗
PubMed1997

Evaluation of logistic versus linear regression models for predicting pulmonary hypertension syndrome (ascites) using cold exposure or pulmonary artery clamp models in broilers.

Syndromes such as ascites (pulmonary hypertension syndrome) present difficulties both in the interpretation of associated physiological observations and in their analyses. The ability to predict which physiological variables have the greatest influence on survival or, more importantly, which individuals are most susceptible or resistant to ascites would be very useful selection tools. When addressed in this manner, ascites data become binary data sets (healthy or affected). Binary data can be problematic in that they do not meet all of the assumptions necessary for more traditional analyses such as ANOVA and linear regression. Binary data are discrete and do not have normally distributed errors, which violates a fundamental assumption of linear models. The predictive abilities of linear and logistic regression were evaluated in two replicated experiments using two methods to induce ascites, cold exposure (COLD) and surgical clamping of one pulmonary artery (PAC). The logistic and linear predictive models were derived using the same data and variables. The first data set from PAC and COLD were used to develop the predictive models and the replicate data sets of PAC and COLD were used as "test data sets" for the prediction of ascites. The linear models developed were complex, using four or five variables and requiring up to seven different measurements. On average, the linear models predicted ascites correctly 87.6% of the time. The logistic models were simple (single variable) models that predicted ascites correctly 92.0% of the time. The variables used in the logistic models were derivations of the ratio of right ventricular weight to total ventricular weight, either corrected for age or the body weight of the bird. Although linear regression predicted the incidence of ascites almost as well as logistic regression did, logistic regression is the more appropriate test statistic to use.

Analysis of Variance↗
PubMed2000

Ascites resistance of progeny from broiler breeders selected for two generations using chronic unilateral pulmonary artery occlusion.

Broilers that survived unilateral pulmonary artery occlusion and lived to maturity comprised the first generation (GEN1) of an ascites-resistant line. Progeny from the GEN1 line previously were shown to tolerate fast growth and cool temperatures with a 50% lower incidence of ascites than chicks from the breeder pullet line serving as the base population for the resistant line. In the present study, progeny from the GEN1 line were subjected to unilateral pulmonary artery occlusion, and survivors were reared to breeding age to serve as the parent stock for the second generation (GEN2) ascites-resistant line. In two experiments (EXP1 and 2), chicks were reared separately by sex but were mixed by line within environmental chambers, where they were grown as rapidly as possible and exposed to cool (14 C) temperatures from 17 to 49 d of age. In EXP1, the ascites incidences in the base population, GEN1, and GEN2 lines, respectively, were 31% (48/157), 15% (8/52), and 4% (3/69) for males and 10% (13/128), 11% (5/46), and 3% (1/36) for females. In EXP2, the ascites incidences in the base and GEN2 lines, respectively, were 44% (71/163) and 6% (7/110) for males and 12% (19/155) and 0% (0/92) for females. The final BW for nonascitic broilers did not differ across lines in EXP1. In EXP2, the final BW was lighter for nonascitic GEN2 males (2,915+/-43 g) and females (2,382+/-17 g) than for nonascitic base population males (3,088+/-42 g) and females (2,493+/-22), respectively. Right:total ventricular weight ratios were higher for ascitic than nonascitic broilers, confirming the primary role for pulmonary hypertension in the pathogenesis of ascites. These experiments demonstrate ongoing improvement in the ascites resistance of progeny from broiler breeders that, for two consecutive generations, have survived the rigorous selection pressure imposed by unilateral pulmonary artery occlusion.

Animal Husbandry↗
PubMed2006

A bivariate mixture model analysis of body weight and ascites traits in broilers.

The objective of the present study was to use bivariate mixture models to study the relationships between body weight (BW) and ascites indicator traits. Existing data were used from an experiment in which birds were housed in 2 groups under different climate conditions. In the first group, BW, the ratio of right ventricular weight to total ventricular weight (RV:TV), and hematocrit value (HCT) were measured in 4,202 broilers under cold conditions; in the second group, the same traits were measured in 795 birds under normal temperature conditions. Cold-stress conditions were applied to identify individuals that were susceptible to ascites. The RV:TV and HCT were approximately normally distributed under normal temperature conditions, whereas the distributions of these traits were skewed under cold temperature conditions, suggesting different underlying distributions. Fitting a bivariate mixture model to the observations showed that there was only one homogeneous population for ascites traits under normal temperature conditions, whereas there was a mixture of (2) distributions under cold conditions. One distribution contained nonascitic birds and the other distribution contained ascitic birds. In the distribution of nonascitic birds, the inferred phenotypic correlations (phenotypic correlations with 2 distinguishing underlying distributions) of BW with RV:TV and HCT were close to zero (0.10 and -0.07, respectively), whereas in the distribution of ascitic birds, the inferred phenotypic correlations of BW with RV:TV and HCT were negative (-0.39 and -0.4, respectively). The negative inferred correlations of BW with RV:TV and HCT in the distribution of ascitic birds resulted in negative overall correlations (correlations without 2 distinguishing distributions) of BW with RV:TV (-0.30) and HCT (-0.37) under cold conditions. The present results indicate that the overall correlations between BW and ascites traits are dependent on the relative frequency of ascitic and nonascitic birds in the population.

Animals↗
PubMed1984

Peritoneovenous shunt therapy for leaking ascites in the cirrhotic patient.

Review of clinical and operative records of 86 patients at the Minneapolis VA Medical Center and Mount Sinai Hospital undergoing peritoneovenous (PV) shunt for intractable ascites revealed a subgroup of patients (n = 9) who developed leaking ascites prior to shunting. The etiology of leaking ascites was as follows: 1) ruptured umbilical hernia ( UH ) (four patients), 2) repeated paracentesis (three patients), and 3) postoperative incisional ascitic fluid leak (two patients). Initial therapy included local sterile compression dressing, intravenous antibiotics, and management of fluid and electrolytes. All nine patients underwent subsequent closure of the fascial defect and PV shunt to prevent reaccumulation of ascites (simultaneous procedures were performed in five patients). No patient developed postoperative septic complications, organ failure, gastrointestinal bleeding, or encephalopathy. There were no early deaths; however, three late deaths (18 months, 2, and 4 years) were due to variceal bleeding and/or liver failure. Ascites was well controlled in seven patients with PV shunt alone, the other two ultimately responding to medical therapy. We conclude that peritoneal fluid leaks can be treated successfully by repairing the fascial defect and placing a PV shunt. In the absence of infected ascites and clinical peritonitis, PV shunt may be performed simultaneously with closure of UH , thus preventing the reaccumulation of ascites during the immediate postoperative period.

Aged↗
PubMed1987

Ascitic fluid bilirubin concentration as a key to choleperitoneum.

Total bilirubin concentration was measured in the ascitic fluid and serum of 65 patients with various types of ascites to determine the normal range of these parameters. The mean (+/- SD) ascitic fluid bilirubin was 0.7 +/- 0.8 mg/dl, and the mean ascitic fluid/serum bilirubin ratio was 0.38 +/- 0.44. Subsequently, I recognized choleperitoneum in a patient with bile-stained ascites preoperatively, because the ascitic fluid bilirubin was 18.5 mg/dl and the ratio was 7.1. Laparotomy documented a ruptured gallbladder. An ascitic fluid bilirubin concentration greater than 6 mg/dl with an ascitic fluid/serum bilirubin ratio greater than 1.0 appears to be characteristic of choleperitoneum.

Aged↗
PubMed1989

Unusual anodic migrating isoamylase differentiates selected malignant from nonmalignant ascites.

Ascitic fluid from nine patients with nonmalignant ascites and nine patients with malignant ascites was subjected to isoamylase analysis. Unusual isoamylase bands that migrate to the anode were demonstrated in seven of eight patients with ovarian carcinoma and in one patient with gastric carcinoma. In no case of nonmalignant ascites was anodic isoamylase found, despite the presence of normal amylase in all samples. This is the first report of anodic isoamylase from ascitic fluid in gastric carcinoma and the first series comparing isoamylase patterns in malignant and nonmalignant ascites. Anodic isoamylase on electrophoresis of ascitic fluid may prove to be useful as a tumor marker in differentiating selected malignancies from nonmalignant ascites.

Amylases↗
PubMed1998

Portal decompression by transjugular intrahepatic portosystemic shunt and changes in serum-ascites albumin gradient.

The serum ascites albumin gradient (SAAG) is widely used to help determine the cause of ascites formation. A serum ascites albumin gradient of > or = 1.1 g/dL reliably distinguishes portal hypertension-related ascites from other causes. To date, there are no published data on the impact of portal decompression on this gradient. The recent development of transjugular intrahepatic portosystemic shunt (TIPS) allows for nonsurgical decompression of portal hypertension by radiologically creating a portosystemic shunt. This study examines the short-term impact of portal decompression on the serum ascites albumin gradient (SAAG) in patients with portal hypertension-related ascites undergoing transjugular intrahepatic portosystemic shunt. Portal pressure measurements were obtained before and after TIPS placement. Serum ascites albumin gradient was determined before and at 6 and 24 hours post-TIPS placement. Fifteen patients were enrolled in the study. The mean portosystemic gradient (PSG) before TIPS was 21.0 +/- 9.2 mmHg, whereas the post-TIPS mean PSG was reduced to 11.0 +/- 6.3 mmHg, consistent with portal decompression (p = 0.005). The mean pre-TIPS serum ascites albumin gradient was 1.9 +/- 0.5 g/dL and was reduced to 1.7 +/- 0.5 g/dL at 6 hours (p = 0.003) and 1.4 +/- 0.4 g/dL at 24 hours (p = 0.002) after TIPS placement. These findings further solidify the association between the SAAG and portal hypertension.

Adult↗
PubMed2001

Effect of ascites on tacrolimus disposition in a liver transplant recipient.

To examine the effects of ascites on tacrolimus disposition, the authors measured tacrolimus concentration in blood and ascitic fluid from a patient with a living related liver transplant recipient who required removal of 500 to 2400 mL ascitic fluid daily. Tacrolimus levels in ascitic fluid ranged from 0.07 to 0.29 ng/mL and in whole blood from 7.5 to 20.3 ng/mL. The tacrolimus concentration in ascitic fluid positively correlated with that in whole blood ( r = 0.878, P <0.0001). Because the amounts of tacrolimus excreted into the ascitic fluid corresponded to only 0.01% to 0.09% of the dose administered, the authors concluded that the effects of ascites on tacrolimus disposition were negligible even though large amounts of ascitic fluid were drained regularly.

Ascites↗
PubMed2004

Nitric oxide and renal function in cirrhotic patients with ascites: from physiopathology to practice.

Patients with cirrhosis and ascites show systemic and splanchnic arterial vasodilation, which causes a reduction in effective arterial blood volume and the activation of hormonal anti-natriuretic systems. Renal impairment is the most important predictor of hospital mortality in cirrhotic patients with SBP. In patients with SBP, the inflammatory response to the infection (TNF-alpha, IL-6) may be an important mechanism of renal dysfunction. Ascitic-fluid NO metabolites are related independently to the development of renal impairment. Treatment of SBP with intravenous albumin in addition to cefotaxime prevents renal impairment and reduces mortality in comparison with treatment with cefotaxime alone. As soon as ascites develops, liver transplantation should be considered in eligible patients, especially when local mean waiting times exceed life expectancy. Nitric oxide (NO), tumour necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) have been implicated in the pathogenesis of circulatory alterations observed in cirrhotic patients with ascites. Kidney failure is one of the main factors associated with mortality in patients with end-stage liver disease developing complications, particularly severe infections and variceal haemorrhage. Renal impairment occurs in patients with the highest concentration of cytokines in plasma and ascitic fluid and is associated with marked activation of the renin-angiotensin system. In patients with spontaneous bacterial peritonitis (SBP), serum and ascitic fluid levels of NO metabolites (nitrites and nitrates) were higher than those of patients with sterile ascites, and renal impairment is considered to be caused by a decrease in effective arterial blood volume as a result of the infection. The administration of albumin prevents deterioration of renal function and reduces mortality in these patients. However, SBP and renal dysfunction are late complications in the course of liver cirrhosis. As soon as ascites develops, liver transplantation should be considered in eligible patients, especially when local mean waiting times exceed life expectancy. A better knowledge of metabolic disorders associated with the early stage of cirrhosis is essential for the development of optimal therapeutic strategies for the prophylaxis and treatment of portal hypertension and its complications.

Ascites↗