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PubMedDate not supplied

Exudative ascites in the course of acute type B hepatitis.

Two patients who presented with an exudative ascites in the course of typical acute type B hepatitis are reported. In one of them, ascites was associated with an exudative pleural effusion. In both patients, the clinical course of the hepatitis was uneventful, and ascites and pleural effusion disappeared spontaneously. Portal hypertension and common causes of exudative ascites were excluded. It is suggested that the development of exudative ascites in these patients represent a hitherto unrecognized manifestation of the hepatitis itself.

Acute Disease↗
PubMedDate not supplied

Nuclear antigens reacted with sera and ascites of hepatocellular carcinoma patients.

In order to study hepatocellular carcinoma-associated antigens, screening of sera and ascites was done from hepatocellular carcinoma patients having antibodies reactive with three hepatocellular carcinoma cell lines (PLC/PRF/5, Hep 3B and HA22T/VGH). The indirect immunofluorescent antibody test was used. Ten of 86 (11.6%) sera and 3 of 14 (21.4%) ascites from hepatocellular carcinoma patients showed positive bindings, whereas only 1 of 35 (2.8%) sera, none of 4 (0%) ascites from chronic hepatitis patients and 3 of 60 (5%) normal human sera had positive immunofluorescent antibody activity. The binding specificities of these positive specimens were further defined by other human cancer cell lines and mouse NIH/3T3 fibroblasts. The antinuclear antibody test against mouse liver sections was also performed. The results suggested that antigens identified by the two tests may not be identical. The nature of nuclear antigens reactive with one of the serum samples, S83, and ascites A83 were characterized. These antigens were sensitive to trypsin but not to RNase A and DNase I. Further studies by radioimmunoprecipitation and two-dimensional gel electrophoresis with serum S83 and ascites A83 showed two acidic phosphorylated antigens with molecular weights of 77 and 79 kd, which had a pI around pH 5.2. The presence of a large amount of these two phosphorylated proteins in 5 of 7 human hepatocellular carcinoma cell lines suggests that these two antigens might play some roles in the carcinogenesis or progression of human hepatocellular carcinoma.

Animals↗
PubMed1992

Globulin correction of the albumin gradient: correlation with measured serum to ascites colloid osmotic pressure gradients.

The albumin difference or gradient between serum ascites is presumed to be an effective estimate of the colloid osmotic pressure gradient, although this has never been directly demonstrated. The colloid osmotic pressure gradient is controlled by the degree of portal hypertension. Thus the albumin gradient is clinically useful in detecting patients with ascites caused by portal hypertension, although some overlap in such patients' albumin gradients exists compared with those of patients without portal hypertension. Part of this overlap is related to the inverse correlation of the albumin gradient with serum globulin; globulins also contribute to colloid osmotic pressure. The ability to calculate colloid osmotic pressure in serum and ascites with albumin and globulin concentration or to correct the albumin gradient for the impact of globulins might improve the clinical usefulness of the ascitic fluid analysis in determining the presence of portal hypertension in ascitic patients with borderline albumin gradients. Thus we developed equations to calculate colloid osmotic pressure from multivariate discriminate analyses of albumin and globulin concentrations in serial dilution samples of pooled serum and subsequently validated these equations, along with older methods of calculating colloid osmotic pressure. In an initial set of dilution experiments, globulin concentration was closely correlated with the colloid osmotic pressure to albumin concentration ratio (r = 0.956; p less than 0.001). Multivariate discriminate analysis yielded an equation for calculating colloid osmotic pressure from albumin (A) and globulin (G) concentration with a ratio of colloid osmotic pressure to albumin (calculated colloid osmotic pressure = A(1.058G + 0.163A + 3.11) and two other equations.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascitic Fluid↗
PubMed2006

Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome.

Several experimental models of cirrhosis have shown dysregulation of renal aquaporins in different phases of liver disease. We investigated the urinary excretion of both aquaporin-1 and aquaporin-2 in patients with cirrhosis at different stages of the disease. Twenty-four-hour urine was collected from 11 healthy volunteers, 13 patients with compensated cirrhosis (without ascites), and 20 patients with decompensated cirrhosis (11 with ascites without renal failure and 9 with hepatorenal syndrome). Aquaporin-1 and aquaporin-2 excretion was analyzed by immunoblotting. Urinary aquaporin-2 excretion was reduced in patients with cirrhosis compared to healthy subjects. A progressive decrease in urinary aquaporin-2 excretion was observed as the severity of cirrhosis increased, from compensated cirrhosis to cirrhosis with ascites and hepatorenal syndrome. Patients with hyponatremia had lower urinary aquaporin-2 excretion than patients without hyponatremia. Vasopressin plasma level did not correlate with aquaporin-2 excretion. There were no differences between healthy subjects and patients with cirrhosis with or without ascites in urinary excretion of aquaporin-1, but urinary aquaporin-1 excretion of those with hepatorenal syndrome was extremely low. In conclusion, patients with cirrhosis appear to exhibit a decreased abundance of renal aquaporin-2 and therefore lower water permeability in the collecting tubules. This may represent an adaptive renal response to sodium retention, with expansion of extracellular fluid volume and dilutional hyponatremia observed in those who have cirrhosis with ascites. Finally, aquaporin-1 does not appear to play a role in the progressive dysregulation of extracellular fluid volume in cirrhosis.

Aquaporin 1↗
PubMed2000

Increased activity of guanosine 3'-5'-cyclic monophosphate phosphodiesterase in the renal tissue of cirrhotic rats with ascites.

A possible defect of guanosine 3'-5'-cyclic monophosphate (cGMP) content in the renal tissue caused by an increased activity of cGMP phosphodiesterase (PDE) has, so far, not been evaluated in the pathogenesis of renal resistance to endogenous natriuretic peptides (ENP) in cirrhosis with ascites. To test this hypothesis the activity of cGMP-PDE and the concentration of cGMP were evaluated in vitro in the renal tissue of 10 control rats and 10 cirrhotic rats with ascites before and after the intravenous (IV) administration of Zaprinast (Sigma, St. Louis, MO), a specific cGMP-PDE inhibitor (30 microgram/kg/min). Moreover, the effects of the intravenous administration of Zaprinast (15 microgram/kg/min and 30 microgram/kg/min) on renal plasma flow (RPF), glomerular filtration rate (GFR), and urinary sodium excretion (U(Na)V) were evaluated in 10 conscious control rats and 10 conscious cirrhotic rats with ascites. The effects of Zaprinast on plasma renin activity (PRA) was also evaluated in 10 control rats and in 10 cirrhotic rats with ascites. Finally, the effect of Zaprinast on RPF, GFR, and U(Na)V were evaluated in 10 cirrhotic rats after the IV administration of the ENP-receptor antagonist, HS-142-1. The renal content of cGMP was reduced in cirrhotic rats because of increased activity of cGMP-PDE. Zaprinast inhibited cGMP-PDE activity and increased the renal content of cGMP in these animals. The inhibition of cGMP-PDE was associated with an increase in RPF, GFR, and U(Na)V and a reduction in PRA. HS-142-1 prevented any renal effect of Zaprinast in cirrhotic rats. In conclusion, an increased activity of the cGMP-PDE in renal tissue contributes to the renal resistance to ENP in cirrhosis with ascites.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2005

Immunotherapy of malignant ascites with trifunctional antibodies.

A new class of intact bispecific antibodies shows unmet effector qualities by activation of not only T cells but also simultaneous activation of Fcgamma receptor type I/III+ cells (macrophages, NK-cells and DC). These trifunctional antibodies (trAb) lead to efficient specific killing of targeted tumor cells without any pre- or co-stimulation. This concept was investigated in vivo in patients with malignant ascites in a clinical situation that allowed monitoring of tumor cell elimination and correlation with clinical effects. In a prospective study, 8 patients with malignant ascites due to peritoneal carcinomatosis were treated with intraperitoneal application of trAb, which bound either the EpCAM- or Her2/neu-antigen on tumor cells. Treatment consisted of 4-6 applications within 9-23 days with a total amount of 145-940 microg. Seven of eight patients required no further paracentesis during follow-up or until death with a mean paracentesis-free interval of 38 weeks (median = 21.5, range = 4-136). Tumor cell monitoring showed a complete elimination of tumor cells in ascites already at total doses as low as 40-140 microg. Clinical response with disappearance of ascites accumulation was seen in all patients, which was correlated with elimination of tumor cells (p = 0.0014). Severe adverse events were not observed. Clinically relevant side effects were fever, moderate abdominal pain and skin reactions. Intraperitoneal immunotherapy with trAb showed convincing efficacy in patients with malignant ascites. This treatment offers new therapeutic options for patients with peritoneal carcinomatosis.

Ascites↗
PubMed1977

Biological characterization of a tumour-growth-promoting factor from ascitic fluid of tumour-bearing mice.

Tumour-growth-promoting activity has been observed in ascitic fluids of mice with progressively growing SV40- and chemically induced tumours. Administration of ascitic fluid to animals together with a normally non-tumorigenic dose of SV40- transformed tissue culture cells (TU-5) will cause these cells to grow progressively and eventually kill the animals. Also, the mKSA-specfic, immunologically non-responsive state (the eclipse phase) of mice bearing large mKSA tumours can be maintained by administration of ascitic fluid or serum from tumour-bearing animals after the tumours have been surgically removed. Normally, complete immunity to a secondary tumour cell challenge is re-established approximately 10 days after removal of the primary tumour, but daily injections of ascitic fluid or serum will maintain sclipse so that a secondary challenge of tumour cells will grow progressively. The active component apparently acts non-specifically, since ascitic fluid from an unrelated tumour also is able to maintain the mKSA-specific eclipse phase. Thascitic fluid has no apparent immunosuppressive activity in vivo.

Animals↗
PubMed1984

Influence of ascites on tobramycin pharmacokinetics.

The influence of ascites on the disposition of tobramycin was examined in eight subjects with cirrhosis of the liver. Five of these subjects had resolution of ascites so they could be used as their own controls. While there was no significant effect of ascites on the clearance and half-life of tobramycin, the volume of distribution of tobramycin was significantly larger when ascites was present, 0.32 versus 0.26 liter/kg (P less than 0.01). There was a trend for the volume of distribution to be larger in those patients with larger ascitic fluid volume.

Adult↗
PubMedDate not supplied

Thickening of the gallbladder wall in ascites.

The thickening of the gallbladder wall in patients with ascites is commonly related to hypoalbuminemia and/or portal hypertension. To evaluate the pathogenetic role of these two factors, we correlated gallbladder wall thickness (GBWT) with the albuminemia and the serum-ascites albumin gradient (SAAG), an index of portal hypertension, in 47 patients with ascites caused by cirrhosis of the liver or abdominal malignancy. We found a thickened gallbladder wall in 30/47 patients. The correlation between GBWT and SAAG was 0.64 (n = 47 p less than 0.001). No correlation was found between GBWT and albuminemia (r = 0.04). We suggest that the sonographic finding of ascites and gallbladder wall thickening should be considered a valuable sign of transudative ascites and of portal hypertension whatever its cause.

Abdominal Neoplasms↗
PubMed2005

Presence and specificity of tumor associated lymphocytes from ascites fluid in prostate cancer.

BACKGROUND: In the present study, we had the rare opportunity to study immunological responses of TAL from ascites fluid in a patient with hormone-refractory prostate cancer. METHODS: We evaluated tumor antigen-specific T-cell responses, induced by either prostate specific antigen (PSA) pulsed dendritic cells (DCs) or PSA peptides, in TAL and peripheral blood lymphocytes. RESULTS: DC stimulation with PSA protein induced recognition of naturally processed PSA epitopes by both blood and ascites T cells. In contrast, only ascites T cells recognized the PSA-3 peptide, after stimulation with PSA-pulsed DCs or peptides. Finally, although IFNgamma secreting T cells were detectable in both blood and ascites by ELISPOT, multiplex cytokine assay detected the presence of predominantly Th2 cytokines. CONCLUSIONS: Although tumor antigen-specific TAL were detected in ascites fluid, these cells were producing immunosuppressive cytokines which may contribute to tumor escape from recognition and/or destruction by the immune system.

Ascitic Fluid↗
PubMed1996

Distinct composition of viral quasispecies between ascites and serum samples from patients with late stage chronic hepatitis C.

By performing single-strand conformation polymorphism and PCR-cloning followed by sequencing, the amino acid composition of hepatitis C virus hypervariable and variable regions were analyzed in ascites and serum samples from two patients with late stage chronic hepatitis C. In patient-LC, the major ascitic clone was constituted by a minor serum-derived clone, while the major serum derived clone was absent in the ascites. In patient-HCC, the major ascitic clone was defective and genetically different from all the serum-derived clones. In addition, anti-genomic HCV RNA was detected in the ascitic mononuclear cells from patient-LC. These results argued that the peritoneal cavity served as a relatively isolated environment for evolution of distinct composition of viral quasispecies.

Aged↗
PubMed1997

A randomized trial of paracentesis plus intraperitoneal tumor necrosis factor-alpha versus paracentesis alone in patients with symptomatic ascites from recurrent ovarian carcinoma.

PURPOSE: Previous phase I and II studies of intraperitoneal recombinant human tumor necrosis factor-alpha (rhTNF-alpha) suggested a high degree of efficacy in reducing or eliminating ascitic fluid. To more accurately determine the efficacy of this agent, the role of paracentesis versus paracentesis plus intraperitoneal rhTNF-alpha was studied in a randomized trial. PATIENTS AND METHODS: Thirty-nine patients with symptomatic ascites with a volume of > 1000 ml from recurrent epithelial ovarian carcinoma or primary peritoneal carcinoma, which was refractory to standard therapy, were randomized either to receive 0.06 mg/m2 rhTNF-alpha (Knoll, Canada) (the dose determined optimal from phase I and II studies) intraperitoneally after drainage of fluid or to receive drainage alone. A maximum of three treatments were given at weekly intervals. Eighteen patients were randomized to receive rhTNF-alpha. RESULTS: None of 18 evaluable rhTNF-alpha patients had either a complete response (CR) (no clinical evidence of ascites and < 400 ml of fluid on ultrasound) or a partial response (PR) (asymptomatic ascites and < or = 1000 ml of fluid ultrasound). There were no CRs or PRs in the 17 evaluable patients who received drainage alone. The intraperitoneal infusion of rhTNF-alpha was generally well tolerated. Moderate to severe toxicity consisted of pain/discomfort in 42.1%, fever/chills in 36.9%, nausea/vomiting in 10.5%, edema in 10.5%, and hypotension in 5.3% of patients receiving rhTNF-alpha. CONCLUSION: rhTNF-alpha, as given in this study, was not effective in preventing recurrence of ascites in this patient population.

Ascites↗
PubMed1998

Intraperitoneal pressures and clinical parameters of total paracentesis for palliation of symptomatic ascites in ovarian cancer.

OBJECTIVE: The present study was designed to prospectively evaluate the intraperitoneal pressure, as well as clinical and hemodynamic effects of total paracentesis, as palliation of symptomatic ascites in ovarian cancer patients. METHODS: Prospective study of 35 sequential total paracenteses was performed using a Veres cannula on patients with advanced recurrent ovarian cancer with symptomatic tense ascites. Relevant clinical symptoms and patient well-being were evaluated. Vital signs, abdominal parameters, and hydrostatic intraperitoneal pressure were recorded before, during, and after the procedure. RESULTS: Intraperitoneal pressure dropped from 30 +/- 7 cmH2O before paracentesis to 13 +/- 6 cmH2O after the procedure (P < 0.0001). Marked symptomatic improvement was observed in all patients (89% complete relief, 11% partial relief), while all the patients tolerated the procedure well without any complications. The mean volume of ascitic fluid removed was 4800 ml. Mean respiratory rate and mean heart rate were both significantly decreased following the procedure (29.3 to 21.4 respirations per min and 101.5 to 93.6 beats per min, respectively). Mean systolic blood pressure mildly decreased (6.6 mmHg), while the mean diastolic blood pressure did not significantly change. None of the patients presented signs or symptoms of hypovolemia during or after the total paracentesis. CONCLUSIONS: Measurement of intraperitoneal pressures during total paracentesis for tense ascites in ovarian cancer patients indicated that the severity of symptoms correlated with the intraperitoneal pressure prior to paracentesis, but not with the volume of ascites. Intraperitoneal pressures measured following total paracentesis in patients with ovarian cancer were similar to the baseline intraperitoneal pressure measured in patients undergoing peritoneal dialysis.

Ascites↗
PubMed1999

Involvement of peritoneal macrophage in the induction of cytotoxicity due to apoptosis in ascitic fluid associated with severe acute pancreatitis.

The aim of this study was to assess the significance of peritoneal macrophage in inducing cytotoxicity in ascitic fluid associated with severe acute pancreatitis. The involvement of peritoneal macrophage was examined experimentally in rats by macrophage depletion with peritoneal lavage prior to the development of pancreatitis. More than 94% of the cellular components collected from peritoneal cavities by the lavage are macrophages. Although the ascitic fluid collected from the rats with necrotizing pancreatitis showed cytocidal effects via apoptosis on Madin-Darby canine kidney cells in a dose- and time-dependent manner, cytotoxicity or apoptosis-inducing activity almost disappeared from the ascitic fluid by the preceding peritoneal lavage. The ascitic fluid did not show significant differences by the lavage in osmolarity and in concentrations of albumin, bilirubin, amylase, and lipase. Although a slight reduction of tumor necrosis factor-alpha was noted with the lavage, tumor necrosis factor-alpha failed to induce apoptotic cell death in the cells, and the neutralization by antibody ameliorated neither cell death nor apoptosis. We conclude that peritoneal macrophages secrete apoptosis-inducing factor(s) into pancreatitis-associated ascitic fluid, other than tumor necrosis factor-alpha.

Acute Disease↗
PubMed1989

Oral pharmacokinetics and ascitic fluid penetration of ofloxacin in cirrhosis.

Plasma and ascitic fluid concentrations of ofloxacin were determined in 12 cirrhotic patients after a single dose and repeated 200 mg oral doses. The single dose kinetics were compared to those obtained in 12 healthy volunteers. Mean plasma elimination half-life was 11.6 h in cirrhotics and 7.0 h in controls. Mean total clearance was 2.3 times lower in patients than in controls, due to a significant decrease of renal clearance of the drug, unrelated to creatinine clearance. Mean apparent volume of distribution was 1.2 l/kg in patients and 1.8 l/kg in controls. Estimated by the ratio of AUC in peritoneal fluid and plasma, ascitic fluid penetration was 80% after the first oral dose. Ascitic fluid concentrations equaled corresponding plasma concentrations after 10 h, without pronounced accumulation of ofloxacin in ascites. We may conclude that, in cirrhotic patients with normal serum creatinine, a significant impairment of renal tubular handling of ofloxacin could be observed and led to a delayed elimination half-life of the drug. Because of its broad spectrum of activity, low side-effect profile, and large ascitic fluid penetration after oral administration, ofloxacin appears to be a new therapeutic approach of severe infections in cirrhotic patients, in particular spontaneous bacterial peritonitis.

Administration, Oral↗
PubMed1978

Resistant ascites in alcoholic liver cirrhosis: course and prognosis.

A group of 29 patients with decompensated cirrhosis of the liver who retained a large amount of ascites under a hospital regimen during two months or longer was identified. The prognosis for this selected group of patients, while grave [during continuous hospitalization 11 out of 29 patients (= 38%) died], is not without hope: 18 patients (62%) improved and could be discharged from the hospital. Their further course was influenced by resumption of alcohol usage. Five of 11 (45.4%) who resumed drinking died due to hepatic causes within 10 months. Of the remaining six only one lost his ascites. Those who abstained (7 patients) remained alive for an average follow-up of 33 months and all lost their ascites. Alcohol resumption significantly decreased both survival (P less than 0.05) and ascites resorption (P less than 0.0015). Continued abstinence from alcohol may thus obviate the need for surgical measures to relieve ascites in these patients.

Alcohol Drinking↗
PubMed1978

Studies on the ascites fluid of acute pancreatitis in man.

Total protein, alpha1-antitrypsin, alpha2-macroglobulin, amylase, methemalbumin, tryptic amidase activity, radioimmunoassayable elastase 2, and three lysosomal hydrolases were determined in the ascites fluid from patients with acute pancreatitis. In eight patients methemalbumin was detected in ascites and serum, supporting the diagnosis of hemorrhagic pancreatitis. Significant levels (4-45 microgram/ml) of tryptic amidase activity were detected in ascites samples from all patients. Evidence is presented which demonstrates that the tryptic amidase activity is due to alpha2-macroglobulin-bound trypsin. Pancreatic elastase 2, determined with a new sensitive and specific radioimmunoassay, ranged from 400 to 2100 ng/ml in serum and from 650 to 4460 ng/ml in ascites fluid. Substantial amounts of alpha2-macroglobulin-bound trypsin and elastase 2, entering the circulation from the peritoneal cavity, might be responsible for certain serious complications seen in acute pancreatitis. However, with the exception of serum calcium and methemalbumin and the ascites fluid methemalbumin and total protein, none of the biochemical parameters studied showed a distinct correlation with the patient's outcome.

Acute Disease↗
PubMed1987

Proteases and antiproteases related to the coagulation system in plasma and ascites--influence of dexamethasone.

Fibrinolysis induced by the infusion of plasminogen activators into the circulation has been shown to cause coagulation disorders in ascites retransfusion. Dexamethasone is known to inhibit the synthesis of plasminogen activators by peritoneal macrophages. We therefore assessed its potential in preventing the occurrence of fibrinolysis by injecting 16 mg dexamethasone intraperitoneally in 10 patients 24 h before ascites retransfusion was performed. In addition, the effect of dexamethasone upon the activity or concentration of several proteases and antiproteases related to coagulation in plasma and ascites was analyzed on 15 occasions. An increase of the activity of plasminogen, alpha 2-antiplasmin, and antithrombin III, and in the concentration of alpha 1-protease inhibitor in ascites was induced by the dexamethasone injection. However, the reaction was not identical in all patients. Those patients having an increase of plasminogen activities of 0.6 CTA U/ml or more did not show signs of fibrinolysis during retransfusion. The results obtained indicate that intraperitoneal injection of dexamethasone decreases the concentration of plasminogen activators in ascites and thereby reduces the risk of coagulation disorders during retransfusion procedures. Since the effect is variable and not sustained, assessment of preoperative plasminogen concentrations is mandatory in order to prevent complications.

Antithrombin III↗