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PubMedDate not supplied

Refractory ascites: definition, pathogenesis and treatment.

Refractory ascites, that is ascites which cannot be mobilized by low sodium diet and maximal doses of diuretics (up to 400 mg spironolactone or potassium canrenoate and 160 mg furosemide per day), occurs in 5% of cirrhotic patients with ascites. The development of refractory ascites is mainly related to the progression of arterial vasodilation-mediated vascular underfilling and to the imbalance between reduced synthesis of renal vasodilating factors (especially renal prostaglandins) and extreme activation of vasoconstricting systems. Further features include increased sodium reabsorption in the proximal tubule and altered pharmacokinetics and pharmacodynamics of diuretics. In patients with impaired renal function (as is the case for most patients with refractory ascites), the marked reduction of renal perfusion and glomerular filtration rate, with the consequent decrease of filtered sodium load, becomes the main pathogenetic factor. The principal therapeutic options for refractory ascites include repeated paracentesis and implantation of the LeVeen shunt. Paracentesis is a rapid and safe procedure to remove ascites, but it does not correct sodium retention. Ascites recurrence, therefore, may occur after a brief interval. The LeVeen shunt allows for better long-term control of ascites, but severe complications may supervene, and shunt occlusion is common. Neither therapeutic procedure improves survival. Different experimental therapeutic procedures have been proposed. Administration of ornipressin corrects hyperdynamic circulation and improves renal function. Thromboxane synthase inhibitors, by reducing renal synthesis of thromboxane A2, potentiate the diuretic and natriuretic response to furosemide. More invasive procedures, including portosystemic shunt and transjugular intrahepatic stent, are rarely used in the treatment of refractory ascites.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascites↗
PubMed1981

Persistence of colchicine resistance in Ehrlich-Lettré ascites tumors and cell strains.

The effect of colchicine on mitoses of mutant HD33 Ehrlich-Lettŕe ascites cells growing in vivo and in vitro was studied. HD33 mouse ascites tumors are colchicine-resistant. The LD50 of colchicine in mice bearing HD33 ascites tumors was 1.4 mg/kg body weight (b.w.), but a single dose of 3.33 mg colchicine/kg b.w. failed to suppress the anaphase of HD33 tumor mitoses for 24 h. No change in the level of colchicine resistance was observed after 269 weekly transplantations of HD33 ascites tumors without colchicine. In suspension culture, growth of HD33 ascites cells ceased at 1.5 x 10(-6) M colchicine. 10(-5) M colchicine suppressed the anaphase of HD33 mitoses and produced typical C-mitoses within one hour. The same effects on mitoses of colchicine sensitive Ehrlich ascites cells in vitro were achieved with 10(-6) M colchicine. In HD33 ascites cell cultures grown without colchicine, only a slight increase in colchicine sensitivity was registered after 5 years. Parallel cultures were propagated for the same period in the presence of 10(-7) M colchicine (HD33C ascites cells) without detectable growth alterations; the resistance level increased slightly. The limit of 10(-6) M colchicine was tolerated by the ascites cells in permanent culture without growth reduction (HD33CS ascites cells). 3H-colchicine binding studies suggest a permeability barrier of the plasma membrane as a mechanism of genetically fixed resistance.

Animals↗
PubMed2003

Treatment of Ascites.

Ascites is the most common complication of cirrhosis and occurs in more than half of all patients with cirrhosis. The development of ascites indicates progression of the underlying cirrhosis and is associated with a 50% 2-year survival rate. Conventional therapies used for the treatment of ascites include sodium restriction (<88 mmol/d), diuretics, and large volume paracentesis (LVP) (>5 L). The most effective diuretic combination is that of a potassium-sparing, distal-acting diuretic (eg, spironolactone) with a loop diuretic (eg, furosemide). LVP provides rapid resolution of symptoms with minimal complications and is well tolerated by most patients. Post-paracentesis circulatory dysfunction (PPCD) may occur after LVP and is characterized by hyponatremia, azotemia, and an increase in plasma renin activity. PPCD is associated with an increased mortality and may be prevented by administration of albumin intravenously (6 to 8 g/L of ascites removed) along with LVP. The development of either diuretic-resistant or diuretic-intractable ascites occurs in approximately 5% to 10 % of all cases of ascites. This is a poor prognostic sign, as 50% of such patients die within 6 months of its development. The only definitive therapy for refractory ascites with cirrhosis is orthotopic liver transplantation. The other options that are available include LVP, peritoneovenous shunts, and transjugular intrahepatic portosystemic shunts (TIPS). The TIPS procedure has not been shown to have any influence on survival in patients with cirrhosis and refractory ascites, and TIPS is contraindicated in patients who have advanced liver failure because it can hasten death in such individuals. Peritoneovenous shunts are associated with a high incidence of complications and frequent occlusion. They are, therefore, rarely used for refractory ascites. Spontaneous bacterial peritonitis (SBP) is a common complication of cirrhotic ascites. It may precipitate hepatorenal syndrome. The overall mortality rate from an episode of SBP is approximately 20%. Following an episode of SBP, the 1-year mortality rate approaches 70%. Hospitalized patients should be treated with intravenous third-generation cephalosporins (eg, cefotaxime), and patients at risk should receive prophylaxis with either orally administered quinolones (eg, norfloxacin) or cotrimoxazole.

Journal Article↗
PubMed1999

Ascites in poultry: recent investigations.

In recent years, ascites research has centred on gaining an increased understanding of pulmonary hypertension syndrome together with the potential role of primary cardiac pathologies. The impact at a cellular level of factors which trigger ascites and substances that protect against it has also been documented. Primary pulmonary hypertension has been induced when birds are exposed to hypoxia during incubation. The conditions experienced during this phase of development may impact on the ability of the bird to regulate its basal metabolic rate through endocrine signals controlled by thyroid activity. The extent of ventilation in the lung influences the ability of the bird to oxygenate haemoglobin. Ventilation/ perfusion mismatches may occur prior to or post-hatching. This factor has been studied extensively using the pulmonary artery/bronchus clamp model. At high altitude, a decreased ventilation/perfusion ratio may occur following the effective increase in physiological dead space due to the lowered oxygen tension at the level of the parabronchi. This explains the mechanism by which ascites is triggered by hypoxia in this particular situation. The effects of ascites are ameliorated by the use of beta agonists and dietary arginine, which act by increasing ventilation and blood flow in the lungs and thus correcting a ventilation/perfusion mismatch. Transient bacterial and viral infections may also influence the induction of pulmonary hypertension. The increases in blood viscosity associated with ascites are most probably a consequence of the condition rather than a cause. A bird may alleviate the effects of pulmonary hypertension by decreasing blood viscosity through inhibition of platelet function, increased erythrocyte deformability and the production of coronary relaxants. Evidence is accumulating that primary cardiac pathology may be associated with a number of ascites cases. Broilers that subsequently develop ascites, exhibit lower heart rates than their normal flock mates. Furthermore, during ascites, hypoxic broilers exhibit bradycardia as opposed to the expected tachycardia. In these cases, a tachycardia induced by feed restriction may protect the bird by raising its cardiac output. Right atrio-ventricular regurgitant flow velocities in chickens are relatively slow compared with similar regurgitant flows induced by pulmonary hypertension in other species. The conduction system in the avian heart is specialized and contains a recurrent bundle branch that innervates the right atrio-ventricular valve, thus initiating active valve closure before right ventricular systole. This predisposes the heart to right ventricular volume overload through a valvular incompetance following a failure of valvular innervation. The resultant elevated diastolic wall stress can trigger the production of angiotensin II and its converting enzyme, which mediate ventricular hypertrophy. Subclinical myocardial damage, irrespective of its cause, can be detected by the presence of troponin T in the blood. Reactive oxygen species may damage cell membranes compromising cellular function in a number of body systems. A positive correlation exists between oxidized glutathione concentrations and right ventricular weight ratio. This indicates a failure to cope with oxidative stress at the level of the respiratory membrane. It is not known if it is possible to modulate levels of antioxidants at this location and hence protect the bird. The final description of the ascites aetiology may lie in the concept of a circuit of events between the cardiac, pulmonary and vascular systems that satisfy the metabolic requirements of the bird. A deficit in one of these systems, at a level that prevents adequate compensation from other components, triggers the pathological cascade that results in the end point of clinical ascites.

Journal Article↗
PubMed2006

Disaggregation and invasion of ovarian carcinoma ascites spheroids.

BACKGROUND: Malignant ascites often develops in advanced stages of ovarian carcinoma, consisting of single and aggregated tumor cells, or spheroids. Spheroids have commonly been used as tumor models to study drug efficacy, and have shown resistance to some chemotherapies and radiation. However, little is known about the adhesive or invasive capabilities of spheroids, and whether this particular cellular component of the ascites can contribute to dissemination of ovarian cancer. Here, we examined the invasive ability of ascites spheroids recovered from seven ovarian carcinoma patients and one primary peritoneal carcinoma (PPC) patient. METHODS: Ascites spheroids were isolated from patients, purified, and immunohistochemical analyses were performed by a pathologist to confirm diagnosis. In vitro assays were designed to quantify spheroid disaggregation on a variety of extracellular matrices and dissemination on and invasion into normal human mesothelial cell monolayers. Cell proliferation and viability were determined in each assay, and statistical significance demonstrated by the student's t-test. RESULTS: Spheroids from all of the patients' ascites samples disaggregated on extracellular matrix components, with the PPC spheroids capable of complete disaggregation on type I collagen. Additionally, all of the ascites spheroid samples adhered to and disaggregated on live human mesothelial cell monolayers, typically without invading them. However, the PPC ascites spheroids and one ovarian carcinoma ascites spheroid sample occasionally formed invasive foci in the mesothelial cell monolayers, suggestive of a more invasive phenotype. CONCLUSION: We present here in vitro assays using ascites spheroids that imitate the spread of ovarian cancer in vivo. Our results suggest that systematic studies of the ascites cellular content are necessary to understand the biology of ovarian carcinoma.

Journal Article↗
PubMed1994

Angiotensin II immunoreactivity is elevated in ascites during severe ovarian hyperstimulation syndrome: implications for pathophysiology and clinical management.

OBJECTIVE: To investigate the ovarian renin-angiotensin system (RAS) during severe ovarian hyperstimulation syndrome (OHSS). DESIGN: Simultaneous sampling of blood and ascitic or peritoneal fluid (PF) during therapeutic paracentesis or laparoscopy. SETTING: University Hospital. PATIENTS: Twelve patients were investigated: three patients presenting severe OHSS, three patients with a spontaneous first trimester pregnancy, three normally cycling women during the early luteal phase, and three patients with ascites of nonovarian origin. MAIN OUTCOME MEASURE: Renin-like activity and angiotensin II (ANG II) immunoreactivity were measured simultaneously in the plasma and the ascites or PF. RESULTS: Angiotensin II immunoreactivity was much higher in the ascites or PF than in corresponding plasma during severe OHSS, first trimester pregnancy, and in the early luteal phase, while it was lower in ascites of nonovarian origin. Renin-like activity and ANG II immunoreactivity were the highest in the ascites of severe OHSS and in the PF from part of the patients with a spontaneous first trimester pregnancy. CONCLUSIONS: The present findings argue for the ovarian origin of the elevated renin-like activity and ANG II immunoreactivity in the ascites of severe OHSS and suggest a stimulatory role of hCG on the ovarian RAS whether during severe OHSS or first trimester spontaneous pregnancy. The vasoactive peptide ANG II may contribute to the maintenance of the ascites in severe OHSS but is probably not responsible for the formation of the ascites. The efficiency of paracentesis during severe OHSS could be explained at least partially by the removing of great amounts of ANG II from the peritoneal cavity.

Adult↗
PubMedDate not supplied

Influence of ascites on the chemotaxis of granulocytes in patients with cirrhosis.

Spontaneous bacterial peritonitis is a specific infectious complication in liver cirrhosis. The reasons for the preferred location of infection on the peritoneum are not clear. The aims of the present study were to ascertain whether hepatogenic ascites fluid is chemotactically effective, what part is played by complement factor C3 and whether there are inhibitors of chemotaxis in ascites. Chemotaxis of granulocytes in serum and ascites fluid was measured in 18 patients with cirrhosis and ascites and in 18 healthy individuals using the Boyden chamber method. In the patients, the chemotactic effect of serum was reduced significantly. Ascites fluid had lower chemotactic activity than autologous serum (P < 0.01), directly correlated to C3 levels (P < 0.025). There was a significant correlation between chemotaxis in serum and in ascites fluid (P < 0.005). Adding ascites fluid to serum led to reduction of chemotactic activity only in the patients (P < 0.025). In conclusion, the chemotactic effect of ascites fluid is considerably lower than that of serum and is proportional to local concentrations of C3. Chemotaxis-inhibiting factors can also be identified in ascites fluid, their pathogenetic relevance being limited.

Adult↗
PubMed2004

Advantages of assaying telomerase activity in ascites for diagnosis of digestive tract malignancies.

AIM: To evaluate the diagnostic value of assaying telomerase activity in ascites cells for the differential diagnosis of malignant and non-malignant ascites. METHODS: Ascites from 40 patients with hepatocellular carcinoma (HCC), 31 with non-HCC gastrointestinal carcinoma (CA), and 24 with liver cirrhosis (LC) were analyzed for telomerase activity. The telomerase activities in cell pellets from ascites were measured according to the Telomeric Repeat Amplification Protocol (TRAP) and quantified with a densitometer. RESULTS: Positive telomerase activity was detected in 16 of 31 (52%) CA patients, 10 of 40 (25%) HCC patients, and 1 of 24 (4%) LC patients (P<0.001). The telomerase activity was higher in the ascites of CA patients than in the ascites of HCC or LC patients (CA: 22.9 +/- 5.8, HCC: 6.7 +/- 2.5, LC: 1.3 +/- 1.3, P = 0.001). Cytology was positive in 18 CA patients (58%) and 1 HCC patient (2.5%), respectively. The positive telomerase activity was not related to patients' age, gender, and ascitic protein concentration, but to white blood count (r = 0.31, P = 0.002), neutrophil count (r = 0.29, P = 0.005), and the C-reactive protein level (r = 0.29, P = 0.018). When the results of both cytological examination and telomerase assay were considered together, the sensitivity increased to 77% for CA patients, 25% for HCC patients, and 48% for all 71 gastrointestinal cancer patients. CONCLUSION: Combining cytological examination of ascites with telomerase activity assay significantly improves the differential diagnosis between malignant and non-malignant ascites.

Aged↗
PubMed1997

Management of ascites. Paracentesis as a guide.

All patients with new-onset ascites or with known ascites and any change in their condition, such as the appearance of fever, abdominal pain, renal insufficiency, or encephalopathy, should undergo diagnostic paracentesis to characterize the ascitic fluid, detect infection, and aid differential diagnosis. A serum-ascites albumin gradient greater than 1.1 g/dL indicates portal hypertension. Spontaneous bacterial peritonitis is a common and serious complication of ascites and is best diagnosed by the number of neutrophils in the ascitic fluid. Patients with the condition should be treated with parenteral antibiotics, and response to therapy should be assessed with repeated paracentesis. Hospitalized patients with low-protein ascites should receive antibiotic prophylaxis. Sodium restriction and diuretics are the cornerstones of therapy for ascites. In refractory cases, alternative forms of therapy, such as large-volume paracentesis, peritoneovenous shunting, or transjugular intrahepatic portosystemic shunting, may be of benefit. Patients with refractory ascites should be considered for liver transplantation.

Anti-Infective Agents↗
PubMed1999

[Dynamics of ascitic fluid in decompensated cirrhosis].

The ascitic fluid in decompensated liver cirrhosis constitutes a continuously circulating pool which carries on sustained water exchanges with plasma and extracellular fluids through the whole peritoneal membrane. The actual ascites volume results therefore from the steady-state between the formation and reabsorption transperitoneal water flows. The ascitic reabsorption concerns both the "iso-osmotic" (i.e. the portion bound to the ascitic proteins and solutes) and the "free-water" (i.e. the amount exceeding the osmotic bounding ability of the peritoneal solutes) fractions of total ascitic water. By means of a simple dilution test, it is possible an in vivo estimation of both the ascites volume and the rate of transperitoneal free-water reabsorption, which is the actual free-water peritoneal clearance (CPAL) and an evaluation of the total intra-abdominal pressure (PIA). PIA results from the sum of the ascitic hydrostatic pressure, and the tension of the abdominal wall. Diuretic administration is able to significantly reduce CPAL, inducing a negative sodium balance and thus leading to a readjustment of ascites steady-state. This fact may cause reductions of ascites volume and PIA only after several days of diuretic treatment. An acute diuretic treatment by itself, even if intensive and resulting in a rapid diuresis and a significant modification of CPAL, does not appear able to determine rapid and detectable modifications of PIA. CPAL has an intrinsic prognostic value in patients with decompensated cirrhosis, since the cumulative mortality was reported to be significantly higher in the patients with lower CPAL levels. The peritoneal clearance ability may be regarded as a compensatory mechanisms of portal hypertension, and its estimate may be a reliable index of patient's aptitude to a lower hydro-retentive trend, which is in turn correlated to a greater cirrhosis severity and a worse prognosis.

Ascites↗
PubMedDate not supplied

Use of a variety of biological parameters in distinguishing cirrhotic from malignant ascites.

Twenty-two different protein measurements were taken in the serum and ascitic fluid of fifty consecutive patients in an attempt to investigate which tests are the most reliable for the differential diagnosis of ascites. Serum and ascitic fluid total proteins (TPR), albumin (ALB), lactate (LAC), ferritin (FER), C3 and C4 complement factors, C-reactive protein (CRP), ceruloplasmin (CER), alpha2-macroglobulin (alpha2MG), haptoglobin (HAP), alpha1-antitrypsin (alpha1AT), alpha1-acid glycoprotein (alpha1AG), transferrin (TRF), immunoglobulins IgG, IgA, IgM and cytokines such as interleukin-1alpha (IL-1alpha), interleukin-1beta (IL-1beta), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) were measured to distinguish between malignant and cirrhotic ascites. Correlations and non-parametric Mann-Whitney tests were used for ascitic fluid:serum ratio comparisons between the two groups. Multivariate analyses were used to determine the most significant biochemical ratio predictors for the differential diagnosis and a recursive partitioning model was constructed. Highly positive correlations (r>0.50) were found between the ratios IgA, IgG, IgM, CER, alpha2 MG, HAP, alpha1AT, alpha1AG and TRF. There was evidence that TPR, ALB, LAC, FER, IgG, CER, alpha2MG, alpha1AT, alpha1AG, TRF and IL-8 ascitic fluid:serum ratios are significnatly higher in patients with malignant neoplasms than in cirrhotics. In the recursive partitioning model the most significant parameters were found to be the ratios of albumin and IL-1alpha. The model fitted allowed for 100% correct classification of ascites. In conclusion, we have shown that a simple and very accurate model based on two ascitic fluid: serum measurements is able to differentiate between malignant and non-malignant ascites.

Acute-Phase Proteins↗
PubMed1987

[Recent aspects in the diagnosis and therapy of ascites].

In the diagnosis of malignant ascites the cytological examination of ascitic fluid lacks sensitivity. Therefore, other parameters for the differentiation of malignant and hepatic ascites are needed. Determination of ascitic fluid cholesterol or fibronectin is superior to the traditional protein measurement in the differential diagnosis of ascites. In the therapy of cirrhotic ascites, physical maneuvers as well as dietary sodium and water restriction have long been known. Diuretic therapy, fraught with considerable side effects, has been applied to cirrhotics with ascites for more than 30 years. However, efficacy of only few regimens has been proven by randomized studies. Recently developed diuretics as well as the novel hormone Atrial Natriuretic Factor might bring about therapeutic advances. Paracentesis combined with intravenous albumin infusion might be reconsidered in severe ascites. Refractory ascites may be treated by implantation of peritoneo-venous shunts.

Ascites↗
PubMed1997

[Clinical evaluation of polyamine assay in diagnosis of malignant ascites].

Polyamine levels were determined by precolumn derivation RH-HPLC in 68 patients with ascites including 21 malignant ascites, 28 liver cirrhosis and 19 tuberculosis. The total polyamine, especially the contents of cadaverine (CA) and spermidine (SPD) in malignant ascites were significantly higher than that in cirrhosis and tuberculosis. Among them CA levels in malignant ascites and cirrhotic and tubercular ascitic fluid were 2.26 +/- 1.83 nmol.ml-1, 0.75 +/- 0.52 nmol.ml-1 and 0.76 +/- 0.47 nmol.ml-1 respectively, demonstrated the most obvious difference. Using 1.0 nmol.ml-1 as a threshold cut off point to differentiate the malignant ascites from non-malignant ascites, the from non-malignant ascites, the sensitivity, specificity and accuracy reached 76. 2%, 83.0% and 80.9% respectively. The results suggest that polymine level in ascites might be regard as one of the cancer-associated markers.

Ascites↗
PubMedDate not supplied

Increase in ascites white blood cell and protein concentrations during diuresis in patients with chronic liver disease.

Serum and ascites protein concentration and ascites cell concentration alterations with determined serially during diuresis in 27 patients with uncomplicated liver disease. The total protein concentration in ascites increased from 1.38 +/- 0.96 gm% to 2.86 +/- 1.28 gm% (p less than 0.001); the serum protein concentration from 6.26 +/- 0.81 gm% to 7.24 +/- 0.93 gm% (p less than 0.001), and the ascites to serum ratio of the total protein concentration from 0.21 +/- 0.13 to 0.38 +/- 0.14 (p less than 0.001). The white blood cell (WBC) concentration in ascites increased from 289 +/- 179 cells per mm3 to 1,108 +/- 924 cells per mm3 (p less than 0.001). Despite the increase in WBC concentration, the polymorphonuclear cell concentration remained constant (42 +/- 52 cells per mm3 to 68 +/- 96 cells per mm3). Protein concentration of the ascitic fluid greater than 3.0 gm% was demonstrated in 12 patients before completion of diuresis and ascitic fluid WBC concentration was greater than 750 cells per mm3 in 17 patients. Ten of 27 patients eventually developed ascites which had a combination of more than 3.0 gm% total protein concentration and greater than 750 cells per mm3. Ascitic fluid protein and WBC concentrations are not "fixed" at a low level in chronic liver disease since each rose during diuresis. Thus, the interpretation of these parameters must be made with caution in patients following significant diuresis.

Ascitic Fluid↗
PubMed2004

Ascites after liver transplantation--a mystery.

Ascites after liver transplantation, although uncommon, presents a serious clinical dilemma. The hemodynamic changes that support the development of ascites before liver transplantation are resolved after transplant; therefore, persistent ascites (PA) after liver transplantation is unexpected and poorly characterized. The aim of this study was to define the clinical factors associated with PA after liver transplantation. This was a retrospective case-control analysis of patients who underwent liver transplantation at the University of Pennsylvania. PA occurring for more than 3 months after liver transplantation was confirmed by imaging studies. PA was correlated with multiple recipient and donor variables, including etiology of liver disease, preoperative ascites, prior portosystemic shunt (PS), donor age, and cold ischemic (CI) time. There were 2 groups: group 1, cases with PA transplanted from November 1990 to July 2001, and group 2, consecutive, control subjects who underwent liver transplantation between September 1999 and December 2001. Both groups were followed to censoring, May 2002, or death. Twenty-five from group 1 had ascites after liver transplantation after a median follow-up of 2.6 years. In group 1 vs group 2 (n = 106), there was a male predominance 80% vs 61% (P =.10) with similar age 52 years; chronic hepatitis C virus (HCV) was diagnosed in 88% vs 44% (P <.0001); preoperative ascites and ascites refractory to treatment were more prevalent in group 1 (P =.0004 and P =.02, respectively), and CI was higher in group 1, (8.5 hours vs 6.3 hours, P =.002). Eight of the 25 (group 1) had portal hypertension with median portosystemic gradient 16.5 mm Hg (range, 16-24). PS was performed in 7 of 25 cases, which resulted in partial resolution of ascites. The development of PA after liver transplantation is multifactorial; HCV, refractory ascites before liver transplantation, and prolonged CI contribute to PA after liver transplantation.

Ascites↗
PubMed1993

Comparison of antigen expression on fresh and cultured ascites cells and on solid tumors of patients with epithelial ovarian cancer.

The antigenic phenotype of malignant cells from ascites of patients with epithelial ovarian cancers was examined and compared to that of their primary and metastatic sites. Cell-surface antigens on frozen sections of primary and metastatic tumors and frozen cell pellets from ascites were analyzed with a panel of murine monoclonal antibodies using the indirect immunoperoxidase method. In addition, ascites cells cultured with and without autologous cell-free ascitic fluid were evaluated by immunofluorescence. The pattern of antigen expression detected on fresh and cultured ascitic epithelial cells was shown to be identical to the expression in autologous solid tumor tissues. When placed in culture, malignant epithelial cells generally persisted for a minimum of one, but no more than five, passages. Addition of autologous ascitic fluid to cultures of ascites cells did not alter the phenotype of the epithelial tumor cell population and did not enhance the growth of these cells. From one culture of ascites cells a permanent malignant epithelial ovarian cancer cell line (designated SK-OV-8) was established. The demonstration that epithelial tumor cells found in ascites of patients with epithelial ovarian cancer have the identical antigenic phenotype as their solid tumor counterpart, at least for the panel of antigens studied, may be useful in planning imaging and therapeutic trials with monoclonal antibodies.

Adult↗
PubMed1997

The in vitro effect on T cell function of soluble IL-2Ralpha from advanced ovarian cancer ascites.

Activated T cells not only secrete interleukin-2 (IL-2) and express cell surface interleukin 2 receptor alpha (IL-2R alpha), but also shed IL-2R alpha. This soluble receptor is a truncated form of the membrane-bound p55 receptor with a similar binding affinity. It has been proposed that soluble IL-2R alpha (sIL-2R alpha) could negatively modulate local immune response. High levels of sIL-2R alpha have been found in the serum and ascites of ovarian cancer patients. The purpose of this investigation is to determine the amount of in vitro T cell inhibition seen in ovarian cancer ascites that is attributable to high levels of sIL-2R alpha. Purified sIL-2R alpha at levels up to 100,000 pg/ml was placed in lymphocyte proliferation assays. Soluble IL-2R alpha was removed from the ascites of three patients with advanced ovarian cancer. Lymphocyte proliferation assays utilizing phytohemaglutin (PHA) stimulation were carried out with this ascites. Untreated ascites from each patient served as control. Addition of purified sIL-2R alpha to lymphocyte proliferation assays failed to demonstrate significant lymphocyte suppression. Addition of ascites to the lymphocyte assays resulted in up to an 80% decrease in lymphocyte proliferation. Neutralization of ascites sIL-2R alpha as well as removal of sIL-2R alpha via a protein G column failed to reverse any of the observed lymphocyte suppression. We conclude that although sIL2R alpha is elevated in ascites of patients with ovarian cancer, it does not account for the profound ascites-induced T cell suppression observed in vitro.

Adult↗
PubMed2002

One-week losartan administration increases sodium excretion in cirrhotic patients with and without ascites.

BACKGROUND: Losartan, a highly selective angiotensin II type 1 receptor antagonist, has been reported to have a significant portal hypotensive effect in cirrhotic patients. A recent study also showed that losartan exerted a dramatic natriuretic effect in preascitic cirrhosis. The influence of losartan on renal hemodynamics and sodium homeostasis in cirrhotic patients with ascites is unclear. This study was undertaken to evaluate the renal effects of 1-week losartan treatment in cirrhotic patients with and without ascites. METHODS: All 12 patients in the study received a daily oral dose of 25 mg losartan for 7 consecutive days. Effective renal plasma flow, urine volume, creatinine clearance, 24h urine sodium excretion and fractional excretion of sodium, blood urea nitrogen, and serum creatinine were measured before and after treatment. RESULTS: In cirrhotic patients without ascites, creatinine clearance, 24-h urinary sodium excretion, and fractional excretion of sodium were significantly increased after losartan administration. Effective renal plasma flow and serum creatinine showed almost no change after treatment. In cirrhotic patients with ascites, creatinine clearance, 24-h urinary sodium excretion, fractional excretion of sodium, and effective renal plasma flow were significantly increased after losartan administration. In addition, the magnitudes of the increases in the fractional excretion of sodium and in the 24-h urinary sodium excretion were greater in cirrhotic patients with ascites than in those without ascites. CONCLUSIONS: One-week treatment with losartan increases sodium excretion in association with an improvement of renal function in cirrhotic patients with and without ascites. The natriuretic effect was more profound in cirrhotic patients with ascites than in those without ascites.

Aged↗