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PubMed1987

Mechanisms of malignant ascites production.

The accumulation of malignant ascites is determined primarily by the obstruction of diaphragmatic lymphatics with tumor inhibiting the outflow of peritoneal fluid. An abnormal increase in peritoneal fluid production has been shown to contribute to ascites formation by a marked neovascularization of the parietal peritoneum. Cell-free malignant ascitic fluid obtained from rats with intra-abdominal Walker 256 carcinoma when infused into the peritoneal cavities of normal animals causes an increase in edema formation and an increase in the permeability of protein from normal omental vessels. Protamine sulfate, a known inhibitor of angiogenesis when infused into the peritoneal cavity along with cell free malignant ascitic fluid, significantly reduces the leak of protein from the intravascular space when compared to ascites alone. Persistent permeability changes continue to exist even after the inhibition of vessel proliferation. These results indicate that angiogenesis is responsible for a major portion of the increase in permeability caused by malignant ascitic fluids. Other tumor-induced factors may be present which alter vascular permeability by other mechanisms which remain to be elucidated.

Animals↗

PubMed1990

Adenosine deaminase (ADA) in peritoneal tuberculosis: diagnostic value in ascitic fluid and serum.

Simultaneous determination of ascitic fluid and serum adenosine deaminase (ADA) activity was evaluated as a diagnostic aid in peritoneal tuberculosis. The ascites was due to peritoneal tuberculosis (group 1), cirrhosis of the liver (group 2), cirrhosis of the liver with spontaneous bacterial peritonitis (group 3), peritoneal malignancy (group 4), Budd-Chiari Syndrome (group 5) and miscellaneous conditions (group 6). Serum from patients of pulmonary tuberculosis and healthy volunteers was analysed for enzyme activity. In patients with peritoneal tuberculosis the ascitic fluid and serum ADA activity was significantly higher than for the other groups (P less than 0.001). Levels above 36 u/l in ascitic fluid and above 54 u/l in the serum suggest tuberculosis. The ascitic fluid/serum ADA ratio was also higher in patients with peritoneal tuberculosis than with other causes of ascites (P less than 0.01). A ratio of more than 0.984 was suggestive of tuberculosis.

Adenosine Deaminase↗

PubMed1984

Peritoneo-cystic shunt for malignant ascites.

Peritoneo-venous shunting has been used extensively in the treatment of benign ascites and, to a limited extent, in the palliative management of malignant ascites. Acceptance of this therapy for malignant ascites has been slow because of concern over intravascular dissemination of disease. Recently a patient with advanced drug-resistant ovarian carcinoma was treated with peritoneo-cystic shunt. This patient's tumor had progressed on multiple chemotherapeutic agents. She continued to work 40 hr per week but her activity was limited by massive ascites. The Denver Shunt (Storz) was selected in preference to the strut-type shunt. The Denver Shunt has a miter valve which is less likely to become occluded by fibrinous and cellular debris, and manual compression of the pumping chamber allows flushing and control of flow. This patient's shunt remained patent for 5 months, until her death, documented by urine cytology and cystoscopy. Initial control of ascites was only fair, probably due to the virtual absence of a pressure gradient between the peritoneal cavity and the bladder. Without a pressure gradient, spontaneous flow would be expected to be nil. Though feasible and well tolerated, this technique is probably not useful in the management of malignant ascites. If modifications of the device could be made to increase the manual flow rate, then this technique might be acceptable.

Ascites↗

PubMed1986

Treatment of cancer ascites by intraperitoneal administration of a streptococcal preparation OK-432 with fresh human complement--role of complement-derived chemotactic factor to neutrophils.

The role of complement in the polymorphonuclear leukocyte (PMN)-mediated tumor cell destruction in cancer ascites was investigated in relation to a streptococcal preparation OK-432, a so-called biological response modifier. Incubation of OK-432 with fresh human serum at 37 degrees C for 60 min resulted in the generation of C3a and C5a chemotactic factors. Intraperitoneal (i.p.) injection of the mixture to a patient with cancer ascites revealed an accumulation of PMNs in the ascitic fluid for a longer period with a rapid reduction of the ascitic fluid, than an intraperitoneal injection of OK-432 alone examined in the same patient. PMNs were found to invade clusters of the tumor cells and then form rosettes followed by the destruction of tumor cells. These findings induced by OK-432 continued over 10 days in the presence of fresh serum, while diminished within 3-4 days when OK-432 alone was injected. When fresh human plasma or fresh frozen plasma was used instead of serum and i.p. injected with OK-432 avoiding preincubation, the same cytological and clinical changes were observed in other patients. These data strongly indicate that OK-432 activates human complement either in vitro or in the peritoneal cavity, and induces PMNs to accumulate in the ascitic fluid. Although the mechanism of killing of tumor cells by PMNs is obscure, addition of human serum or plasma to i.p. use of OK-432 seems to be valuable for the management of patients with malignant ascites.

Ascites↗

PubMed1995

Idiopathic dialysis ascites in the nineties: resolution after renal transplantation.

The incidence of idiopathic dialysis ascites seems to have decreased since the introduction of more effective techniques for control of fluid overload and uremia in chronic hemodialysis patients. Most of the patients reported so far had some predisposing factor, such as malnutrition or sustained fluid overload. We report a case of idiopathic dialysis ascites in a young well-nourished woman with an excellent control of fluid overload and in whom biocompatible dialyzer membranes and volumetric controlled ultrafiltration had been used since her onset of chronic dialysis. Extensive studies excluded the existence of an underlying cause for ascites. Ascitic fluid had the characteristics of an exudate, and a peritoneal biopsy specimen showed chronic nonspecific inflammatory changes. Massive ascites persisted for 6 months, requiring repeated paracentesis, until the performance of a successful renal transplantation. Coinciding with the recovery of renal function, a dramatic disappearance of ascites was observed.

Adult↗

PubMed1985

Demonstration of hepatic triglyceride lipase-like activity in ascites fluid of mice with sarcoma 180.

The contents of apolipoproteins of plasma and ascites fluid of mice with Sarcoma 180 were measured. The apolipoprotein A-I contents of plasma decreased with development of the tumor. The apolipoprotein C-II and C-III contents of plasma reached a maximum on day 7 after tumor inoculation and then decreased. The apolipoprotein A-I content of the ascites fluid was lower than that of normal mouse plasma. In contrast, the apolipoprotein C-II and C-III contents of the ascites fluid were higher than those of normal mouse plasma. The ascites fluid of mice with Sarcoma 180 was found to contain at least two lipases. One had a pH optimum of 5.5-7.0 and was strongly inhibited by chlorpromazine. The other had an alkaline pH optimum and was inhibited only slightly by chlorpromazine. When the ascites fluid was applied to a heparin-Sepharose column 40-45% of the applied triglyceride lipase activity was retained on the column, which was eluted with 0.75 M NaCl. This fraction was inhibited by heat-inactivated (56 degrees C, 10 min) human serum, and was relatively resistant to l M NaCl. These results suggest that one of the lipolytic enzymes present in the ascites fluid of mice with Sarcoma 180 is hepatic triglyceride lipase.

Animals↗

PubMed1990

Chylous ascites after whole-abdomen irradiation for gynecologic malignancy.

From November 1981 through December 1987, 207 patients received whole-abdomen irradiation (WAI) for gynecologic malignancies at the Mayo Clinic. In seven (3%) of these patients, chylous ascites subsequently developed; one additional patient with chylous ascites after WAI for a gynecologic malignancy was referred to us from another institution. In these eight patients, irradiation was done either adjuvantly (five patients) or as salvage therapy after chemotherapy failure (three patients). Chylous ascites was confirmed by laboratory analysis in six cases and was presumed based on the clinical course in two cases. Mean cumulative radiation doses were 2,925 and 5,122 cGy to the abdomen and pelvis, respectively, with para-aortic boosts administered in six cases to a mean cumulative dose of approximately 4,200 cGy. The mean time from completion of WAI to development of ascites was 12 months (range, 6 to 18 months). In six patients, therapy was conservative-observation and diuretics. Two other patients required multiple paracenteses for relief of abdominal distention. Parenteral nutrition was given to two patients who had associated radiation enteritis. The ascites resolved in all eight cases at a mean of 18 months (range, 8 to 30 months) after development. At a mean follow-up of 57 months after initial diagnosis and 16 months after resolution of the ascites, seven patients are without evidence of disease and one patient died of recurrent carcinoma. Distinguishing this clinical entity from recurrent carcinoma is important because of its benign course and its resolution with conservative management.

Adenocarcinoma↗

PubMed1994

Soluble intercellular adhesion molecule-1 (ICAM-1) is released into the serum and ascites of human ovarian carcinoma patients and in nude mice bearing tumour xenografts.

We have demonstrated that patients with ovarian carcinoma have higher levels of soluble intercellular adhesion molecule-1 (ICAM-1) in their serum and ascitic fluids than serum from normal individuals and non-neoplastic gynaecological disease or ascites from patients with cirrhosis. In order to investigate the source of the ICAM-1, and to study the mechanisms which regulate ICAM-1 release in ovarian carcinoma, we have employed the nude mouse model system. Three different human ovarian carcinoma (HOC) cell lines were grown as ascitic tumours in the peritoneal cavity of nude mice. HOC xenografts harvested from nude mice expressed comparable levels of ICAM-1 on their cell surface. Human ICAM-1 was detected, with a species-specific ELISA, in serum and ascitic fluid of tumour-bearing mice, confirming that the tumours were the source of the ICAM-1. The three HOC xenografts showed different levels of ICAM-1 release, but within each xenograft model the level of ICAM-1 in serum and ascitic fluid correlated with the tumour burden. The level of ICAM-1 released by the HOC xenografts could be increased by in vivo treatment with interferon gamma (IFN-gamma). Interleukin 1 (IL-1), tumour necrosis factor (TNF) and IFN gamma increased the cell surface expression of ICAM-1 and caused the release of soluble ICAM-1 from HOC cells established in vitro. The nude mouse provides a useful system in which to study the effects of modulating ICAM-1 release on the progression of ovarian carcinoma and suggests that measuring ICAM-1 levels in the blood or ascites of patients may provide an indication of tumour burden.

Animals↗

PubMed2005

Management of ascites in cirrhosis.

Onset of ascites in cirrhosis of the liver is associated with worsened quality of life, increased risk of spontaneous bacterial peritonitis, and renal failure. Portal hypertension produces splanchnic vasodilation that triggers the cascade of events leading to release of Na retentive vasoconstrictor hormones. Management of ascites caused by cirrhosis is based on improving the Na excretion with diuretics and Na restriction in diet. Refractory ascites and hepatorenal syndrome are the complications of ascites that carry a very high mortality. Large volume paracentesis and transjugular intrahepatic porto-systemic shunts are useful in managing patients with refractory ascites. Liver transplant is the only way to improve survival in ascites caused by cirrhosis.

Ascites↗

PubMed2005

A novel sodium overload test predicting ascites decompensation in rats with CCl4-induced cirrhosis.

BACKGROUND/AIMS: We aimed to develop a non-invasive test to identify the initial alterations of sodium homeostasis and prospectively predict decompensation in preascitic cirrhotic rats. METHODS: The sodium overload test (SOT) was performed in control (CT) and CCl4-induced cirrhotic rats (CH) by calculating the percentage of sodium excreted in the urine after NaCl oral administration (0.5 g/kg). Liver fibrosis was quantified by image cytometry. RESULTS: From the 8th week of CCl4 intoxication, while the daily sodium balance did not change in CH and CT, SOT became significantly lower in the former (62.1+/-13.2 vs 78.8+/-13.2%; P=0.035). At sacrifice, ascites was only present in one animal. The degree of liver fibrosis correlated with SOT. In subsequent experiments, 17 cirrhotic rats developed ascites between the 9th and 14th weeks. SOT remained stable up to 3 weeks before ascites appearance, while it fell significantly to 35+/-19 and 26+/-21% at 2 and 1 week before ascites diagnosis, respectively. Nearly all the rats (95%) with a SOT<60% developed ascites within 3 weeks. CONCLUSIONS: In preascitic cirrhotic rats, SOT unveils sodium metabolism abnormalities earlier than the daily sodium balance and prospectively predicts ascites appearance, identifying rats in a homogeneous stage of cirrhosis, which is essential in pathophysiological studies on sodium retention.

Animals↗

PubMed2004

Chylous ascites following para-aortic lymphadenectomy: a case report.

BACKGROUND: Chylous ascites is an uncommon complication following para-aortic lymph node dissection in the management of gynecologic malignancies. Treatment options are serial paracentesis, medium-chain triglyceride diet, total parenteral nutrition and somatostatin as conservative management and peritoneovenous shunting, and surgical exploration for refractory cases. CASE: A 31-year-old female patient developed chylous ascites following para-aortic lymph node dissection for borderline mucinous tumor of the ovary. Conservative management options failed with recurrence of chylous ascites. Chylous ascites resolved after surgical closure of the lymphatic fistula on the cisterna chyli. There was no evidence of ascites at 10 months follow-up. CONCLUSION: If the patient is a good surgical candidate, surgical exploration should be considered earlier in the treatment of refractory chylous ascites.

Adult↗

PubMed2006

The use of bevacizumab to palliate symptomatic ascites in patients with refractory ovarian carcinoma.

OBJECTIVE: To evaluate our experience with the use of bevacizumab in patients with heavily pretreated recurrent ovarian carcinoma who have symptomatic ascites. METHODS: Four patients were identified who were previously heavily pretreated for recurrent ovarian carcinoma. Each had symptomatic ascites and required frequent therapeutic paracenteses. Each was treated with bevacizumab with the intent to palliate symptomatic ascites. Clinical data including demographic data and clinicopathologic variables was abstracted. RESULTS: The four patients demonstrated symptomatic relief of ascites. Toxicity was manageable in all patients with no grade 3/4 toxicity observed. In addition to symptomatic relief of ascites, no therapeutic paracenteses were required after initiation of therapy with bevacizumab. CONCLUSIONS: Bevacizumab may be a viable palliative option in patients with end stage ovarian carcinoma who have symptomatic ascites.

Angiogenesis Inhibitors↗

PubMed2002

Vascular endothelial growth factor immunoneutralization plus Paclitaxel markedly reduces tumor burden and ascites in athymic mouse model of ovarian cancer.

Ovarian cancer is characterized by rapid growth of solid intraperitoneal tumors and production of large volumes of ascites. Our previous studies of intraperitoneal ovarian carcinoma in an athymic mouse model demonstrated that a monoclonal antibody (mAb) to human vascular endothelial growth factor (VEGF) could prevent ascites formation. Although ascites was almost completely inhibited, tumor burden was variably reduced. To develop more effective therapy, we assessed the combination of a human VEGF mAb plus paclitaxel. Four groups of female athymic nude mice were inoculated intraperitoneally with OVCAR3 cells. Two weeks after inoculation, one group was treated with a human VEGF mAb intraperitoneally twice weekly plus paclitaxel intraperitoneally three times weekly for 6 weeks. The second group was treated with VEGF mAb alone. The third group was treated with paclitaxel alone. The remaining group was treated with vehicle only. Tumor burden in the VEGF mAb plus paclitaxel and paclitaxel alone groups was reduced by 83.3% and 85.7% and 58.5% and 59.5%, respectively, in two separate experiments, compared to controls. VEGF mAb alone caused no significant decrease in tumor burden, nor did treatment of mice inoculated intraperitoneally with HEY-A8 cells, a non-VEGF-secreting ovarian cell line. Virtually no ascites developed in the combined treatment group or the group treated with VEGF mAb alone. Paclitaxel alone reduced ascites slightly, but not significantly. Morphological studies demonstrated that VEGF immunoneutralization enhanced paclitaxel-induced apoptosis in these human ovarian cancers. Thus, combination therapy with inhibitors of VEGF plus paclitaxel may be an effective way to markedly reduce tumor growth and ascites in ovarian carcinoma.

Animals↗

PubMed2001

Ascitic fluid carcinoembryonic antigen and alkaline phosphatase levels for the differentiation of primary from secondary bacterial peritonitis with intestinal perforation.

BACKGROUND/AIMS: In cirrhotic patients, spontaneous bacterial peritonitis (SBP) may be difficult to distinguish from secondary peritonitis with occult intestinal perforation; Runyon's criteria (based on ascitic fluid glucose, protein and lactate dehydrogenase levels) are sensitive but not specific. Ascitic fluid carcinoembryonic antigen (CEA) and alkaline phosphatase (AP) are potential markers for secondary peritonitis. METHODS: Ascitic fluid CEA and AP levels were prospectively compared among three subject groups--cirrhotic patients with sterile ascites, cirrhotic patients with SBP, and patients (cirrhotic and non-cirrhotic) with perforation-related secondary peritonitis. RESULTS: The secondary peritonitis group (n = 38 including 11 cirrhotic patients) had significantly higher mean CEA and AP levels than the SBP (n = 34) and sterile ascites patients (n = 63). Of secondary peritonitis patients, 92% fulfilled predetermined criteria (either CEA >5 ng/ml or AP >240 units/l) versus only 12% of SBP patients; sensitivity was 92% and specificity 88% for differentiating secondary peritonitis from SBP. Runyon's criteria had a sensitivity of 97% and specificity of 56%. Stratification of secondary peritonitis patients by the presence or absence of cirrhosis did not alter our results. CONCLUSIONS: Ascitic fluid CEA or AP elevations appear to be sensitive and specific markers for perforation-related secondary peritonitis in cirrhotic as well as non-cirrhotic patients.

Adult↗

PubMed1992

Ascites dynamics in cirrhosis. Proposal and validation of a methylene blue dilution test.

In order to investigate ascites dynamics, we examined a simple compartmental model based on the analysis of the peritoneal clearance rate of methylene blue in 58 patients with cirrhosis and ascites. After abdominal injection of 10-50 mg methylene blue, the ascitic concentration of the dye progressively decreased, following an exponential trend. The dye distribution volume (7.1 + 0.61, mean + SE) and its peritoneal clearance (87.6 + 5.0 ml/min) were determined by mathematical analysis. The accuracy of volume determinations was controlled in 5 subjects by total paracenteses. In 6 patients, methylene blue clearances were also compared with free-water peritoneal clearances, estimated by a deuterium oxide dilution technique. The decrease in the ascitic concentrations of both tracers followed a corresponding exponential decay in all patients, and the parameters of ascites dynamics determined by the two techniques (peritoneal volumes and clearance values) showed no statistical difference. We therefore suggest the use of the methylene blue dilution test to estimate free-water transperitoneal dynamics, which may be useful in the evaluation and control of cirrhotic patients with ascites.

Adult↗

PubMed1996

Hemodynamic effects of peritoneovenous shunts in hemodialysis patients with ascites.

Ascites in hemodialysis patients has been reported in association with systemic diseases, such as cirrhosis or congestive heart failure, and as an idiopathic form. Regardless of the etiology, these patients often are refractory to treatment with intradialytic ultrafiltration because of recurrent hypotensive episodes. In this report we describe the hemodynamic effects of peritoneovenous shunts (PVSs) in three hemodialysis patients with ascites refractory to conventional treatment. One patient had idiopathic ascites and the other two had associated liver disease. Patients were monitored for lowest blood pressure, number of intradialytic hypotensive episodes, number of grams of albumin infused to treat hypotensive episodes, interdialytic weight gain, and hemodynamic stability (defined as the difference between the predialysis mean arterial pressure and the lowest intradialytic mean arterial pressure). In all three patients the hemodynamic parameters stabilized after PVS placement despite equal or greater ultrafiltration during dialysis (due to a significant increase in the lowest measured intradialytic blood pressure). The total number of hypotensive episodes decreased from 219 prior to PVS placement to zero after shunt placement. The need for albumin infusion during hemodialysis (for blood pressure support) decreased (significantly in two patients), as did the volume of ascites in all three patients. One patient required PVS replacement secondary to infection, which was the only complication. We believe that refractory ascites in end-stage renal disease patients can be successfully treated by placement of a PVS, which often results in relief of the ascites and significant improvement in intradialytic hemodynamic stability.

Aged↗

PubMedDate not supplied

A bcl-x(S) adenovirus demonstrates therapeutic efficacy in an ascites model of human breast cancer.

OBJECTIVES: To determine whether a Bcl-x(S) adenoviral vector has therapeutic potential in an ascites model of human breast cancer in nude mice. METHODS: Advanced ascites were developed by injecting mice intraperitoneally (IP) with MDA-MB-231 human breast carcinoma cells. Mice received sequential IP injections of the Bcl-x(S) virus or a control lac-Z adenovirus. A third group of mice received no virus. Tumor burden and survival were monitored. Histopathology and necropsies were performed on mice. RESULTS: A single injection of the Bcl-x(S) adenovirus produced no systemic or local toxicity and no abnormal histopathology in normal mice. However, abdominal organs within these mice were transduced with the Bcl-x(S) vector. Adenoviral gene transduction efficiency in MDA-MB-231 ascites was 36+/-6.40% (n = 3). Percent weight change differences revealed that ascites bearing mice injected three times with the Bcl-x(S) vector showed a statistically significant decrease in tumor burden compared with lac-Z-injected mice (n = 7; P = .012 on days 10-15 after the first injection). Mice injected with the Bcl-x(S) vector had significantly greater survival relative to lac-Z-injected mice (n = 7; P = .0004). Bcl-x(S) protein expression was detected in aspirates of mice injected with the Bcl-x(S) vector but not the lac-Z vector. Necropsies revealed that ascites bearing mice injected with Bcl-x(S) vector lacked carcinoma in the peritoneal cavity compared with control mice. CONCLUSION: The Bcl-x(S) adenovirus can reduce tumor burden and increase survival in an ascites model of advanced stage breast cancer.

Adenoviridae↗

PubMed2001

Clinical management of ascites and its complications.

Development of ascites is a poor prognostic sign with a 1 year mortality rate of up to 50%. Cirrhotic patients who develop ascites should therefore be evaluated for liver transplantation. Even though current therapies of ascites are not associated with a survival benefit, the elimination of ascites will improve quality of life and prevent the development of lethal complications such as SBP and HRS. Therapy of ascites should be directed at correcting the pathophysiologic abnormalities that lead to ascites formation, namely sodium retention, reduced effective arterial blood volume, and sinusoidal hypertension.

Anti-Bacterial Agents↗