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PubMed1993

Fibrinolytic activity of ascites caused by alcoholic cirrhosis and peritoneal malignancy.

Coagulopathy is a well recognised complication of peritoneovenous shunting for ascites. The relative contributions of primary fibrinolysis and disseminated intravascular coagulation remain controversial. Plasminogen activating activity was significantly lower in malignant ascites (n = 10, median < 0.02 (range < 0.02-1.26) IU/ml) than in alcoholic ascites (n = 10, 1.07 (0.30-1.49) IU/ml) (p < 0.05). Fibrinolytic activity was determined by a balance between tissue plasminogen activator and plasminogen activator inhibitor-1. There was no significant difference between the two groups in the concentration of tissue plasminogen activator (34 (12-64) ng/ml in malignant ascites v 29 (12-43) ng/ml in alcoholic ascites), but the concentration of plasminogen activator inhibitor-1 was significantly higher in malignant ascites (736 (213-1651) ng/ml) than in alcohol ascites (29 (12-43) ng/ml) (p < 0.05). Malignant ascites contained significantly higher concentrations of urokinase (0.7 (< 0.1-1.3) ng/ml v 0.2 (< 0.1-0.6) ng/ml in alcoholic ascites) and plasminogen activator inhibitor-2 (33 (< 6-140) ng/ml v 9 (< 6-28) ng/ml alcoholic ascites). The plasminogen activating activity of alcohol ascites may lead to primary fibrinolysis after peritoneovenous shunting. The considerably lower activity found in malignant ascites may explain why coagulopathy after shunting is less pronounced in this group of patients.

Adult↗
PubMed2026

Ascites reprograms innate lymphoid immune cells in ovarian cancer by promoting ILC2 enrichment and dysfunctional NK-cell states.

BACKGROUND: High-grade serous ovarian cancer (HGSOC) is commonly accompanied by malignant ascites, a clinically relevant tumor niche that promotes immune evasion, metastasis, and treatment resistance. Although natural killer (NK)-cell dysfunction has been described in ovarian cancer, the broader innate lymphoid landscape of ascites and the mechanisms linking ascites-derived signals to innate immune suppression remain insufficiently resolved. METHODS: We performed single-cell RNA sequencing of NK/innate lymphoid cells from ovarian cancer ascites to define cellular heterogeneity and differentiation states. Functional assays assessed NK-cell cytotoxicity, degranulation, and receptor expression following exposure to patient-derived ascites, with or without transforming growth factor-&#x3b2; (TGF-&#x3b2;) receptor inhibition. Proteomic profiling was used to characterize the soluble ascites milieu, and clinical associations were examined for innate lymphoid subsets. RESULTS: Single-cell analysis identified eight transcriptionally distinct NK/innate lymphoid states, including cytotoxic, precursor, early-like, tolerant/immunoregulatory, regulatory, proinflammatory, and innate lymphoid populations. Ovarian cancer ascites was characterized by depletion of cytotoxic and precursor NK-cell states together with enrichment of early-like, tolerant, regulatory, pro-inflammatory, and innate lymphoid cell (ILC) populations. Trajectory analysis indicated impaired maturation toward terminally differentiated cytotoxic NK cells. Notably, ascites contained an expanded population of programmed cell death protein 1 (PD-1)+ ILC2s, which were more abundant in patients with shorter progression-free survival. In functional assays, short-term exposure of healthy donor NK cells to ascites suppressed degranulation and tumor-cell killing, reduced expression of activating receptors including NKp30 and DNAM-1, increased inhibitory receptor expression, and shifted NK cells toward a CD56highCD16low phenotype. Proteomic profiling supported a soluble milieu consistent with type 2 immune skewing and NK-cell suppression. Importantly, TGF-&#x3b2; receptor inhibition partially restored NK-cell activation and function in the presence of ascites. CONCLUSIONS: HGSOC ascites establishes a type 2-skewed immunoregulatory niche that coordinately drives NK cell dysfunction and PD-1+ ILC2 accumulation. The findings identify TGF-&#x3b2;-linked suppression and ascites-associated immune regulators as candidate immunotherapeutic vulnerabilities for restoring antitumor immunity in ovarian cancer.

Humans↗
PubMed1988

CT- or sonography-guided biopsy of the liver in the presence of ascites: frequency of complications.

The presence of ascites has been considered a contraindication to percutaneous biopsy of the liver. To determine the validity of this assumption, we performed percutaneous biopsies of the liver under CT or sonographic guidance in 28 patients who had ascites and in 28 patients who did not have ascites and compared the complication rates in the two groups. Twenty-two patients (79%) in the group with ascites and 19 patients (68%) in the group without ascites had biopsies to determine the cause or extent of chronic liver disease. The remainder were oncologic patients who had biopsies to determine the cause of a focal hepatic mass. The complication rate in the patients who had ascites (32%) was less than that in the patients who did not have ascites (43%) (the difference did not reach statistical significance, p less than .30). In the ascites group, complications included transient hypotension (five patients), a mild-to-moderate fall in hematocrit (three patients), and a small leak of ascites from the biopsy site (one patient). In the control group, minor complications included transient hypotension (three patients), a mild-to-moderate fall in hematocrit (seven patients), and a small subcapsular hematoma (one patient). One major complication occurred in the control group: a patient required a blood transfusion because of the fall in his hematocrit. We conclude that the complication rate in liver biopsies guided by CT or sonography in the presence of ascites is not higher than similar biopsies done in the absence of ascites. Ascites should not be considered a contraindication for performing such biopsies.

Adolescent↗
PubMed2005

Low gradient ascites: a seven-year course review.

AIM: To study the patients with low gradient ascites in hospitals of Guilan Province (northern Iran). METHODS: Patients admitted in hospitals of Guilan Province with low gradient ascites from 1993 to 2000 were enrolled in the study. Serum and ascitic fluid albumin levels were determined by biochemical reactions. The serum-ascitic albumin gradient (SAAG) less than 1.1 g/dL was considered low. Statistical analysis was performed with SPSS 9.0 software and P<0.05 was considered statistically significant. RESULTS: Of the 148 patients enrolled in the study, 72 (48.6%) were males and 76 (51.4%) were females with a mean age of 59.03+/-13.54 years. Tuberculous peritonitis was the most frequent cause of low gradient ascites in 68 (45.9%). Other most frequent causes were cancer in 62 (41.9%), nephrotic syndrome in 9 (6%), pancreatitis in 6 (4%). Peritoneal cancer was found in 22 (35%), ovarian and gastric cancers were found in 14 (22.5%) and 12 (19.3%), respectively. All of which were the causes of ascites. The mean SAAG was 0.68+/-0.19 g/dL. The mean serum and ascitic fluid albumin concentrations were higher in tuberculous patients (P<0.006), but lactate dehydrogenase (LDH) level was higher in cancer patients (P<0.0001). In peritoneal tuberculosis, mean ascitic glucose concentration was significantly lower than other patients (P<0.0001). CONCLUSION: Tuberculosis should be considered in all patients with low gradient ascites especially in developing countries (like Iran), as the first cause of ascites. In the approach to patients with low gradient ascites, ascitic fluid glucose, and LDH level are useful indicators for decision making.

Adult↗
PubMed1995

Pathogenesis of ascites tumor growth: fibrinogen influx and fibrin accumulation in tissues lining the peritoneal cavity.

In the immediately preceding paper, we demonstrated that the microvasculature supplying peritoneal lining tissues of mice bearing either of two transplantable ascites carcinomas was hyperpermeable to circulating macromolecules. Solid tumors have been shown to exhibit similar levels of microvascular hyperpermeability, leading to extravasation of plasma proteins, including fibrinogen which clots on extravasation to form an extravascular fibrin gel. To determine whether similar extravasation and clotting of plasma fibrinogen occurred in ascites tumors, we used 125I-labeled fibrinogen (125I-F) as a tracer to measure inflow of fibrinogen into the peritoneal cavities, and influx and accumulation of fibrinogen/fibrin in the peritoneal lining tissues (peritoneal wall, mesentery, and diaphragm) of mice bearing syngeneic TA3/St or MOT ascites tumors. The percentage of circulating 125I-F that extravasated into the peritoneal cavity was increased from 10- to 50-fold in mice bearing either ascites tumor. Influx into the peritoneal walls of ascites tumor-bearing mice was 3-7 times that of control mice and became maximal on day 8 (TA3/St) and day 15 (MOT). Accumulation of 125I-F in ascites fluid and peritoneal lining tissues was also increased substantially in mice bearing these ascites tumors, reaching maximal values on days 7-8 (TA3/St) and 19-29 (MOT) at levels 2- to 3-fold (peritoneal wall) and 33- to 148-fold (ascites fluid) above control levels. Significant amounts of the 125I-F that accumulated in the peritoneal lining tissues of ascites tumor-bearing animals were insoluble in 3 M urea, consistent with clotting of 125I-F to cross-linked fibrin. Autoradiographs of SDS-PAGE gels performed on extracts of peritoneal lining tissues of both ascites tumors revealed the characteristic signature of cross-linked fibrin, i.e., gamma-gamma dimers and alpha-polymers. Fibrin was also identified in peritoneal lining tissues of both ascites tumors by immunohistochemistry. Taken together, these data indicate that fibrinogen, like other circulating macromolecules, extravasates into the peritoneal cavity and peritoneal lining tissues of ascites tumor-bearing mice and does so with kinetics similar to those of other macromolecular tracers we have studied. Moreover, a portion of the fibrinogen that extravasated into peritoneal lining tissues clotted to form a cross-linked fibrin meshwork which trapped tumor cells and favored their attachment to the peritoneal surface. By analogy with solid tumors, such fibrin deposits may also be expected to have a role in initiating angiogenesis and the generation of mature tumor stroma.

Animals↗
PubMed1994

A multicenter, case-controlled study of the clinical presentation and etiology of ascites and of the safety and clinical efficacy of diagnostic abdominal paracentesis in HIV seropositive patients.

OBJECTIVE: To analyze the clinical presentation and etiology of ascites in HIV seropositive patients compared with the general population and to analyze the safety and clinical efficacy of abdominal paracentesis in HIV patients. METHODS: We did a multiyear study of 24 HIV seropositive and 60 control patients with ascites undergoing diagnostic abdominal paracentesis at two university hospitals. RESULTS: HIV seropositive patients presented with similar clinical findings as other patients with ascites, except HIV patients had a significantly higher incidence of pyrexia and a lower serum albumin level and leukocyte count. The two groups had similar mean ascitic fluid values of lactate dehydrogenase, total protein, glucose, and erythrocyte count. HIV patients had a trend of a higher rate of infected ascites than controls (29% vs 12%; odds ratio = 3.12; odds ratio confidence interval = 0.80-12.3; p < 0.06; chi 2). HIV and control patients with culture-proven bacterial peritonitis had similar ascitic fluid leukocyte and absolute neutrophil counts. In eight (33%) of the HIV patients, major new diagnoses were made from ascitic fluid analysis, including spontaneous bacterial peritonitis in four, tuberculous ascites in two, fungal peritonitis in one, and lymphoma in one (control rate = 30%; not significantly different; chi 2). The HIV patients did not experience any complications from paracentesis, whereas the controls experienced one minor complication of prolonged drainage of ascitic fluid from the paracentesis site (not significantly different rates; Fisher's exact test). Six (25%) of the HIV patients had ascites caused by AIDS-defining illnesses of lymphoma, peritoneal tuberculosis, or disseminated candidiasis. CONCLUSIONS: Abdominal paracentesis is a safe and effective clinical diagnostic tool in HIV patients. In addition to standard tests, ascitic fluid should be sent for mycobacterial and mycological histological stains and cultures in HIV patients. AIDS-unrelated causes are the most common cause of ascites in HIV patients, with only about 1/4 of cases due to AIDS-related diseases.

Adult↗
PubMedDate not supplied

Interleukin-12 synergizes with interleukin-2 to generate lymphokine-activated killer activity in peripheral blood mononuclear cells cultured in ovarian cancer ascitic fluid.

OBJECTIVES: The ascites-associated lymphocytes in ovarian cancer have altered immunologic function, and cell-free ascitic fluid has immunomodulating properties. We determined (1) whether interleukin (IL)-2 could induce lymphokine-activated killer (LAK) activity in normal peripheral blood mononuclear cells (PBMC) cultured in ovarian cancer ascitic fluid, and (2) whether IL-12 could synergize with IL-2 to generate LAK activity in normal PBMC cultured in ascitic fluid. METHODS: Normal PBMC were cultured in control medium and in media consisting of 50% ascitic fluid (ascitic medium), with and without IL-2 and IL-12. Cell activation to assess LAK activity (cell lysis) was determined in a 51Cr-release assay with the tumor cell lines FMEX and SKOV3 as target cells. To determine a possible mechanism for any synergistic effect, the expression of perforin, a pore-forming protein, was determined by Northern blot analysis. RESULTS: Interleukin-2 alone could not induce LAK activity in normal PBMC cultured in 50% ascitic fluid for up to 3 days. Interleukin-12 did mediate some or minimal LAK activity after 1, 2, or 3 days of incubation in control medium or in 50% ascitic fluid. When IL-2 and IL-12 were used in combination, PBMC cultured for 3 days in 50% ascitic fluid had remarkably high lytic activity against FMEX and SKOV3 tumor cells. In some experiments, this cytotoxicity was greater than that in PBMC cultured in control medium with IL-2 and IL-12. Lower concentrations of IL-12 (1 U/mL) with IL-2 (100 U/mL) were as effective as, and often more effective than, higher doses of IL-12 with IL-2. Very low-dose IL-12 (0.01-0.03 U/mL) in combination with IL-2 also induced a range of cytotoxicities. Only the combination of IL-2 and IL-12 up-regulated expression of perforin mRNA in ascitic medium. CONCLUSIONS: The cytotoxicity responses of PBMC cultured in ascitic fluid in the presence of IL-2 and IL-12 are complex. Low-dose IL-2 and IL-12 can overcome the inhibitory property of ascitic fluid on LAK generation and can restore and enhance cytotoxic activity, possibly by reconstituting the expression of perforin. These findings may have therapeutic potential.

Ascites↗
PubMed2001

Ascites.

Ascites is the most common presentation of decompensated cirrhosis, and its development heralds a poor prognosis, with a 50% 2-year survival rate. Effective first-line therapy for ascites includes sodium restriction (2 g/d), use of diuretics, and large-volume paracentesis (LVP). Ideally, a combination of a loop-acting diuretic (eg, furosemide) and a distal-acting diuretic (eg, spironolactone) is used. LVP has the advantage of producing immediate relief from ascites and its associated symptoms. When 5 L or more ascitic fluid is removed, albumin (6 to 8 g per liter of fluid removed) should be administered intravenously to minimize hemodynamic and renal dysfunction. The development of refractory ascites is particularly ominous, and 50% of such patients die within 6 months of its development. Liver transplantation is the only effective therapy for patients with refractory ascites associated with cirrhosis; unfortunately, this therapy is not available for many of those with refractory ascites. Other therapies that are available include LVP, peritoneovenous shunts, and transjugular intrahepatic portasystemic shunts (TIPS). LVP alleviates ascites rapidly, but ascites recurs universally, requiring repeated hospitalizations and paracenteses and decreasing patient quality of life. Peritoneovenous shunts rarely are used due to their high complication rate and tendency to become occluded. Recently, the use of TIPS has been shown to be an effective therapy for patients with refractory ascites. It is most effective when liver function is relatively well preserved. On the other hand, TIPS may hasten death in those with advanced liver failure. TIPS has not been shown to have a clear-cut beneficial effect on survival in patients with refractory ascites. Spontaneous bacterial peritonitis is the most common complication of ascites and is associated with a worsening hyperdynamic circulation and a mortality rate of approximately 20%. Following an episode of spontaneous bacterial peritonitis, the 1-year mortality rate approaches 70%. Patients at risk should be considered for prophylaxis with an orally administered quinolone (eg, norfloxacin). Alternatives include trimethoprim/sulfamethoxazole. Active spontaneous bacterial peritonitis should be treated with an intravenously administered third-generation cephalosporins (eg, cefotaxime) in most circumstances.

Journal Article↗
PubMed2002

Vascular endothelial growth factor is increased in ascites from metastatic pancreatic cancer.

INTRODUCTION: Vascular endothelial growth factor (VEGF) is an angiogenic factor that increases vascular permeability. VEGF stimulates capillary formation and has mitogenic effects on vascular endothelial cells. The development of malignant ascites causes significant morbidity. We hypothesized that increased levels of VEGF play a role in the development of malignant ascites in patients with pancreatic cancer. METHODS: Athymic mice underwent orthotopic implantation of human pancreatic ductal adenocarcinoma tumors (250,000 cells) into the body of the pancreas. Tumors were allowed to grow for 12 weeks, at which time ascites develops in 50% of mice. Paracentesis was performed on mice with noticeable ascites. Saline lavage was performed in mice with equivalent pancreatic tumor masses without ascites and served as control. Both ascites and tumor masses were harvested for VEGF protein quantitation by ELISA. RESULTS: VEGF protein levels were elevated in malignant ascites by 15-fold compared to control mice with equivalent tumors (N = 6, P < 0.001, t test). VEGF levels were slightly higher in the primary tumor masses harvested from mice without ascites. Mice with ascites also had metastatic nodules throughout the abdominal cavity. CONCLUSIONS: We are reporting for the first time that VEGF levels are increased in the ascites of nude mice with orthotopically transplanted human pancreatic cancers. VEGF increases vascular permeability and allows for extrapancreatic seeding of tumors. Irrespective of primary tumor size, intraperitoneal VEGF levels are increased when ascites and extrapancreatic nodules are present, while a paradoxical decrease is observed in VEGF levels of primary tumors.

Animals↗
PubMed1993

The hyperfibrinolytic state of liver cirrhosis: possible pathogenetic role of ascites.

We evaluated coagulation and fibrinolytic parameters in both plasma and ascitic fluid of 39 patients with ascites secondary to liver cirrhosis and in 14 cirrhotic patients without ascites, in order to verify if the peritoneal compartment could be involved in the pathogenesis of the hyperfibrinolytic state of the disease. An activation of fibrinolysis, as suggested by increased levels of FDP, D-dimer and tissue plasminogen activator (t-PA) was demonstrated in both ascitic fluid and to a lesser extent in plasma. A positive correlation was also observed between plasma and ascitic fluid plasminogen, anti-plasmin and fibrinogen, while a negative correlation was found between plasma and ascitic fluid plasminogen activator inhibitor-1 (PAI-1). Moreover, plasma PAI-1 was significantly lower in patients with ascites than in those without ascites and among ascitic patients in those who had bleeding into soft tissues when compared to those who did not present haemorrhagic events. Finally, a significant association was also shown between positivity for plasma D-dimer (> 200 ng/ml) and the presence of ascites. Taken together, our data suggest an exchange of some coagulation and fibrinolytic proteins between plasma and ascitic fluid and point out the key role of PAI-1 in regulating plasma fibrinolytic potential and in bleeding complications in cirrhotic patients.

Adult↗
PubMed1986

Elevated ascitic fluid fibronectin concentration. A non-specific finding.

Ascitic fluid fibronectin concentration was measured in 111 specimens by laser nephelometry. Sterile, portal hypertension-related fluid fibronectin concentration (24 +/- 14 micrograms/ml) was significantly lower than the concentration in infected, portal hypertension-related ascites (49 +/- 44 micrograms/ml, P less than 0.001), peritoneal carcinomatosis (123 +/- 45 micrograms/ml, P less than 0.001), massive liver metastases-related ascites (55 +/- 21 micrograms/ml, P less than 0.001), as well as in ascites of other types (94 +/- 42 micrograms/ml, P less than 0.001). The percentage of samples with fibronectin concentration, greater than 75 micrograms/ml, was 0% for sterile, portal hypertension-related ascites, 28% for infected, portal hypertension-related ascites, 89% for peritoneal carcinomatosis, 20% for massive liver metastases-related ascites, and 72% for ascites of other types. Ascitic fluid fibronectin concentration correlated in a linear fashion with ascitic fluid total protein (r = 0.81, P less than 0.001). Fibronectin concentration in ascites appears to be elevated under a variety of conditions and does not appear to be a specific marker for cancer.

Ascites↗
PubMedDate not supplied

Evaluation of fibronectin as a marker of malignant ascites.

The aim of the study was to assess the accuracy of fibronectin, a glycoprotein, for the diagnosis of malignant ascites and to compare it with conventional parameters. Ascitic fluid samples from 50 patients, 25 with intra-abdominal malignancy and 25 without it were analysed for total protein concentration, fluid/serum protein ratio, glucose concentration, leucocyte count, pH, fibronectin concentration (by ELISA) and for malignant cell cytology. Twenty-two of the 25 patients with ascites and intra-abdominal malignancy had documented peritoneal metastases in group A. The 25 patients with non-malignant ascites constituted group B. Mean values of ascitic fluid fibronectin, for groups A and B were 538 +/- 46 micrograms/mL and 60 +/- 4.92 micrograms/mL, respectively (P less than 0.001). Within the group with malignant ascites, patients who had positive malignant cytology (n = 12) exhibited a significantly higher ascitic fluid fibronectin concentration than patients with negative cytology (P less than 0.05). While mean ascitic fluid protein concentration showed a significant difference (P less than 0.01) between the two groups, there was no difference in respect to ascitic fluid pH, glucose concentration and leucocyte count. Malignant cell cytology was positive in 54.5% of group A patients with no false positive report in group B. The diagnostic accuracy for differentiating malignant from non-malignant ascites was 100% for a fibronectin value of greater than or equal to 110 micrograms/mL as compared with 78.7% for ascitic fluid protein concentration greater than or equal to 0.5 g/dL, 57.4% for leucocyte count greater than or equal to 1000/mm3, 59.6% for pH less than 7.45 and 78.7% for malignant cell cytology.

Abdominal Neoplasms↗
PubMed1988

Ascites kinetics in cirrhosis: effects of rapid volume expansion and diuretic administration.

I examined whether the rate of ascites formation in cirrhosis is increased by volume expansion and whether this rate is related to the intensity of renal sodium retention, and I examined the mechanisms by which ascites is mobilized during diuresis. The plasma-ascites filtration rate (PFR) of intravenously injected iodine 125-labeled albumin (the rate of ascites formation by the liver) after volume expansion with normal saline solution in seven patients was similar to that observed in 14 patients who had not received infusions (0.010 +/- 0.003 vs. 0.013 +/- 0.006 L/hr/m2) and was unrelated to natriuresis both before and after intravenous administration of 80 mg furosemide the previous day (r = 0.04 and -0.36). Diuresis of seven patients who had not received infusions reduced PFR (from 0.679 +/- 0.267 to 0.411 +/- 0.198 L/day, P less than 0.05) and total ascites formation rate (from 3.029 +/- 1.620 to 1.465 +/- 1.053 L/day, P less than 0.02) but not plasma volume (from 3.464 +/- 0.646 to 3.391 +/- 0.775 L). Increases occurred in ascites albumin concentration (from 7 +/- 4 to 9 +/- 4 gm/L, P less than 0.05) and in the ascites/serum albumin ratio (from 0.26 +/- 0.12 to 0.35 +/- 0.13, P less than 0.05) but not in the serum-ascites albumin gradient (portal pressure). Fractional changes in ascites volume and albumin concentration were unrelated (r = 0.20). The calculated rate of ascites reabsorption decreased in five patients during diuresis, indicating that ascites was mobilized by decreased formation. Ascites reabsorption increased in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1990

Selective intestinal decontamination increases serum and ascitic fluid C3 levels in cirrhosis.

Selective intestinal decontamination for 7 days with norfloxacin was performed in 14 cirrhotic patients with ascites and low ascitic fluid total protein. Variations in serum and ascitic fluid of C3 and C4 and ascitic fluid total protein after therapy were compared with those of a control group of 14 untreated patients with similar characteristics. After oral norfloxacin administration, we saw a significant increase of C3 in serum (p less than 0.05) and ascitic fluid (p = 0.01). A significant increase was also observed in ascitic fluid total protein (p less than 0.05) but not in serum and ascitic fluid C4. There were no changes in serum C3, ascitic fluid C3, ascitic fluid C4 or in ascitic fluid total protein in group 2. These data demonstrate that selective intestinal decontamination increases serum and ascitic fluid C3 levels and, therefore, might be useful in preventing spontaneous infections in cirrhotic patients at high risk of infection.

Ascitic Fluid↗
PubMed2002

Gallbladder contractility in patients with cirrhotic versus malignant ascites.

PURPOSE: The aim of this study was to evaluate differences in gallbladder contractility by measuring gallbladder wall thickness, fasting and residual gallbladder volume, and gallbladder ejection fraction in patients with cirrhotic and malignant ascites. METHODS: Twenty-four patients (16 women and 8 men) with malignant ascites (2 cervical, 2 colon, 2 stomach, 6 pancreatic, and 12 ovarian carcinomas), aged 59 +/- 12 years, and 26 patients (14 women and 12 men) with cirrhotic ascites, aged 57 +/- 16 years, were included in the study. After patients fasted overnight for 8 hours, gallbladder wall thickness, fasting gallbladder volume, and gallbladder volume and ejection fraction were measured sonographically at 10, 20, 30, 40, 50, 60, 70, 80, and 90 minutes after ingestion of a standard liquid test meal. RESULTS: The mean gallbladder wall thickness was higher in patients with cirrhotic ascites than in those with malignant ascites (5.5 +/- 1.5 mm [standard deviation] versus 3.1 +/- 0.6 mm, respectively; p < 0.001). The mean fasting gallbladder volume was also higher in patients with cirrhotic ascites than in those with malignant ascites (27.3 +/- 11.5 cm(3) versus 17.6 +/- 8.9 cm(3); p < 0.05). Patients with cirrhotic ascites had significantly higher mean postprandial gallbladder volumes and ejection fractions than did those with malignant ascites at all times except 10 minutes after the meal (p < 0.05). CONCLUSIONS: Our findings suggest that gallbladder contractility is greater in patients with cirrhotic ascites than in patients with malignant ascites.

Adult↗
PubMed2000

Ascites after liver transplantation.

Massive ascites after liver transplantation, although uncommon, usually represents a serious adverse event. The pathogenesis of this complication has not been adequately investigated. To determine the incidence, characteristics, and pathogenic factors of massive ascites after liver transplantation (ascitic fluid > 500 mL/d for >10 days), the charts of 378 liver transplant recipients were reviewed. Massive ascites occurred in 25 patients (7%). Mean ascitic fluid production was 960 mL/d (range, 625 to 2,350 mL/d), and the duration of ascites was 77 days (range, 15 to 223 days). The ascitic fluid had a high protein content (36 +/- 7 g/L; range, 25 to 50 g/L). When patients who did and did not develop massive ascites were compared, significant differences were found in receptor sex (men, 88% v 60%, respectively; P <.01) and surgical technique (inferior vena cava preservation with piggyback technique, 72% v 41%; P <.01). Significantly increased wedged and free hepatic venous pressures and gradients between hepatic vein and right atrial pressures were found in patients who developed ascites, suggesting a difficulty in graft blood outflow. Massive ascites was associated with renal impairment, increased incidence of abdominal infection, prolonged hospitalization, and a tendency toward reduced survival. In conclusion, massive ascites after liver transplantation is relatively uncommon but associated with increased morbidity and mortality and is predominantly related to difficulties of hepatic venous drainage. Measurement of hepatic vein and atrial pressures to detect a significant gradient and correct possible alterations in hepatic vein outflow should be the first approach in the management of these patients.

Adult↗
PubMed1976

Ascites in patients undergoing maintenance hemodialysis. Report of six cases and physiopathologic approach.

Six patients with chronic uremia in whom ascites developed during maintenance hemodialysis are described. Their clinical and biochemical findings are reviewed and compared with data of 10 hemodialyzed patients without ascites. Liver cirrhosis was the origin of ascites in only one case. Hypoalbuminemia, liver cirrhosis, congestive heart failure, peritonitis, peritoneal tuberculosis and carcinomatosis were uniformly absent in the other patients. Long-term and marked overhydration seems to be at the origin of ascites. Lack of peripheral edema, probably due to ascites compartmentalization, was a constant finding in every noncirrhotic patient with ascites. When long-term overhydration was stopped after successful kidney transplantation or by means of diminished water and salt ingestion, reversal of the syndrome was attained. Nevertheless, ascites because of liver cirrhosis was not influenced by means of kidney transplantation. In three patients with ascites who did not receive a transplant, a significant reduction in water and salt ingestion was reached after intensive psychotherapy which led to reversal of the ascitic syndrome. In one anephric patient ascites did not develop despite water overloading. Survival has not been influenced by the formation of ascites. Further research is needed to determine the mechanism of sodium transfer across the peritoneal membrane. Influence of humoral factors can be considered, if an active transport mechanism could be demonstrated.

Adolescent↗
PubMed1992

Evidence for the production of high amounts of interleukin-6 in the peritoneal cavity of patients with ascites.

The ascites and serum concentrations of interleukin-6 (IL-6) and interleukin-1 (IL-1) were determined in 21 patients with hepatic ascites and in 9 patients with malignancy-associated ascites. There was no evidence for bacterial peritonitis in any patients. All ascites samples contained high amounts of immunoreactive IL-6 [hepatic ascites 1730 +/- 2130 pg/ml (mean +/- SD), 1160 pg/ml (median); malignant ascites 4020 +/- 1510 pg/ml (mean), 3820 pg/ml (median)] but no IL-1. The mean ascites to serum ratios of IL-6 were 96 (median 49) in patients with hepatic ascites and 587 (median 480) in patients with malignant ascites. Ascites IL-6 was biologically active as determined by the B9 cell bioassay. The results indicate that even in the absence of infection IL-6 is produced in high amounts in the peritoneal cavity of patients with hepatic or malignant ascites.

Adult↗