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At least 19 recordsLinked to original sources
PubMed1978

Quantitation of secretory component levels in cyst fluids, ascitic fluids, and sera from ovarian adenocarcinoma patients.

A secretory component (SC) was detected by radioimmunoassay in the cyst fluids, ascitic fluids, and sera from patients with ovarian adenocarcinomas. Serous cyst fluids and ascitic fluids showed lower levels (expressed as means +/- SE) of SC (1.37 +/- 0.37 and 1.24 +/- 0.24 microgram/ml, respectively) than mucinous cyst fluids (181.50 +/- 50.40 microgram/ml). SC levels in the sera of all patients with ovarian adenocarcinoma were high (12.67 +/- 1.43 microgram/ml) when compared to SC levels in the sera of normal individuals (2.34 +/- 0.41 microgram/ml). Sera from patients with ovarian cancers diagnosed as serous, mucinous, papillary, and poorly differentiated adenocarcinomas showed SC levels of 9.93 +/- 1.68, 22.44 +/- 3.24, 7.35 +/- 1.13, and 10.10 +/- 1.58 microgram/ml, respectively.

Adenocarcinoma↗
PubMed1986

Coagulant, fibrinolytic, and aggregating activity in ascitic fluid.

Ascitic fluid samples from 14 subjects with liver cirrhosis and from 13 patients with malignancy were investigated. Activated FX was present in ascitic fluid in small quantities with a mean value of 8.7 10(-3) IU/ml. The mean thrombin activity was 70.8 10(-3) IU/ml and the mean plasmin activity was 449.6 10(-3) CU/ml. High levels of fibrin/fibrinogen degradation products (mean 75.4 micrograms/ml) and of antithrombin III (mean 43.4%) were found. No statistically significant differences between values in liver cirrhosis and in malignancy were found. In 15 of 17 experiments 10-fold concentrated ascitic fluid caused irreversible platelet aggregation and [14C] serotonin release of normal platelet-rich plasma similar to collagen. The aggregating effect disappeared after addition of collagenase. These results do not support the concept that the coagulopathy after peritoneovenous shunting is a result of direct and rapid intravenous infusion of procoagulant substances. They rather point to a central role of collagen present in ascitic fluid.

Ascitic Fluid↗
PubMed1984

Some aspects of the composition of avian ascitic fluid.

Ascitic fluid from male Single Comb White Leghorn chickens fed a diet containing 20% by weight rapeseed oil rich (51.6 weight percent) in erucic (22:1n9) acid contained 2.84 +/- .09 g/dl protein and 2.55 +/- .22 micrograms/ml DNA. A characteristic feature of ascitic fluid as compared to liver and plasma was its high polyunsaturates, low saturates, and low saturate to unsaturate ratio. In general, the fatty acid profile of ascitic fluid is more comparable to the fatty acid profile of plasma lipids than to that of liver lipids. These data suggest that there is no direct absorption of fat and transfer to the ascitic fluid.

Animal Feed↗
PubMed1988

Detection of human ovarian tumor-associated antigens by antibodies isolated from ovarian carcinoma ascitic fluid.

Ascitic fluid from patients with ovarian epithelial cancer contains large amounts of soluble immune complexes and is a potential source of antibodies and antigens associated with the tumor. The antibodies against tumor-associated antigens were purified from the ascitic fluids of patients with ovarian serous cystadenocarcinoma. These antibodies showed specificity toward ovarian epithelial cancer when tested against ovarian tumor cell lines and paraffin-embedded tissue sections of ovarian cancer. The antigens in sera of patients were separated from IgG and IgG complexes by affinity chromatography and the free antigens were isolated. With the antibodies purified from ascitic fluid, the levels of tumor-associated antigens in sera of 10 patients with serous cystadenocarcinoma and 12 control patients were detected by an enzyme-linked immunosorbent assay. The antigens in patients with ovarian epithelial cancer were 2 to 10 times higher than those in control patients. These studies demonstrate that the antibodies isolated from ascitic fluid detect the tumor-associated antigens on tumor cells as well as the shed antigens present in serum.

Antibodies, Neoplasm↗
PubMedDate not supplied

Identification of transforming growth factor-beta and interleukin-6 in chicken ascites fluid.

Ascites fluids from chickens were analyzed for the occurrence of transforming growth factor-beta (TGF-beta) and interleukin-6 (Il-6) using the mink lung epithelial cell inhibition and B9 hybridoma proliferation assays, respectively. Both of these cytokines were significantly elevated in ascites fluids (TGF-beta, 0.129 +/- 0.017 ng/mg protein; Il-6, 0.054 +/- 0.011 ng/mg protein) relative to serum (TGF-beta, 0.005 +/- 0.003 ng/mg protein; Il-6, < 0.002 ng/mg protein) derived from the same individual birds. TGF-beta occurred in a latent form and required activation by heat or acid (heat, 100%; non-activated, 5.2 +/- 1.1%; acid-activated, 89.5 +/- 12.3%). Heat treatment destroyed Il-6 activity. Both TGF-beta and Il-6 activities could be neutralized by antibodies directed against the recombinant human counterpart of these cytokines. Increasing dilutions of ascites fluid caused proportionate decreases in cytokine activities. Il-6 activity was further characterized by gel filtration using high-pressure liquid chromatography, which yielded a peak of biological activity corresponding to an approximate molecular weight of 35,000. These data suggest that ascites fluid may be an interesting biological model and source for studying avian cytokines and their physiological relevance.

Animals↗
PubMed1978

Immunosuppressive activity and tissue polypeptide antigen content of human ascitic fluids.

Ascitic fluids from patients with cancer, cirrhosis, and congestive heart failure and from a patient with noninfectious tuberculosis contain measurable levels of tissue polypeptide antigen (TPA). Only the cancer patients had levels higher than 2.0 microgram TPA per ml. The average TPA levels of 29 cancer patients was 6.4 microgram/ml compared to 0.9 microgram/ml for the controls. Seventeen of 22 cancer ascitic fluids and 7 of 9 fluids from patients with liver disease were immunosuppressive as measured by the inhibition of [3H]thymidine incorporation into phytohemagglutinin-stimulated lymphocytes. Fluids from a patient with congestive heart failure and a patient with noninfectious tuberculosis were not suppressive. We were unable to obtain a significant correlation coefficient between immunosuppression and TPA levels in these fluids. In addition, TPA levels remained constant over a period of 18 months of testing, whereas the in vitro immunosuppressive activity was lost in 9 to 10 months. Sephadex G-200 fractionation of the ascitic fluid resulted in the TPA and immunosuppressive activity eluting in the first large molecular weight peak from the column. Although the 2 activities eluted together in this fractionation, the data suggest that TPA is not responsible for the immunosuppression.

Antigens↗
PubMed1988

Plasminogen activators and plasminogen activator inhibitor in malignant and non-malignant ascitic fluid.

Ascitic fluid from tumour patients (hepatoma, gastric cancer, gallbladder cancer, colorectal cancer, ovarian cancer) and from non-malignant diseases (liver cirrhosis, congestive heart failure) were compared with respect to their content of determinants of the fibrinolytic system, tissue-type plasminogen activator antigen (t-PAag) and activity (t-PAact), urokinase-type plasminogen activator antigen (u-PA) and plasminogen activator inhibitor activity (PAI). Furthermore, SDS-polyacrylamide slab-gel electrophoresis (SDS-PAGE) was performed to evaluate molecular weight distribution of the detectable fibrinolytic parameters. In malignant ascites, PAI activity was three to four times higher, and increased complex formation of PAI with t-PA could be demonstrated, compared with non-malignant ascitic fluid. Tissue-type plasminogen activator antigen and activity showed a similar concentration in ascites of both study groups. Urokinase-type plasminogen activator antigen was detectable neither in ascites of malignant nor in ascites of non-malignant origin. It is concluded that t-PA is the physiological plasminogen activator in ascites and that increased PAI levels followed by increased complex formation between t-PA and PAI might reflect a reaction of the peritoneum.

Adult↗
PubMed1967

Friend Leukemogenic Virus-neutralizing Antibody from Mouse Ascitic Fluid.

Ascitic fluid antibody produced in C57/B1 mice immunized with Friend leukemogenic virus exhibited potent neutralizing activity. In vitro neutralization tests revealed that a mean neutralization index of 3.0 was achieved, and it was shown by sucrose gradient ultracentrifugation that this antibody resembled the 7S type. A mean yield of 6.7 ml of fluid per mouse per weekly paracentesis was obtained over an 8-week period. The ascitic fluid antibody to Friend virus was also active in vivo. Mice given antibody 3, 5, 7, and 9 days after infection with Friend virus did not develop the splenomegaly characteristic of Friend disease.

Journal Article↗
PubMed1987

[Can the protein concentration of the ascitic fluid in ascites predict the occurrence of an infection?].

In cirrhotic patients, spontaneous bacterial peritonitis is frequent and severe. This study was performed to determine if low protein concentration in ascitic fluid on admission could predict the occurrence of spontaneous bacterial peritonitis during hospitalization. Ninety-two cirrhotic patients with ascites, without spontaneous bacterial peritonitis were studied. Bacteriologic study and cultures of ascitic fluid were performed on admission and repeated every 5 days, and if any suspicion of infection occurred; 11 patients developed spontaneous bacterial peritonitis during hospitalization. Among the 92 patients in the study, protein concentration in ascitic fluid was initially less than 10 g/l in 45 and 10 of these 45 patients (22 p. 100) developed spontaneous bacterial peritonitis during hospitalization; protein concentration in ascitic fluid was initially greater than 10 g/l in 47 patients; only one of these 47 patients (2.1 p. 100) developed spontaneous bacterial peritonitis during hospitalization. This difference (22 p. 100 vs 2.1 p. 100) was significant (p less than 0.01). Ascitic fluid protein concentration (6.9 +/- 2.3 g/l) was significantly lower (p less than 0.01) in the spontaneous bacterial peritonitis group than in patients without peritonitis (13.8 +/- 10.5 g/l). These results suggest that: 1) ascitic fluid protein concentration on admission is lower in patients who will develop spontaneous bacterial peritonitis during hospitalization than in patients without infection and 2) patients with ascitic fluid protein concentration under 10 g/l on admission represent an high risk group for spontaneous bacterial peritonitis.

Ascitic Fluid↗
PubMed1986

Immediate diagnostic criteria for bacterial infection of ascitic fluid. Evaluation of ascitic fluid polymorphonuclear leukocyte count, pH, and lactate concentration, alone and in combination.

We prospectively evaluated the ascitic fluid (AF) polymorphonuclear cell (PMN) count, pH, and lactate concentration in single ascitic fluids from 60 patients to determine their relative predictive values for the immediate diagnosis of ascitic fluid infection. Nine of the 60 ascitic fluids were malignant. Of the remaining 51 samples, nine from cirrhotic patients were infected. The mean AF pH, lactate concentration, and PMN count in the infected group were 7.20 +/- 0.19, 80 +/- 51 mg/dl, and 18,199 +/- 19,650 cells/mm3, respectively, and all were significantly different from the corresponding values in noninfected ascites. Mean arterial blood-ascitic fluid (B-AF) pH and lactate gradients in the infected group were 0.23 +/- 0.17 and -46 +/- 31 mg/dl, respectively, and were significantly different from the corresponding values in noninfected ascites (p less than 0.05). Significant differences were not found between infected and malignant ascites, except for the AF PMN count (p less than 0.001). In cirrhosis with ascites, an AF pH less than or equal to 7.34 was the most specific single test (100%) and had the highest diagnostic accuracy (98%). In the larger group of patients with ascites of diverse etiology, a B-AF pH gradient greater than or equal to 0.10 or an AF PMN count greater than or equal to 500 cells/mm3 were the single tests with the highest diagnostic accuracy (92%). Combining an AF PMN count greater than 500 cells/mm3 with any of the other diagnostic criteria increased the specificity and diagnostic accuracy (up to 98%) compared to the best single criterion. Although our data support the use of a number of different combinations of AF measurements for the immediate diagnosis of infection, the simplest and most readily obtainable measurements are the pH and PMN count. Therefore, in the clinical setting we recommend the use of either an AF pH less than or equal to 7.34 or a B-AF pH gradient greater than or equal to 0.10 in combination with an AF PMN count greater than 500 cells/mm3 to obtain the highest degree of accuracy in the immediate diagnosis of ascitic fluid infection.

Adult↗
PubMed1991

Ascitic fluid pH and lactate: insensitive and nonspecific tests in detecting ascitic fluid infection.

Ascitic fluid pH and lactate concentration have been proposed as useful tests for the detection of ascitic fluid infection. However, past studies involved small numbers of infected patients, and all did not use optimal culture techniques. This large study was performed using highly sensitive culture methods and sought (a) to compare the sensitivity, specificity and accuracy of pH and lactate to that of the ascitic fluid neutrophil count and (b) to determine whether evaluation of ascitic fluid pH or lactate (or arterial-ascitic fluid pH or lactate gradient) would result in improved decision-making regarding empirical treatment of suspected ascitic fluid infection. Analysis of 206 ascitic fluid specimens obtained in 175 patients, including 101 infected specimens, revealed that ascitic fluid (or arterial-ascitic fluid) pH and lactate were less than 50% sensitive in detecting bacterial peritonitis and that these tests did not improve clinical decision-making about empirical treatment of suspected ascitic fluid infection. Although statistically significant differences in ascitic fluid pH were detected between infected samples and control samples, these differences did not appear to be clinically helpful. The ascitic fluid pH was 0% sensitive in detecting the presence of bacteria in the absence of neutrophils (i.e., no such specimens had a pH lower than 7.35). Ascitic fluid pH correlated well with neutrophil count and appears to be, at least in part, an indirect measure of the presence of neutrophils in ascitic fluid. Measurement of pH or lactate (or arterial-ascitic fluid gradients) is not helpful in the clinical management of infected ascitic fluid.

Ascites↗
PubMed1980

Variability of hydrostatic hepatic vein and ascitic fluid pressure, and of plasma and ascitic fluid colloid osmotic pressure in patients with liver cirrhosis.

The variability of hydrostatic hepatic vein and ascitic fluid pressures and of plasma and ascitic fluid colloid osmotic (oncotic) pressures was assessed during hepatic venous catheterization by repeated measurements on different days and at different locations in patients with cirrhosis of the liver. Furthermore, calculation of oncotic pressure from protein determinations was compared to the directly measured value of plasma and ascitic fluid samples. Repeated measurements of hydrostatic pressure in the same hepatic vein within 15 min showed a standard deviation (SD) below 1 mmHg. The variation in hydrostatic hepatic vein pressures, pressure differences and ascitic fluid pressures (when measured at different locations within the liver and peritoneal space during a single examination) was 1.5, 1.0 and 1.0 mmHg (SD), respectively. When measured on different days, the variation of hydrostatic hepatic vein pressures, pressure differences and ascitic fluid pressures was 2.5, 1.6 and 1.3 mmHg (SD), respectively. Repeated measurements of oncotic pressure on the same plasma sample varied 0.3 and 0.6 mmHg (SD) when measured on the same day and a subsequent day, respectively. The variation in plasma and ascitic fluid oncotic pressure, when measured on samples obtained on different days, was 2.0 and 0.6 mmHg, respectively. The error of oncotic pressure calculated from protein determinations was 2.9 and 1.3 mmHg (SD) for plasma and ascitic fluid, respectively. It is concluded that measurements during catheterization give a good reproducibility in determination of the hydrostatic pressures in hepatic vein and ascitic fluid and of the colloid osmotic (oncotic) pressure in plasma and ascitic fluid in the resting supine patient with cirrhosis, which substantiates the use of measurements during a short period as representative for the patients long-time level.

Ascitic Fluid↗
PubMed1994

Phenotypic characteristics of mononuclear cells in human ovarian tumors - with special reference to cystic and ascitic fluid.

The occurrence of mononuclear cells and their cell-surface phenotype was studied in cryo- and paraffin sections in 26 untreated ovarian tumors and in normal ovarian tissue. T cells (positive for CD4 or CD8 markers) were sparsely represented in all sections of normal ovarian tissue and benign ovarian tumors, and in most ovarian cancer sections. B cells were found in three malignant tumors, CD57-positive (natural killer) cells in two, and CD25 (interleukin-2 receptor)-positive cells in one. Macrophages occurred sparsely both in normal ovarian tissue and in benign and malignant ovarian tumors. One endometrioid ovarian cancer, however, manifested rich infiltration of T cells (predominantly positive for CD8 marker). Cystic fluid from malignancies manifested higher prostaglandin concentrations and total cell counts than did benign cystic fluid, but sparse lymphocytes as a rule (5-10% of the total cell count). As compared to cystic fluid, ascitic fluid had higher concentrations both of prostaglandins and cells, with up to 25% lymphocytes in connection with malignancies. Immunogenic activity thus would appear to be weak in ovarian cancer. The harvest of tumor-infiltrating lymphocytes (TIL) from cystic fluid in ovarian cancers is moderate, compared to that of tumor-associated lymphocytes (TAL) from corresponding ascitic fluid samples.

Journal Article↗
PubMed2001

Tumor necrosis factor-alpha, interleukin-6, and nitric oxide in sterile ascitic fluid and serum from patients with cirrhosis who subsequently develop ascitic fluid infection.

Ascitic fluid infection probably results from repeated episodes of bacteremia and seeding of ascitic fluid. The outcome of these episodes of colonization is probably a function of serum and ascitic fluid defense mechanisms and the virulence of the organism. Patients who develop spontaneous bacterial peritonitis may have serum and ascitic fluid characteristics that are different from those who do not develop infection. We prospectively collected serum and ascitic fluid specimens at the time of admission from patients with sterile cirrhotic ascites, and tested these specimens for interleukin-6, tumor necrosis factor-alpha, and nitric oxide and compared these results as well as other characteristics of patients who did not develop infection to those who did. An elevated baseline serum tumor necrosis factor-alpha as well as an increased proportion of polymorphonuclear leukocytes in sterile ascitic fluid from patients who subsequently developed infection probably represent a subclinical activation of defense mechanisms from prior silent colonizations with bacteria.

Adult↗
PubMed1992

Enhancement of normal polymorphonuclear cells respiratory burst in ascitic fluid by fibronectin. Comparison between cirrhotic and malignant ascitic fluids.

The chemiluminescence (CL) response of normal peripheral blood polymorphonuclear cells (PMN) in ascitic fluids (cirrhotic = 32; malignant = 17) was studied independently of the ascitic fluid complement activity. CL response and fibronectin levels were higher in malignant ascitic fluid than in cirrhotic ascitic fluid (p less than 0.001). Addition of pure fibronectin or malignant ascitic fluids to cirrhotic ascitic fluids increased the CL response of normal PMN. These findings suggest that the susceptibility of cirrhotic patients to spontaneous bacterial peritonitis (SBP) is a multifactorial defect involving factors distinct from low C3 levels. Fibronectin is an important factor in the promotion of the respiratory burst of normal PMN stimulated by opsonized zymosan or PMA in ascitic fluid. Our results suggest that low levels of ascitic fluid fibronectin could partly explain the high susceptibility of cirrhotic patients to spontaneous bacterial peritonitis.

Adult↗