Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASCITES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1995

Ascitic fluid cholesterol in malignant and tubercular ascites.

Cholesterol was estimated in ascitic fluid of 44 patients (29 malignant and 15 tubercular). Mean ascitic cholesterol level was significantly higher in malignant ascites (89.52 mg/dl) as compared to tubercular ascites (35.07 mg/dl). At a cut off value of 54.5 mg/dl (mean in tubercular ascites + 2SD), the sensitivity, specificity, positive and negative predictive value and overall diagnostic accuracy for differentiating malignant from tubercular ascites was found to be 89.65%, 100%, 100%, 83.33% and 93.18% respectively. Ascitic fluid cholesterol estimation is a reliable and simple test for differentiating malignant ascites from tubercular ascites.

Adult↗
PubMed1991

Ascitic fluid analysis for the differentiation of malignancy-related and nonmalignant ascites. Proposal of a diagnostic sequence.

The authors tried to differentiate malignancy-related from nonmalignant ascites with a sequence of sensitive followed by specific ascitic-fluid parameters. There were four results of this study. First, of nine parameters investigated in a first series of 48 patients, 28 with nonmalignant and 20 with malignancy-related ascites, ascitic-fluid cholesterol and fibronectin yielded the best negative predictive value of 92% each. Carcinoembryonic antigen (CEA) and cytologic examination both showed a positive predictive value of 100%. Second, combining cytologic examination (sensitivity, 70%) and CEA determination (sensitivity, 45%) increased the sensitivity to 80%. Third, cytologic findings were negative in all ascitic-fluid samples with a cholesterol concentration below the cutoff value of 45 mg/100 ml. Fourth, based on the results of the first series of 48 patients, the diagnostic sequence with cholesterol as a sensitive parameter, followed by the combination of cytologic examination and CEA determination as specific parameters, was tested in a second series of 71 patients, 37 with nonmalignant and 34 with malignancy-related ascites. Again cytologic examination was negative in all samples with cholesterol levels below 45 mg/100 ml. In the total of 119 patients, this diagnostic sequence did not identify 9% of patients with malignancy-related ascites, and 82% of samples classified as malignancy related by cholesterol levels above 45 mg/100 ml were confirmed by positive cytologic examination and/or CEA level above 2.5 ng/ml. Thus, a diagnostic sequence with ascitic-fluid cholesterol determination, followed by cytologic examination and CEA determination, in samples with cholesterol levels above 45 mg/100 ml should permit a cost-efficient routine differentiation of malignancy-related from nonmalignant ascites.

Adult↗
PubMed1996

Ultrasound demonstration of gallbladder wall thickening as a method to differentiate cirrhotic ascites from other ascites.

RATIONALE AND OBJECTIVES: Gallbladder wall thickness was measured by ultrasound in 16 patients with ascites caused by liver cirrhosis and in 16 noncirrhotic patients with ascites. This study was performed to evaluate if gallbladder wall thickening could differentiate cirrhotic ascites from ascites due to other causes. METHODS: Gallbladder thickness was measured by duplex ultrasound in 16 cirrhotic patients with ascites and in 16 noncirrhotic patients with ascites. Measurements of portal vein flow and serum albumin also were performed. RESULTS: Gallbladder wall thickness was 0.76 +/- 0.21 cm in cirrhotic patients and 0.24 +/- 0.09 in noncirrhotic patients (P < 0.001, Student's t test for unpaired data). Gallbladder wall thickening was significantly more frequent in patients with cirrhotic ascites than in patients with noncirrhotic ascites (P < 0.001, chi-square test). CONCLUSIONS: The authors feel that the ultrasound finding of gallbladder wall thickening in patients with ascites is highly predictive of liver cirrhosis diagnosis.

Aged↗
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↗
PubMed1991

Ascites adenosine deaminase activity is decreased in tuberculous ascites with low protein content.

The value of adenosine deaminase activity (ADA) in ascitic fluid was examined in 12 patients with confirmed peritoneal tuberculosis and compared with that of 96 patients with ascites of other different etiologies as an age-matched control group, to determine the diagnostic value of the ADA activity in tuberculous ascites. The mean adenosine deaminase activity (ADA) value in ascitic fluid of the tuberculous peritonitis group was 47.9 +/- 21.9 IU/L and in the control group 9.6 +/- 5 U/L (mean +/- SD); p less than 0.01. A different method than that usually reported in tuberculous peritonitis was used for ascites ADA estimation. The best sensitivity and specificity was obtained when greater than 32 U/L was used as a cutoff point. The ascites ADA activity correlated with the ascites total protein concentration in the tuberculosis group (r = 0.842). Our findings confirm other results and support the ADA activity determination in ascitic fluid as a useful noninvasive screening test in the diagnosis of peritoneal tuberculosis in endemic areas or in high risk patients. However, false-negative results may occur in those patients in which ascites total protein concentration is low.

Adenosine Deaminase↗
PubMed1993

Ascitic fluid cholesterol in differential diagnosis of ascites.

Cholesterol was estimated in ascitic fluid of 89 patients (29 malignant and 60 non-malignant ascites). Mean ascitic cholesterol level was significantly higher in malignant ascites (89.52 mg/dl) as compared to non-malignant ascites (29.93 mg/dl). At a cut off value of 48 mg/dl, the sensitivity, specificity, positive and negative predictive value and overall diagnostic accuracy for diagnosing malignant ascites is 96.5%, 96.6%, 93.3%, 98.3% and 96.6% respectively. Ascitic fluid cholesterol estimation is an easy and reliable test for differentiating malignant ascites from non-malignant ascites.

Ascites↗
PubMed1998

Efficacy of extracorporeal ultrafiltration of ascitic fluid as a treatment of refractory ascites.

BACKGROUND: Refractory ascites is recognized in patients with various conditions. Although intravenous reinjection of ascitic fluid after its filtration and concentration (IRA) is an effective method of treating this condition, many associated side-effects have been reported. We performed extracorporeal ultrafiltration of ascitic fluid (EUA) to demonstrate the efficacy and advantages of this method of treating refractory ascites. METHODS: EUA was performed in seven patients with hepatic cirrhosis (3 cases), lupus nephritis, diabetic nephropathy, and carcinomatous peritonitis (2 cases) for a total of 122 sessions. IRA was performed in three of these seven patients for a total of 12 sessions. RESULTS: The average volumes of ascitic fluid removed by EUA and IRA were 3.94+/-1.45 litres and 2.87+/-0.69 litres (mean+/-SD) respectively. Although chills and acute renal failure were recognized as complications of IRA in five and one sessions respectively, the only complication of EUA was severe intra-abdominal haemorrhage, which resolved spontaneously. In spite of rapid and massive removal of ascitic fluid (maximum 2.0 litres per 15 min), significant changes in blood pressure were not noted during EUA. In three patients (hepatic cirrhosis, lupus nephritis, and diabetic nephropathy), de novo production of ascitic fluid disappeared. In one patient with hepatic cirrhosis and chronic renal failure on haemodialysis, 67 sessions of EUA have been performed under stable conditions. Three patients (one case of hepatic cirrhosis and two cases of carcinomatous peritonitis) died of their primary diseases. CONCLUSIONS: We conclude that EUA is a useful method for the treatment of massive refractory ascites.

Adult↗
PubMedDate not supplied

The importance of serum and ascites fluid alpha-fetoprotein, carcinoembryonic antigen, CA 19-9, and CA 15-3 levels in differential diagnosis of ascites etiology.

BACKGROUND/AIMS: Clinical usage of tumor markers is being limited due to low specificity. Elevated plasma levels of tumor markers may be seen in diseases other than malignancy, i.e., kidney, liver or circulatory disturbances. METHODOLOGY: In our study, we studied serum and ascites fluid alpha-fetoprotein, carcinoembryonic antigen, CA 19-9, CA 15-3 levels in patients with chronic liver disease, spontaneous bacterial peritonitis, malignancy, tuberculous and congestive heart failure in a total of 76 patients. RESULTS: The sensitivity and specificity for ascites fluid alpha-fetoprotein levels were 28.5% and 100%, for serum alpha-fetoprotein levels 28.5% and 98.1%, for ascites fluid carcinoembryonic antigen levels 38.0% and 98.1%, for serum carcinoembryonic antigen levels 57.1% and 90.0%, for ascites fluid CA 19-9 levels 19.0% and 94.5%, for serum CA 19-9 levels 33.3% and 21.8%, for ascites fluid CA 15-3 levels 28.5% and 92.7%, and for serum CA 15-3 levels 47.6% and 81.8%, respectively. CONCLUSIONS: In conclusion, the sensitivity of serum and ascites fluid tumor markers was found to be low. High specificity may be due to low number of study participants. Serum and ascites fluid tumor markers are not found to be useful in the differential diagnosis of ascites etiology.

Adult↗
PubMed2004

Gemcitabine suppresses malignant ascites of human pancreatic cancer: correlation with VEGF expression in ascites.

It has been reported that vascular endothelial growth factor (VEGF) is a potent angiogenic factor that also has the ability to increase vascular permeability. VEGF plays an important role in the development of malignant ascites in various cancers. Gemcitabine has been prescribed for patients with inoperable human pancreatic ductal carcinoma as a first-line chemotherapy. However, the response rates of patients with malignant ascites who were undergoing systemic chemotherapy were extremely limited. In the present study, we investigated the role of VEGF and the effects of gemcitabine on malignant ascites of human pancreatic ductal carcinoma. As an in vitro assay, the human pancreatic cancer cell line (SUIT-2) was incubated in DMEM supplemented with serially diluted concentrations of gemcitabine for 24 h. The expression levels of VEGF in culture media were assayed using an enzyme-linked immunosorbent assay (ELISA). As an in vivo assay, a cell suspension (1 x 10(7) cells in 100 microliters PBS) was injected into the intraperitoneal region. The mice were randomly divided into two groups (control and treated with gemcitabine). The mice were sacrificed four weeks after inoculation, the ascites volume was measured, and the extent of peritoneal dissemination was examined. The expression levels of VEGF and CD31 in peritoneal nodules were examined by immunohistochemistry. In addition, secreted VEGF protein levels were quantified using ELISA. The results show that VEGF levels in the culture medium decreased in response to gemcitabine in a dose-dependent manner. The ascites formation and peritoneal dissemination within mice were suppressed by the treatment with gemcitabine. Immunohistochemical analysis suggested that expression of VEGF and CD31 in peritoneal nodules was suppressed by gemcitabine treatment, and the VEGF protein level in ascites was significantly decreased by gemcitabine (p<0.05). These results suggest that gemcitabine controls malignant ascites and peritoneal dissemination, either directly or indirectly, via VEGF. Moreover, intraperitoneal administration of gemcitabine may be a useful therapeutic approach for patients with malignant ascites in pancreatic carcinoma.

Animals↗
PubMed2000

Discrimination between malignant and nonmalignant ascites using serum and ascitic fluid proteins in a multivariate analysis model.

Our objectives were to study the value of different proteins in the serum and ascitic fluid and assess their potential in discriminating between malignant and nonmalignant ascites in a model that could be developed to aid clinical diagnosis. In all, 57 different measurements (30 in serum and 27 in ascitic fluid) including erythrocyte sedimentation rate, number of white blood cells, cytokines, interleukin-1a (IL-1a), IL-1b, IL-2, IL-6, IL-8, tumor necrosis factor-alpha, immunoglobulins (IgG, IgA, IgM), complement factors C3 and C4, acute-phase proteins such as alpha1-acid glycoprotein, alpha2-macroglobulin, alpha1-antitrypsin, haptoglobin, C-reactive protein, ferritin, ceruloplasmin and transferin, were performed in 61 patients with ascites (25 with malignant exudates, 13 with nonmalignant exudates, and 23 with transudates). Patients with sepsis were excluded. Correlation tests and one-way ANOVAs were used for comparisons between different groups. Discriminant analyses were used to assess the significance of each parameter in the differentiation process. Correct classification of 100% of cases required the use of all 57 ascitic fluid measurements in the model, which was not considered practical in clinical diagnosis. Discriminant analysis showed that five ascitic fluid measurements-total protein, LDH, TNF-alpha, C4, and haptoglobin-were sufficient for a model to correctly classify 89% of cases. Cross-validation showed that 70% of unknown cases were correctly classified using this model. In conclusion, we have shown that five easily taken protein measurements in the ascitic fluid can differentiate to a large extent between cases with ascites and have proposed a relatively simple statistical model with these parameters that could be developed to be extremely useful in the clinical setting.

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↗
PubMed1987

[The management of malignant ascites with a streptococcal preparation, OK-432: relation between the clinical effect and auto-tumor cell killing activity by OK-432-induced ascites-derived lymphocytes].

Twelve patients with malignant ascites caused by gastro-intestinal cancer were treated by intraperitoneal administration of OK-432. Tumor cells from these patients were separated from ascitic fluid and cultured in vitro before OK-432 therapy. OK-432 was given intraperitoneally one to two times a week at doses ranging from 5 to 20 KE suspended in saline. Mononuclear lymphocytes were collected from the fluid at various intervals throughout the therapy. The effect of ascites-derived lymphocytes on ascites-derived autologous tumor cell growth was studied in vitro using microplate assay. Nine (responders) of 12 patients showed complete disappearance or significant reduction of ascitic fluid. Ascites-derived lymphocytes slightly inhibited autologous tumor cell growth only in one case before OK-432 therapy. Lymphocytes collected from ascites after OK-432 injection significantly inhibited auto-tumor cell growth in all of 9 responders. In 3 non-responders, however, auto-tumor cell growth inhibition was found only in one case. Interestingly, lymphocytes from non-responders significantly inhibited the growth of tumor cells taken from responders. Conversely, lymphocytes from responders did not inhibit non-responder-derived tumor cell growth. These findings imply that auto-tumor killing by OK-432-induced lymphocytes may depend more on the condition of the tumor cells than on the condition of the lymphocytes, and that the measurement of auto-tumor killing activity by ascites-derived lymphocytes may be useful as an indicator in OK-432 therapy.

Abdominal Neoplasms↗