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At least 469 records · Page 26Linked to original sources
PubMed1982

Mononuclear-cell infiltration in ovarian cancer. II. Immune function of tumour and ascites-derived inflammatory cells.

Mononuclear cell fractions were isolated from blood, ascites and solid tumours of patients undergoing surgery for Stages III and IV adenocarcinoma of the ovary, and evaluated for their response in NK, ADCC and PHA assays. Control experiments with the same fraction of normal blood indicated that these responses were not influenced by the enzymes used to isolate the tumour and ascites inflammatory cells. The inflammatory cell fractions isolated from both tumour sites which sedimented in the velocity range of blood mononuclear cells were adequate in number and composition for comparison with similar cells from blood. E RFC values in both ascites and tumour fractions exceeded those of patient blood. However, there was a marked difference in distribution of the T subsets between blood, ascites and tumour, which could cause the variable test results between the different cell sources. PHA responses of patient blood and ascites fractions were about half that of normal blood. Tumour-infiltrating lymphocytes (TIL) were less than 10% as responsive as normal blood. The depressed PHA responses of the TIL were not due to the presence of a suppressor cell population. NK activity of patient blood was less than that of normal blood, but not as much as the ascites of TIL cells. The activity of the ascites-derived lymphocytes was enhanced by treatment with interferon. ADCC activity against both CRBC and SB cells was normal or higher than controls in patient blood, and depressed in the ascites-derived fractions. TIL responded to less than 10% of the patient blood values. The results indicate a lack of response by ascitic and TIL cells in assays dependent on FcR-bearing effector cells and a greater loss of PHA-reactive cells from the tumour than from blood and ascites. These data could result from intratumour inactivation, or a failure of the particular subset to localize either in the ascites or the tumour site.

Adenocarcinoma↗
PubMedDate not supplied

The effect of ascites, mass volume, and peritoneal carcinomatosis on serum CA125 levels in patients with ovarian carcinoma.

The aim of this study is to investigate the effects of ascites, ovarian mass volume, and peritoneal carcinomatosis on serum CA125 levels in patients with nonmucinous epithelial ovarian carcinoma. Serum CA125 levels were determined by a commercial enzyme immunoassay kit in a series of 98 patients with stage I-IV nonmucinous epithelial ovarian carcinoma. Amounts of ascites were determined in each patient with ascites. Ovarian mass volumes were calculated in 22 patients with stage I disease without ascites. Peritoneal carcinomatosis was detected in 35 ovarian cancer patients. Serum CA125 levels were compared among the patients with different clinical conditions. Serum CA125 levels were significantly higher in cases of ovarian cancer with ascites when compared with those without ascites (P < 0.01). Abnormal levels of serum CA125 were found in 80% of all patients; these abnormal levels were detected in 92% and 97% of the patients with ascites and with peritoneal carcinomatosis, respectively. A positive correlation between serum CA125 levels and ascites amounts was found in patients with ascites (P < 0.01, r = 0.74). However, there was no correlation between ovarian mass volumes and levels of serum CA125 in patients having stage I disease but no ascites (P = 0.5, r = 0.15). Our results showed that serum CA125 levels might be affected by the amount of ascites and the presence of peritoneal carcinomatosis but not with ovarian mass volume. However, these findings need to be confirmed in more and larger studies. These results may be beneficial in the management of ovarian carcinoma patients with elevated CA125 levels.

Adult↗
PubMed2003

Haematological characteristics predicting susceptibility for ascites. 2. High haematocrit values in juvenile chickens.

1. Male broilers of two different genetic stocks, a pure broiler sire line (A) and commercially available Ross broilers (B), were used to study the effect of differences in haematocrit values in 12-d-old chickens on the development of ascitic symptoms. Body weight gain (BWG), feed intake (FI) and feed conversion ratio (FRC) were measured from 2 to 5 weeks of age. Mortality was recorded from 2 to 6 weeks. The birds were kept at a low ambient temperature to stimulate the incidence of ascites. 2. From each stock 32 birds with the highest (High Ht) and 32 birds with the lowest (Low Ht) haematocrit values in venous blood were selected at 12 d of age for an examination on susceptibility for the ascites syndrome at 5 weeks. 3. At 2 weeks 448 birds per stock (including High Ht and Low Ht birds) were allotted to 32 floor pens (1 High Ht and 1 Low Ht in each pen). Venous blood samples were taken weekly in High Ht and Low Ht birds for haematocrit measurements and at week 5 also thyroid hormone (T3, T4) concentrations in plasma were measured. At 5 weeks all High Ht and Low Ht birds were examined post-mortem and arterial pressure index, heart weight, lung weight and liver weight (all relative to body weight) were recorded. High values for arterial pressure index, relative heart and liver weights and low values for relative lung weights and plasma thyroid hormone were considered to be indicators for ascites susceptibility. 4. Stock A, with the highest ascites mortality, had lower values for BWG and FCR than stock B. Throughout, a clear difference in Ht values between High Ht and Low Ht birds was maintained. No significant effects of 12-d haematocrit values were found on the incidence of ascitic symptoms until week 5. High Ht values tended to correlate with low relative lung weights and low plasma T3 concentrations in High Ht birds. 5. Within the groups of selected birds, there was an effect of stock on ascitic symptoms (arterial pressure index, relative heart weight and T3 values) at week 5. This is consistent with a higher ascites mortality in flock A than in flock B, over the whole period up to 6 weeks. Until 4 weeks both A and B were similar with respect to mean Ht values of High Ht and Low Ht groups. After 4 weeks Ht values were very high in the High Ht birds of stock A, possibly as a result of the susceptibility for ascites of stock A. There was a significant interaction between stock and Ht values on the ascites-related variable arterial pressure index. Only in stock A was high arterial pressure at 5 weeks related to high Ht values at d 12. 6. Overall it was concluded that a high Ht in blood of juvenile chickens has limited practical value in predicting incidence of ascites at 5 weeks of age.

Animals↗
PubMed2005

Genetic parameters of ascites-related traits in broilers: correlations with feed efficiency and carcase traits.

(1) Pulmonary hypertension syndrome followed by ascites is a metabolic disorder in broilers that occurs more often in fast-growing birds and at cool temperatures. (2) Knowledge of the genetic relationships among ascites-related traits and performance traits like carcase traits or feed efficiency traits is required to design breeding programmes that aim to improve the degree of resistance to ascites syndrome as well as production traits. The objective of this study was to estimate these genetic correlations. (3) Three different experiments were set up to measure ascites-related traits (4202 birds), feed efficiency traits (2166 birds) and carcase traits (2036 birds). The birds in different experiments originated from the same group of parents, which enabled the estimation of genetic correlations among different traits. (4) The genetic correlation of body weight (BW) measured under normal conditions and in the carcase experiment with the ascites indicator trait of right ventricle to total ventricle ratio (RV:TV) measured under cold conditions was 0.30. The estimated genetic correlation indicated that single-trait selecting for BW leads to an increase in occurrence of the ascites syndrome but that there are realistic opportunities of multi-trait selection of birds for improved BW and resistance to ascites. (5) Weak but positive genetic relationships were found between feed efficiency and ascites-related traits suggesting that more efficient birds tend to be slightly more susceptible to ascites. (6) The relatively low genetic correlation between BW measured in the carcase or in the feed efficiency experiments and BW measured in the ascites experiment (0.49) showed considerable genotype by environment interaction. (7) These results indicate that birds with high genetic potential for growth rate under normal temperature conditions have lower growth rate under cold-stress conditions due to ascites.

Animal Nutritional Physiological Phenomena↗
PubMed2006

Echocardiographic characteristics of chickens with ascites syndrome.

1. B- and M-mode echocardiography was used to compare cardiac function in broilers with spontaneous ascites syndrome with that of normal chickens. 2. Thirty ascitic chickens and 15 normal chickens aged three, 4, 5, and 6 weeks from the same flock (180 birds in total) were examined. They were restrained gently in a natural standing position, and echocardiographs were obtained from a 7.0-MHz linear transducer placed on the left pectoral apterium. Indices of cardiac structure and functioning were calculated from the echocardiographs, and some were normalised to body weight. Heart rate was also measured. 3. All cardiac structural indices in both ascitic and normal chickens increased with age. Compared with normal chickens, right ventricular diameter at the end of systole in ascitic chickens was greater at 4, 5 and 6 weeks of age. Ventricular septal thickness at the end of both systole and diastole was greater in ascitic chickens at 5 and 6 weeks. Left ventricular free wall thickness at the end of diastole was less in ascitic chickens at 3 weeks. However, all the structural indices decreased with age after normalisation with body weight. 4. The heart rate of ascitic chickens was lower at 4, 5 and 6 weeks. Normalised left ventricular fractional shortening was lower in ascitic chickens at 4, 5 and 6 weeks, as was normalised right ventricular fractional shortening. Incrassation of the ventricular septum (Delta T), which changed little in normal chickens, was less at 4, 5 and 6 weeks in ascitic chickens. Left ventricular fractional shortening, right ventricular fractional shortening and Delta T were all negatively correlated with ascites heart index at all ages. 5. Taken together the results suggest heart failure of both ventricle, but that right ventricular dysfunction is more extensive than left ventricular dysfunction. We suggest that secondary pulmonary hypertension would result in these ascitic chickens due to volume overload.

Animals↗
PubMed1996

Tumor necrosis factor effects on ascites formation in an experimental tumor model.

In humans, treatment of malignant ascites with bolus TNF leads to resolution of the ascites. In an experimental model NMRI nude mice were inoculated intraperitoneally with human NIH-OVCAR3 adenocarcinoma cells, resulting in production of ascites and intraperitoneal tumor growth. Ascites formation and tumor growth after IP injection of recombinant human TNF was determined. Depending on the treatment schedule, a dual effect of TNF on the development of ascites was seen. Doses of TNF (1-10 micrograms/g) given once per week completely prevented ascites production, whereas the same doses of TNF given on a daily schedule induced enhanced ascites formation in an inverse TNF dose relationship. The area of tumor cell-covered peritoneal lining corresponded to these findings, indicating a correlation of tumor mass with ascites production. In an attempt to prevent renewal of ascites after drainage, neither inhibition nor enhancement in ascites production was seen when TNF was given five times per week. However, doses of 10 micrograms/g of TNF once per week led to almost complete inhibition of ascites reappearance. Histological examination of animals that received repeated TNF treatment demonstrated chronic peritonitis with strong stromal proliferation, angiogenesis, and increased adhesion of tumor cells to the peritoneum.

Animals↗
PubMed1997

Spontaneous ascitic infection in different cirrhotic groups: prevalence, risk factors and the efficacy of cefotaxime therapy.

OBJECTIVE: To investigate the prevalence of spontaneous ascitic infection (SAI) in different cirrhotic groups, the risk factors for development of SAI, and the efficacy of cefotaxime therapy. DESIGN: A prospective study. SETTING: In-patient clinic of a university hospital. PATIENTS: Eighty cirrhotic patients with ascites were assigned to four groups: hepatitis B or D virus-related 34, alcoholic 18, hepatitis C virus-related 14, miscellaneous 14. INTERVENTIONS: Paracentesis was performed on 80 patients during 92 consecutive hospitalizations. Ascitic fluid was cultured by the method of bedside inoculation of blood culture bottles with ascites. The patients with SAI were treated with cefotaxime (2 g, three times daily, intravenously) for 5 days. MAIN OUTCOME MEASURES: Frequency of SAI in cirrhotic groups; clinical, bacteriological and biochemical findings of SAI; rate of recovery-from infection. RESULTS: Twenty SAI episodes (22%) were found in 16 patients; 8 episodes were spontaneous bacterial peritonitis, 2 bacterascites, and 10 culture-negative neutrocytic ascites. SAI occurred more frequently in patients with hepatitis B or D virus-related liver cirrhosis (32%) than in the alcoholic (6%, P < 0.05), hepatitis C virus-related (14%) or miscellaneous (14%) cirrhotic groups in multivariate analysis, independent predictive factors associated with the development of SAI are chronic hepatitis B virus infection, ascitic fluid total protein and serum bilirubin. Escherichia coli was obtained in 5 of 10 positive ascitic fluid cultures. Cure of the infection was achieved in 95% of episodes. Hospitalization mortality rate in infected patients was 20%. CONCLUSION: Spontaneous ascitic infection occurs in approximately 20% of cirrhotic patients hospitalized with ascites. The patients with low ascitic protein concentration, high serum bilirubin level or hepatitis B virus cirrhosis are more predisposed to SAI. Cefotaxime may be an effective first-choice antibiotic for ascitic fluid infection.

Adult↗
PubMed2005

Haeme oxygenase mediates hyporeactivity to phenylephrine in the mesenteric vessels of cirrhotic rats with ascites.

BACKGROUND AND AIMS: Haeme oxygenase could play a role in the pathogenesis of arterial vasodilation in cirrhosis. The aim of this study was to verify the role of haeme oxygenase in the hyporesponsiveness to phenylephrine of small mesenteric arteries in rats with CCl(4) induced cirrhosis, with and without ascites. METHODS: Pressurised small resistance mesenteric arteries were challenged with increasing doses of phenylephrine. Dose-response curves were evaluated under basal conditions, after inhibition of haeme oxygenase with chromium-mesoporphyrin, after inhibition of nitric oxide synthase (NOS) with N(G)-nitro-L-arginine-methyl-ester (L-NAME), and then after inhibition of both NOS and haeme oxygenase. Haeme oxygenase protein expression was also analysed. RESULTS: Twenty six control rats and 35 rats with cirrhosis (17 with and 18 without ascites) were studied. Response to phenylephrine was lower in non-ascitic and ascitic cirrhosis than in controls. Chromium-mesoporphyrin increased the response to phenylephrine only in ascitic cirrhosis (p<0.001). L-NAME increased the response to phenylephrine in controls (p<0.001) and in ascitic and non-ascitic cirrhosis (p = 0.002, p<0.001, respectively) but the final response in non-ascitic cirrhosis was similar to that of control rats while it remained impaired in ascitic cirrhosis. Addition of chromium-mesoporphyrin to L-NAME improved the response to phenylephrine in ascitic cirrhosis (p<0.01), with final values not different from those of the other two groups. Protein expression of the inducible isoform of haeme oxygenase was increased in the mesenteric vessels of cirrhotic rats. CONCLUSION: Haeme oxygenase mediates hyporeactivity to phenylephrine in the mesenteric vessels of experimental cirrhosis with ascites. NOS plays a major role only in the first stage of the disease.

Animals↗
PubMed2000

Correlation between increased colloid osmotic pressure and the resolution of refractory ascites after transjugular intrahepatic portosystemic shunt.

BACKGROUND: This study compared the changes in serum albumin, globulin, and colloid osmotic pressure (COP) before and after transjugular intrahepatic portosystemic shunt (TIPS) or large volume paracentesis (LVP) in patients with ascites. METHODS: Of 23 patients with refractory ascites, 17 had TIPS and 6 had LVP with infusion of albumin. Colloid osmotic pressure measurements were calculated, using the formula previously proposed by Hoefs: COP = A (1.058G + 0.163A + 3.11) where A = serum albumin and G = serum globulin. RESULTS: After 1 month, ascites resolved in 9 of the 17 patients who had TIPS and in none of the 6 who had LVP. Colloid osmotic pressure increased significantly in patients whose ascites resolved after TIPS. Colloid osmotic pressure did not change in the patients whose ascites did not resolve after TIPS, and COP decreased significantly in the LVP group. A statistically significant difference was found in the pre-TIPS COP measurements between those patients who had resolution of ascites and those who did not. A pre-TIPS COP of < or =20 mm Hg predicted resolution of ascites with an 88% sensitivity and a 78% specificity. CONCLUSIONS: Serum COP increased significantly in patients with resolution of ascites but remained unchanged in patients with persistent ascites after TIPS. Serum COP decreased after LVP. A statistically significant difference in the pre-TIPS COP was found between patients whose ascites resolved and patients having persistent ascites.

Adult↗
PubMedDate not supplied

Suppression of ascites formation and re-accumulation associated with human ovarian cancer by an anti-VPF monoclonal antibody in vivo.

Ascites formation is often observed in ovarian cancer patients. Vascular permeability factor (VPF) may induce ascites formation. We established an animal model of ascites formation and re-accumulation by i.p. transplantation of a human ovarian adenocarcinoma cell line, NOS2, into nude mice. The formation of ascites was observed after 10 days of tumor inoculation and continued for up to 4 weeks. In the ascitic fluid, biologically active VPF was detected. The repeated i.p. administration of an immunoneutralizing monoclonal antibody (MAb) to VPF, MV833, significantly inhibited the formation of ascites throughout the experiments. Re-accumulation of ascites occurred quickly in control mice after aspiration of ascites and these mice died within 20 days. MV833 again inhibited the re-accumulation of ascites and significantly prolonged the life span of mice without any side effect. These results indicate that VPF plays an important role in the accumulation of ascites induced by ovarian cancer and an anti-VPF MAb is a new specific drug to suppress the formation and re-accumulation of ascites. This MAb may contribute to ameliorating quality of life of cancer patients as well as prolong their survival.

Animals↗
PubMed2001

Ascites due to hypothyroidism in a patient with alcoholic cirrhosis.

Myxedema is the cause of ascites in less than 1% of new-onset ascites cases, where as only 4% of patients with hypothyroidism present ascites. When ascites is the first manifestation of thyroid insufficiency, there is usually a delay in diagnosis. We report here a case of myxedema ascites occurring in a patient with alcoholic cirrhosis, that was first thought to be the cause of the ascites, and review the features of 48 cases previously reported. Some clinic and analytical findings that have been commonly reported, are the long duration of the ascites before diagnosis, the prompt response (with resolution of ascites) to thyroid replacement treatment, a high total protein concentration in ascites fluid, white moderate white blood cell counts and a lymphocyte predominance. Serum-ascites albumin gradient has been postulated to be high in myxedema ascites, but we believe this has been studied in too few cases thus far, to be conclusive.

Ascites↗
PubMedDate not supplied

Diuretic-resistant ascites in cirrhosis. Mechanism and treatment.

Refractory ascites (or diuretic-resistant ascites), i.e. ascites that cannot be mobilized by medical treatment (low sodium diet and high doses of furosemide and spironolactone) is an infrequent phenomenon in cirrhosis. It usually occurs in patients with functional renal failure as a consequence of alteration in both pharmacokinetics and pharmacodynamics of diuretics. Peritoneovenous shunting, a procedure which improves systemic hemodynamics and renal function and suppresses the plasma levels of renin, aldosterone, norepinephrine and antidiuretic hormone in cirrhotics with ascites, has been proposed as the treatment of choice in patients with refractory ascites. Unfortunately it is associated to a high rate of severe complications and does not prolong the survival of these patients. Moreover, in approximately one third of the patients the shunt becomes occluded within the first year after operation. Recent studies have shown that repeated large volume paracentesis (4-64 per day until disappearance of ascites) or total paracentesis (complete mobilization of ascites in only one paracentesis session) associated to i.v. albumin infusion are an effective and safe therapy of ascites. At present, there is only one controlled trial comparing therapeutic paracentesis versus peritoneo-venous shunt in the management of patients with refractory ascites. In this study, there were no significant difference between both therapeutic groups with respect to survival. However, the incidence of readmission to hospital for the treatment of ascites was higher in the paracentesis group. Therefore, both procedures are valid therapeutic alternatives for that type of patients. Future studies are necessary to investigate if there are subsets of cirrhotics with refractory ascites in which one of these two types of treatment is especially indicated.

Ascites↗
PubMed1989

Management of cirrhotic ascites.

The pathogenesis and diagnosis of cirrhotic ascites are reviewed, and the treatment options are described, focusing on pharmacologic management. The major theories on the pathogenesis of cirrhotic ascites are the underfill and overflow theories. The underfill theory states that ascites formation results in decreased plasma volume leading to renal sodium and water retention. The overflow theory states that the initial event in ascites formation is renal sodium retention. Evidence suggests that the formation of ascites is a continuum involving both overflow (early) and underfill (late) mechanisms. Although the most frequent cause of ascites is hepatic cirrhosis, analysis of the ascitic fluid is important to exclude other causes (e.g., neoplasm, peritonitis, pancreatitis). Patients who do not respond to treatment with sodium restriction and bed rest require diuretic therapy. Spironolactone is the agent of choice for treatment of the nonazotemic patient with cirrhotic ascites. Combination therapy with spironolactone and furosemide or spironolactone and metolazone may be used in those patients who do not respond to spironolactone. Patients with impaired renal function should not be treated with spironolactone because of the risk of hyperkalemia. Paracentesis with albumin replacement has been used successfully for treatment of patients with tense cirrhotic ascites. Initial management of cirrhotic ascites is conservative, with sodium restriction and bed rest. Spironolactone is a good first-choice drug for treatment of ascites. Daily weight, serum electrolytes, and renal function should be monitored to assess the effectiveness and potential adverse effects of diuretic therapy.

Ascites↗
PubMed1989

[Influence of ascites on splanchnic and systemic hemodynamics in patients with alcoholic cirrhosis].

The effect of ascites on splanchnic and systemic hemodynamics was retrospectively studied in 256 patients with alcoholic cirrhosis. The patients were divided into 3 classes: no ascites, moderate ascites, and large ascites. They were also classed into 3 groups according to a modified Pugh classification (ascites was not taken into account). In patients without ascites, cardiac output was positively related to the severity of liver disease. This result was not found in patients with large ascites. Similarly, in patients with no or moderate ascites, the degree of portal hypertension estimated by the hepatic venous pressure gradient was associated with liver failure. In patients with large ascites, hepatic venous pressure gradient was higher than in patients without ascites but this relation was observed only in patients without liver failure. These results show that ascites reduces the relation between cardiac output and liver failure and increases the degree of portal hypertension but not cardiac output.

Ascites↗
PubMed1983

Serum protein concentration and portal pressure determine the ascitic fluid protein concentration in patients with chronic liver disease.

UNLABELLED: The ascitic fluid and serum concentrations of albumin and globulin were measured simultaneously with transhepatic portal pressure determination in 56 patients with chronic liver disease to determine whether (1) portal pressure correlated with (S-Asc)A and (2) the majority of variation in ascitic fluid protein concentration between patients was related to fluid balance from serum to ascites. The mean ascitic fluid albumin concentration was 1.04 +/- 0.73 gm/dl; globulin concentration 1.31 +/- 0.80 gm/dl; and ascitic fluid total protein concentration 2.35 +/- 1.49 gm/dl. The mean serum albumin concentration was 2.58 +/- .57 gm/dl; globulin concentration 3.91 +/- .86 gm/dl; and total protein concentration 6.49 +/- 1.30 gm/dl. The (S-Asc)A was 1.54 +/- .45 gm/dl. The mean PPIVC was 14.5 +/- 4.3 mm Hg. The (S-Asc)A correlated directly with PPIVC (r = 0.73; p less than 0.0001). The ascitic fluid protein correlated with three variables that did not correlate with each other: serum albumin (r = 0.67; p less than 0.0001), serum globulin (r = 0.44; p less than 0.001), and PPIVC (r = -0.48; p less than 0.0005). The sum of the squared correlation coefficients with these latter uncorrelated variables equaled 0.87 and partial correlation coefficient analyses demonstrated an increase in the correlation of the ascitic fluid protein with the serum albumin concentration when corrected for serum globulin and (S-Asc)A (r = 0.97; p less than 0.0001) or PPIVC (r = 0.90; p less than 0.0001). Thus most of the variation in ascitic fluid protein between patients in this study could be related to serum protein concentrations and PPIVC or (S-Asc)A. Furthermore, multivariate discriminant analysis of patients with an ascitic fluid protein less than or equal to 2.5 vs. greater than 2.5 gm/dl indicated that the majority of differences between the two groups could be attributed to differences in serum albumin and serum globulin in combination with the (S-Asc)A (canonical correlation = 0.808) or PPIVC (canonical correlation = 0.806). These factors could correctly identify the low or high ascitic fluid protein groups in 96% and 93% of patients, respectively. IN CONCLUSION: (1) the (S-Asc)A is associated with the degree of portal pressure elevation and (2) the majority of variation in ascitic fluid protein concentration between patients with chronic liver disease is associated with differences in portal pressure and serum protein concentrations.

Analysis of Variance↗
PubMed1997

Treatment and prevention of malignant ascites associated with disseminated intraperitoneal malignancies by aggressive combined-modality therapy.

No satisfactory treatment exists to treat or prevent malignant ascites secondary to nonovarian intraperitoneal (IP) disseminated malignancies. A Phase I/II clinical trial combining radical cytoreductive surgery (CS) and IP hyperthermic chemotherapy (IPHC) with mitomycin C is presented. Between December 9, 1992 and July 31, 1995, 39 patients (pts) were explored for IP cancer. Five pts with known liver metastases were excluded, leaving 34 pts (15 female, 19 male) of median age 53 (range, 17-76). The majority of pts had disseminated IP cancers of gastrointestinal origin (80%). Prior therapy included the following: chemotherapy, 20 pts (59%); surgery, 29 pts (85%); and radiation, 2 pts (6%). Following CS, IPHC with mitomycin C was done. At surgery, 12 pts (35.3%) had frank ascites, and 12 pts (35.3%) had positive IP cytology without ascites. The median hospital stay was 9 days (range, 5-65) with no 30-day mortality. Complications for 36 treatments included: thrombocytopenia Eastern Cooperative Oncology Group grade 3 or 4, two cases (5.6%); neutropenia requiring granulocyte colony-stimulating factor, seven cases (19.4%); sepsis, four cases (11.1%); bowel leak, two cases (5.6%); and serous wound leak, two cases (5.6%). Ascites correlated with worse resection status (P = 0.025). Ascites was controlled in 9 of 12 (75.0%) pts, with failures at 1, 4, and 14 months (median follow-up, 7.5 months). No cytology-positive ascites-negative pts developed clinical ascites (median follow-up, 9.4 months). The median survival time in pts with ascites was 10.1 months versus 32.7 for patients without ascites (P = 0.013). For the entire study population, the 1- and 2-year survival rates were 74.6 and 48.5 per cent, respectively (median follow-up, 18.2 months). In this study, malignant ascites was controlled in 75 per cent of cases and prevented in all pts with positive IP cytology. CS plus IPHC appears to be relatively well tolerated and may be effective for the treatment and prevention of malignant ascites.

Antibiotics, Antineoplastic↗
PubMedDate not supplied

[The analysis of ascitic fluid].

The approach to the study of the patient with ascites should include biochemical and cytologic analysis of the ascites. The albumin ascites serum gradient and total proteins separate the ascites ascites caused by portal hypertension from the neoplastic ascites and peritoneal tuberculosis. Other parameters are the measurement of fibronectin and cholesterol, both of them with the cytology make the diagnosis of malignant ascites. More than 250 leukocytes per mm3 in the ascites, predominantly lymphocytes, peritoneal tuberculosis can be the cause. In conclusion the ascites analysis is the first election procedure for the study of the cause of ascites.

Ascites↗
PubMed2006

Ascites in childhood liver disease.

Ascites is a common clinical problem in children with liver disease. The peripheral arterial vasodilation hypothesis is mostly accepted as the pathophysiological basis of ascites. The most important complication is spontaneous ascitic fluid infection in the form of spontaneous bacterial peritonitis (SBP) and its variants. Aerobic gram-negative bacteria, primarily Escherichia coli, are the most common isolates. Diagnostic paracentesis is done in patients with ascites when diagnosed first time and at the beginning of each admission to hospital. Ascitic fluid is evaluated for cell count with differential, albumin level, total protein and culture. Serum-ascites albumin gradient (SAAG) is the best single test for classifying ascites into portal hypertensive (SAAG> 1.1 g/dL) and non-portal hypertensive (SAAG < 1.1 g/dL) causes. In patients with tense ascites LVP should be performed. A neutrophil count of > 250 cells/mm3 is highly suggestive of bacterial peritonitis. Intravenous cefotaxime is the empiric antibiotic of choice. Long-term administration of oral norfloxacin 5-7.5 mg/Kg once a day in cirrhotic patients with ascitic fluid protein content of < 1g/dL or prior episode of SBP is recommended for prevention of SBP. Oral dual diuretic therapy of single morning dose of spironolactone along with furosemide in the ratio of 5:2 is recommended. While obtaining satisfactory diuretic response dual diuretic therapy can be changed over to monotherapy with spironolactone. Patients should be on sodium restricted diet. Management of ascites might ultimately require liver transplantation.

Ascites↗