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PubMed2005

Usefulness of routine analysis of ascitic fluid at the time of therapeutic paracentesis in asymptomatic outpatients. Results of a multicenter prospective study.

AIM: The guidelines of the American Association for the Study of Liver Diseases recommend performing exploratory paracentesis on each patient with cirrhosis and chronic ascites. The aim of the study was to evaluate the prevalence of spontaneous bacterial peritonitis and culture-negative neutrocytic ascites in a large population of consecutive asymptomatic cirrhotic ascitic ambulatory patients. METHODS: Patients with cirrhosis and tense ascites hospitalized from January to September 2000 in 5 hepatogastroenterology units prospectively underwent an exploratory paracentesis with cytobacteriological, biochemical and bedside inoculation into aerobic and anaerobic blood culture bottles. Patients studied were not receiving antibiotics except for norfloxacin and had no obvious sign of infection such as fever or hypothermia, chills, unusual abdominal tenderness, de novo or worsening hepatic encephalopathy, recent gastrointestinal bleeding, acute renal failure or marked arterial hypotension. Clinical and biological findings and ascitic fluid cytological and bacteriological results were evaluated at each exploratory paracentesis. The results are given in mean +/- standards deviations with range. RESULTS: Sixty-seven cirrhotic patients (48M/19F, mean age 59 +/- 9 years) had 270 therapeutic paracenteses, preceded by an exploratory aspiration. Fifty-nine patients (88%) had alcoholic cirrhosis. Twenty-five patients (37.3%) received norfloxacin. At first paracentesis 41 (61.2%) and 26 (38.8%) patients were class B and C respectively according to the Child-Pugh classification; the mean Child-Pugh score was 9 +/- 1.5. None had suspicion of infection. The mean number of paracenteses was 5 +/- 4.3 per patient; 59.6% of the paracenteses (161) were compensated with human albumin. Ascitic protein concentration was 17.5 +/- 8.6 g/l, ascitic fluid cell count and number of neutrophils were 127 +/- 155/mm3 and 5.9 +/- 14/mm3 (0-60), respectively. No patient had spontaneous bacterial peritonitis nor culture-negative neutrocytic ascites; 10 cases of monomicrobial bacterascites were observed, all with commensal germs. CONCLUSIONS: In the absence of obvious signs of infection, the prevalence of spontaneous bacterial peritonitis and culture-negative neutrocytic ascites in asymptomatic cirrhotic outpatients with ascites is near 0%. Moreover, for 100 large volume paracenteses, not performing exploratory paracentesis corresponds to a savings of 5,500 euros, without risk for these patients.

Adult↗
PubMed1988

Finding the cause of ascites. The importance of accurate fluid analysis.

Diagnostic paracentesis with ascitic fluid analysis is critical to the accurate diagnosis and management of ascites. Recent advances have improved the evaluation of ascitic fluid, among them the serum-ascites albumin difference for discriminating between ascites caused by liver disease and ascites due to malignancy. The ascitic fluid polymorphonuclear leukocyte concentration is the best index for the rapid presumptive diagnosis of spontaneous bacterial peritonitis. Familiarity on the part of the clinician with ascitic fluid interpretation and with ascitic fluid characteristics in various diseases will increase the chances of controlling ascites early.

Ascites↗
PubMed1980

Analysis of Twenty-three plasma proteins in ascites. The depletion of fibrinogen and plasminogen.

The concentrations of 23 plasma proteins were measured by radial immunodiffusion in the plasma and ascites of 17 patients with cirrhosis and four patients with intraperitoneal malignancies, to learn whether there is a selectivity in the movement of proteins from plasma into ascites, analogous to that of proteinuria. Additionally, since some of the proteins are involved in coagulation, we hoped to clarify the coagulopathy frequently seen following peritoneovenous shunting of ascites. Analysis was by groups: group 1 consisted of nine patients with cirrhosis with an ascites-total protein content less than 2.5 g/dl; group 2 consisted of eight patients with cirrhosis with ascites-total protein content greater than or equal to 2.5 g/dl; and group 3 consisted of four patients with malignant ascites. The ratio of the plasma concentration/ascites concentration ([P]/[A]) for each protein was calculated for each patient. In each group the median [P]/[A] for each protein was plotted against the natural logarithm of its molecular weight (In MW). For 21 of the 23 proteins, [P]/[A] showed a close linear relationship to In MW. Fibrogen and plasminogen showed significant (p < 0.0002) elevation above the regression line relating [P]/[A] to In MW. This indicates depletion of fibrinogen and plasminogen in ascites. The ascites in group 1 showed moderate selectivity, defined as the slope of the regression line (1.59), while groups 2 and 3 were essentialy nonselective (0.35 and 0.50). Fibrin-split products were elevated in all ascites but not in plasma, indicating either fibrinolysis or fibrinogenolysis within the ascites. A normal ratio for prothrombin suggests fibrinogenolysis may be the dominant mechanism. Thus the coagulopathy induced by LeVeen valve insertion may be in part secondary to the infusion of plasmin or a plasminogen activator into the circulation.

Afibrinogenemia↗
PubMed1986

Malignant ascites. Clinical and experimental observations.

Malignant ascites formation is a grave prognostic sign, but palliative efforts seem justified in some patients. Lack of knowledge concerning the natural history of this process hinders the choice of therapeutic options. Over 5 years, 107 patients with untreated malignant ascites were reviewed to define their survival. Pancreas (20), ovary (18), and colon (18) were the most frequent tumors, with 52% of patients presenting with ascites at the time of the initial cancer diagnosis. Cytology evaluation of the ascitic fluid was positive for tumor cells in 57% of cases and a high protein content was noted in 65%. Mean survival of the entire series was only 20 weeks from the time of diagnosis of ascites, with tumors of ovarian and lymphatic origin having better mean survivals of 32 and 58 weeks, respectively. Patients with high ascitic protein levels fared better than those with low levels. In an effort to explain this correlation of elevated protein levels and a favorable survival rate, a hypothesis was proposed that certain tumors secrete a factor, which alters vascular permeability and causes fluid accumulation in the absence of lymphatic obstruction. In an experimental rat model of malignant ascites, the intraperitoneal infusion of cell-free malignant ascitic fluid caused an increase in edema formation and a significant increase in capillary permeability to protein in the omentum. This demonstrated change in the leak of protein explains the formation of ascites by some tumors in the absence of tumor obstruction of the draining lymphatics of the peritoneal cavity and suggests another important mechanism in the genesis of malignant ascites.

Adult↗
PubMed2001

[Ascitic fluid puncture in the treatment of severe forms of ovarian hyperstimulation syndrome].

OBJECTIVE: Evaluate the contribution and complications of ascitic fluid puncture in the treatment of severe ovarian hyperstimulation syndrome. DESIGN: Retrospective analysis of 18 patients. SETTING: Department of Gynaecology and Obstetrics, University Hospital, Palacky University, Olomouc. METHODS: 18 patients with the diagnosis of severe ovarian hyperstimulation syndrome admitted to intensive care unit from January 1996 to June 2000 were analysed. As a part of the therapy of severe OHSS 11 punctures of ascitic fluid was performed. In 3 patients the reinfusion of the ascites into the blood circulation was performed. RESULTS: The transabdominal paracentesis under the ultrasound control in 11 patients was performed. In 6 patients the puncture had to be repeated. The amount of removed ascitic fluid in single procedure was between 600-3750 ml. Total amount of fluid in different patients was between 1500-17,300 ml. Sterility of ascites and high contents of proteins was proved. In 3 patients with the refractory ascites the reinfusion of the ascitic fluid to the circulation was performed. No serious complications of the punctures were observed, 4 patients had a slight rise of body temperature, which fell down without antibiotics therapy. CONCLUSION: Puncture of the ascitic fluid is a save and effective part of the therapy of severe OHSS. In the treatment of the refractory ascites the reinfusion of the ascitic fluid should be used.

Ascites↗
PubMedDate not supplied

[The validity of the proteins concentrations in the ascitic liquid and serum for the differential diagnosis of the ascitis].

Prospective evaluation was performed in 60 in-patients, carriers of ascites of different etiologies, analyzing the validity of the parameters depending on protein and albumin dosage, both in the ascitic serum and fluid, for the discrimination of possible etiological causes of ascites, including in these parameters Protein Concentration in the Ascitic Fluid, the Serum-Ascites Albumin Gradient, the Protein Ascites/Serum Ratio, and the Albumin Concentration in the ascitic fluid. Average age was 46.9 +/- 19.6, all female; 21 cases were associated with Chronic Hepatic Disease, 14 to Tuberculosis, 11 to Malignant Neoplasia, 7 to Nephrotic syndrome, 4 to Congestive Heart Failure, 2 to Collagen Disease, and 1 to a severe Malnutrition case. The evaluation parameters correlate with the oncotic and hydrostatic pressures of the Starling Law, on the basis of what they could be compared with, demonstrating that their sensitivity levels and their specificity may be used as positive or negative predictive values in the discriminative evaluations of ascites in relation to its probable etiological causes. Even though the Serum-Ascites Albumin Gradient may be useful in the separation of ascites cases with portal hypertension, it is also useful for classifying exudates and transudates. However, the other parameters must not be excluded for the evaluation of those cases, aiming at establishing whether the peritoneum has been affected and hence the terms transudates and exudates should still be used on the basis of the high sensitivity value and specificity of theses tests, which do not differentiate them statistically from the Serum-Ascites Albumin Gradient. Using the cut-off points for each parameter, the most adequate for our population would be 1.5 gr/dl for Albumin and 2.5 gr/dl for protein, with the additional lower cost benefit.

Adolescent↗
PubMed1979

Pancreatic Ascites.

Ascites occurring in patients with a history of alcoholism is usually due to cirrhosis but clinically significant ascites also occurs in association with pancreatic disease. We reviewed 265 cases of pancreatitis over a five-year period. There were 129 blacks and 136 Caucasians. Ages ranged from 19-86 years with a mean of 46.2 years. Eight of these cases (3%) were found to have pancreatic ascites. The initial serum and urinary amylase had no prognostic value regarding the subsequent development of pancreatic ascites. The mean ascitic fluid amylase was 14,426 Somogyi units (range 1,279-67,774). The mean ascitic fluid protein was 4.6 gm./100ml. (range 1.4-7.2). High enzyme and protein concentration in the ascitic fluid are characteristic of pancreatic ascites. Out of eight cases, two were associated with a pseudocyst, three with hemorrhagic pancreatitis and three with acute edematous pancreatitis. Four of these eight (50%) died. Pancreatic ascites is a distinct clinical entity which should be differentiated from cirrhotic, tuberculous or malignant ascites.

Adult↗
PubMed1998

Differential inhibition of fluid accumulation and tumor growth in two mouse ascites tumors by an antivascular endothelial growth factor/permeability factor neutralizing antibody.

In the accompanying paper (Luo et al., Cancer Res., 58: 2652-2660, 1998), we demonstrated that vascular endothelial growth factor (VEGF), also designated vascular permeability factor (VPF), significantly accumulated in all mouse malignant ascites tested, suggesting its fundamental role in ascites tumors. Removal of VEGF may inhibit the development of ascites tumors. In this study, using a goat antimouse VEGF-neutralizing antibody, we tested this hypothesis with two well-defined syngeneic mouse ascites tumors: MM2 breast adenocarcinoma and OG/Gardner lymphoma 6C3HED (expressing moderate and low levels of VEGF, respectively). This antibody significantly inhibited MM2 and OG cell-free ascites fluid-induced hyperpermeability of mouse peritoneal microvessels and in vitro endothelial cell growth. Mice bearing tumors were administered i.p. daily with the antibody or normal goat IgG as controls for 8 days, at doses of 20-fold (for MM2-bearing mice) or 40-fold (for OG-bearing mice) the estimated amounts of VEGF that kinetically accumulated in the ascites fluid after the tumor inoculation. The average volume of ascites fluid, number of tumor cells and leaked RBCs, and the peritoneal microvessel permeability in MM2-bearing mice that received the antibody treatment were significantly lower than those in the matched controls (P < 0.01). Unexpectedly, OG-bearing mice did not show satisfactory response to the anti-VEGF treatment. This discrepancy was not likely due to inadequate doses or different host immune responses, but it was quite possibly to the different characteristics of MM2 carcinoma and OG lymphoma tumors, the latter being strongly invasive, and/or the existence of an inflammatory mediator(s), such as bradykinin or cytokine(s) other than VEGF. In summary, our results directly demonstrated, for the first time, differential roles for VEGF in ascites tumors in vivo and suggest the potential of VEGF inhibition as a specific therapy for ascites tumors of carcinoma origin, which are the major cause of the malignant ascites in adult humans.

Animals↗
PubMed1998

Significant expression of vascular endothelial growth factor/vascular permeability factor in mouse ascites tumors.

Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, is believed to be a potent mediator of peritoneal fluid accumulation and angiogenesis and of tumor growth in ascites tumor. Such roles, however, have not been generally established because of insufficient quantitative and systemic analyses. To address this, we examined the expression of VEGF in 13 mouse ascites tumors (5 sarcomas, 3 carcinomas, 2 lymphomas, 1 leukemia, 1 mastocytoma, and 1 plasmacytoma). Using a newly developed sensitive and specific radioreceptor binding assay and functional assays, we found that active VEGF was significantly accumulated (6-850 ng/ml) in the ascites fluids of all 13 tumors. VEGF concentrations are higher in the tumors of sarcoma and carcinoma origin (430.4 +/- 234.2 ng/ml) than in those of lymphoma and hematological tumor origin (19.2 +/- 10.45 ng/ml). VEGF that accumulated in the peritoneal fluids or expressed in the ascites tumor cells was easily visualized with immunoprecipitation Western blot analysis with a rough correlation to the expression levels of VEGF gene in these tumor cells, suggesting that the tumor cells, at least in part, contributed to the production of the VEGF that accumulated in the ascites fluid. Most ascites tumors expressed VEGF; the 164-amino acid isoform was predominant, the 120-amino acid isoform was less abundant, and the 188-amino acid isoform was least abundant. Several representative ascites tumors expressed similar, if not higher, levels of VEGF when they were cultured at normoxic states, suggesting that they expressed VEGF at high levels in a constitutive manner. The microvessel densities in the peritoneal walls of tumor-bearing mice, which are significantly higher than those in normal mice, basically correlated to but did not parallel the VEGF concentrations in their respective ascites fluids. Thus, a complicated relationship may exist between the VEGF production and angiogenesis associated with ascites tumor in vivo. Taken together, our observations suggest that VEGF plays a fundamental role in ascites tumor formation; however, its importance may vary according to tumor origin.

Animals↗
PubMed1988

Simultaneous soft agar cloning of ascites and solid tumor specimens from patients with ovarian cancer.

Concurrent Cloning Efficiencies (CE) of both ascites and solid tumor samples from 36 patients with ovarian carcinoma were studied using the soft agar assay. The CE of both were highly variable (range, 0-1.234% and 0-0.802%, respectively). There was marked intrapatient and interpatient heterogeneity in the CE. Of the 36 tested, comparative CE were evaluable in 29. CE was 0 in both solid tumor and ascites in one patient. CE was 0 in four other ascites samples from four patients. In other 24, the relative CE of solid tumor/ascites from each patient ranged from 0.066 to 435. In the 29 patients with samples of ascites and a solid tumor evaluable for concurrent CE, the median colony counts of solid tumors was more than tenfold higher than ascites. The solid tumors obtained from 31 patients had a significantly higher CE than tumor cells obtained from ascites samples from 32 patients. Solid tumors were significantly better than ascites for in vitro testing based on the data that 75% (27/36) of solid tumors and only 31% (11/36) of ascites formed greater than or equal to 30 colonies. The drug sensitivity profiles of tumor cells from a solid tumor and ascites of the same patient appear similar. Based on these observations, it may be more cost and labor effective to do soft agar in vitro chemotherapy assays using a solid tumor than ascites in ovarian carcinoma.

Agar↗
PubMed1998

The diagnostic and predictive value of ascites nitric oxide levels in patients with spontaneous bacterial peritonitis.

Nitric oxide (NO) is a messenger molecule involved in pathogen suppression. Cirrhosis is characterized by an increased risk for infections, including spontaneous bacterial peritonitis (SBP). The role of NO in the infections that develop in cirrhosis has not been clearly established. The aim of this study was to investigate the utility of measuring ascites NO in the diagnosis of SBP and/or in determining the predisposition of cirrhotic patients to develop this infection. Nitric oxide metabolites (nitrites + nitrates [NOx]) were measured by chemiluminescence in 105 ascites samples obtained from 87 cirrhotic patients and in 87 simultaneously obtained serum samples. Ascites NO levels were not significantly different among ascites from patients with SBP (n = 39; median, 48 micromol/L), patients with sterile ascites (n = 54; median, 42 micromol/L), and samples obtained after patients with SBP had been treated (n = 12; median, 62 micromol/L). No differences in ascites NO levels were observed between culture-positive and culture-negative peritonitis. Among 50 patients with sterile ascites on initial paracentesis, 7 patients developed peritonitis during follow-up; no differences in baseline NO levels were observed between patients who developed peritonitis (median, 46 micromol/L) and those who did not (median, 41 micromol/L). Among patients with SBP, mortality was significantly higher in those with NO levels >60 micromol/L. A very significant direct correlation was found between ascites and serum NO levels (r2 = .86). In conclusion, ascites NO levels in cirrhotic patients are not useful either to diagnose or to determine predisposition to SBP. Rather, ascites NO levels reflect serum levels, are higher in cirrhotic patients with more severe liver disease, and may be a useful prognostic marker.

Ascites↗
PubMed1996

The prognostic implication of ascites in advanced-stage ovarian cancer.

Ovarian carcinoma accounts for greater than 50% of the gynecologic cancer deaths in the United States each year. One of the central reasons for this dismal outcome is that many patients present with advanced disease. In this series, a retrospective review of 130 patients with stage III and IV invasive epithelial ovarian carcinoma was performed to determine the prognostic significance of ascites. Patients were divided into two study groups based upon the presence or absence of ascites. Survival for the entire study group was 15%, but differed markedly when separated for the presence of ascites. In these patients, ascites was associated with a statistically decreased 5-year survival of 5% versus 45% without ascites (P = 0.0001). Individuals were found to be similar in each group when examined for age, height, weight, cell type, grade, and surgical and chemotherapeutic treatment modalities. More patients proportionately with stage IIIC disease had ascites than those without ascites (P = 0.0015). More of the individuals without ascites underwent second-look laparotomies and achieved a negative result than those with ascites (P = 0.04; P = 0.0038). We conclude that ascites in the presence of stage III and IV disease produces an almost uniformly fatal outcome.

Antineoplastic Agents↗
PubMedDate not supplied

Differentiation of exudate from transudate ascites by Doppler sonography.

BACKGROUND: We investigated whether the addition of Doppler sonography (US) increases the diagnostic confidence of US for estimating the nature of ascites. METHODS: Of the 127 cases reviewed in this study, there were 42 cases of transudate and 85 of exudate ascites. We reviewed the US, power Doppler, and pulsed Doppler images of these cases. RESULTS: With US, the transudate ascites was imaged as free of echo in 38 of 42 cases (90.5%). The exudate ascites was imaged as free of echo in 22 of 85 cases (25.9%) and with internal echo spots in 63 of 85 cases (74.1%). With Doppler US, we obtained distinct pulsed signals from the transudate ascites in only two of 36 cases (5.6%). In contrast, we obtained distinct Doppler signals from the exudate ascites in 66 of 79 cases (83.5%). Those 66 cases included 16 of the 22 cases with echo-free ascites. CONCLUSION: The presence or absence of echo spots within the ascites helped differentiate transudate from exudate ascites, as reported in the literature. However, the addition of Doppler US contributed to the differentiation of echo-free exudate (Doppler signals present) from echo-free transudate (Doppler signals absent) ascites.

Abdomen↗
PubMed2001

Ascites following ventriculoperitoneal shunting in children with chiasmatic-hypothalamic glioma.

OBJECT: Optic pathway gliomas in children can involve the optic nerve, chiasm, and hypothalamus. This uncommon, slowly growing tumor can cause hydrocephalus, which usually requires placement of a ventriculoperitoneal (VP) shunt. Symptomatic ascites may occasionally develop as a complication of the VP shunt procedure. The purpose of this study was to assess the risk factors associated with CSF ascites in children with optic pathway gliomas. METHODS: Twenty-two children (ages 4 months to 20 years) with chiasmatic-hypothalamic optic gliomas participated in this study. Four children were diagnosed with a chiasmatic glioma, 7 with a hypothalamic glioma, and 11 with a glioma involving both the optic chiasm and hypothalamus. Twelve children (55%) developed hydrocephalus and required VP shunt placement. Of the 12 shunted children, 4 (33%) developed CSF ascites. The incidence of ascites was not associated with infection, tumor metastasis, or multiple shunt revisions. There was no correlation with the size of the tumor. All 4 children with ascites had tumor involving the optic chiasm or optic nerve. None of the 5 children with pure hypothalamic glioma who underwent VP shunt placement have developed ascites. Among the 7 children suffering from chiasmatic or optic nerve gliomas who developed hydrocephalus, the risk of developing ascites as a complication of VP shunt placement was 57% (4/7). Ventriculoatrial (VA) shunt was the treatment of choice for children with VP shunt-induced ascites. After placement of a VA shunt the ascites subsided. The children did not develop further complications. CONCLUSION: We conclude that glioma involving the optic chiasm or nerve is associated with a high risk of developing ascites following VP shunt placement. VA shunt may be the treatment of choice for children with chiasmatic or optic nerve gliomas who require a CSF diversion procedure.

Adolescent↗
PubMed1991

Muscle sympathetic nerve activity and renal responsiveness to atrial natriuretic factor during the development of hepatic ascites.

PURPOSE: Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive antinatriuretic forces such as the sympathetic nervous system and vasodilatory natriuretic agents such as atrial natriuretic factor (ANF). With the development of refractory ascites, cirrhotic patients become unresponsive to the natriuretic effect of ANF. Animal data suggest that the sympathetic nervous system plays a key role in mediating the refractoriness to ANF. We therefore studied the relationship between sympathetic nerve activity (SNA) and the natriuretic response to ANF in normal subjects and cirrhotic patients. We also attempted to localize the intrarenal site of refractoriness to ANF by lithium clearance. PATIENTS AND METHODS: Twenty-six patients with biopsy-proven cirrhosis and seven age- and sex-matched normal volunteers were studied after a week of 20 mmol/day sodium intake and no diuretics. Muscle SNA was recorded from the peroneal nerve (microneurography) and correlated with responsiveness to a 2-hour ANF infusion. Lithium clearance was used as a marker of sodium reabsorption proximal to the intramedullary collecting duct, the main site of ANF action. Plasma norepinephrine, renin, and aldosterone levels were also determined. Patients were categorized into three groups: nine patients free of ascites (by ultrasonography), five ascitic patients who responded to a 2-hour ANF infusion (i.e., had a natriuretic response to ANF above 0.83 mmol/hour), and 12 ascitic patients who did not respond. RESULTS: Muscle SNA was greatly increased in the ascitic nonresponder patients compared with the normal subjects (64 +/- 4 versus 27 +/- 7 bursts/minute, p less than 0.001), moderately increased in ascitic responders (47 +/- 6 bursts/minute, p less than 0.05), but not significantly increased in nonascitic patients with cirrhosis (34 +/- 5 bursts/minute). SNA was positively correlated with plasma norepinephrine levels (r = 0.69; p less than 0.005) and inversely correlated with peak sodium excretion during the ANF infusion (r = -0.63; p less than 0.001). Plasma renin activity and aldosterone were markedly elevated in ascitic nonresponders, and normal in ascitic responders and nonascitic patients. Lithium clearance was reduced in ascitic patients compared with nonascitic patients, did not change after the ANF infusion, and correlated inversely with SNA (r = -0.61; p less than 0.01). CONCLUSION: These results support the concept that the sympathetic nervous system is a factor in renal sodium handling in cirrhosis, especially in the initiation of sodium retention and the development of refractory ascites. Refractoriness to ANF might be explained, at least in part, by increased neurally mediated sodium reabsorption proximal to the intramedullary collecting duct, the main site of ANF action.

Adult↗
PubMed1988

Ascites fluid lipoproteins in experimental nephrotic syndrome.

Lipoprotein content and composition were studied in ascites fluid of puromycin aminonucleoside-nephrotic rats. All of the lipoprotein density classes were found in ascites fluid. Protein levels compared to plasma were: very low density lipoprotein (VLDL, d less than 1.006), 1.2%; intermediate density lipoprotein (IDL, 1.006 less than d less than 1.02), 2.6%; low density lipoprotein (LDL, 1.02 less than d less than 1.063), 1.0%; and high density lipoprotein (HDL, 1.063 less than d less than 1.21), 1.1%. The predominant protein in ascites fluid was albumin, present at 1.9% of the plasma level. Radioiodinated VLDL and HDL injected intravenously into nephrotic rats appeared in lipoprotein fractions of the ascites fluid. VLDL and IDL triacylglycerol content and particle diameter were low compared with plasma particles, suggesting peritoneal triacylglycerol lipase activity; such lipase activity could account for the increased proportion of LDL in the ascites fluid. Ascites fluid LDL and HDL phospholipid and free cholesterol were high and cholesteryl ester was low. Ascites lipoproteins contained the same apolipoproteins as plasma, but in different proportions. Ascites VLDL had higher apolipoprotein B and lower apolipoprotein E, while LDL and HDL had higher apolipoprotein E. Ascites HDL could be separated by heparin-Sepharose affinity column chromatography into a retained and a non-retained fraction, while nearly all nephrotic plasma HDL was non-retained. These data suggest that modification of ascites fluid lipoproteins occurs prior to their entry into the lymph and return to the blood, perhaps mediated by peritoneal macrophages.

Animals↗
PubMed1994

Dextran sulphate activation of the contact system in plasma and ascites.

We have previously reported on the presence of proenzymes and inhibitors of the contact system in ascitic fluid. Malignancy-related ascites was also found to contain both high and low molecular weight kininogen (HK and LK). On this basis we have studied a possible activation of the contact system in ascites. Generation of amidolytic activity towards the chromogenic substrate S-2302 after incubation with dextran sulphate (DXS), was found in ascites from patients with gastrointestinal cancer, but not in ascites from patients with benign liver disease. It is concluded that malignancy-related ascites allows contact activation to take place, while benign ascites does not. This activation process, generating bradykinin, could possibly be of relevance to the mechanism of ascites generation. Plasma samples from patients with ascites were also tested in relation to activation of the contact system. Activation was evaluated by immunoblotting, studying the disappearance of intact HK after the initiation of activation with different concentrations of DXS. In control plasma, activation took place at low concentrations of DXS (25 - 50 micrograms/ml). In plasma samples from patients with malignancy-related or benign ascites, contact activation was depressed. In some samples concentrations of DXS up to 1 mg/ml, were not able to activate the contact system at all. Concentrations of proenzymes and relevant inhibitors in the contact system, HK and total protein were also determined. We found the concentration of prekallikrein to be positively correlated with the degree of activation. Concentrations of inhibitors such as C1-inhibitor, did not show any correlation with activation.

Adult↗
PubMed1992

Diuresis increases ascitic fluid opsonic activity in patients who survive spontaneous bacterial peritonitis.

Patients with low protein ascites and deficient ascitic fluid opsonic activity have been shown to be unusually predisposed to development of spontaneous bacterial peritonitis. Survivors of spontaneous peritonitis frequently develop recurrent infection. Diuresis has been shown to increase the ascitic fluid opsonic activity of patients who have never had spontaneous bacterial peritonitis. Patients with adequate opsonic activity are protected from ascitic fluid infection. Theoretically, the subset of patients who develop spontaneous peritonitis may have such severe liver disease that (i) their ascites is refractory to diuretic therapy or (ii) their ascitic fluid opsonic activity does not increase in response to diuresis. In this study, opsonic activity and concentrations of total protein and complement components were measured in the ascitic fluid of 11 patients who were hospitalized with spontaneous bacterial peritonitis and who responded to oral diuretics. The mean values of all of these parameters were found to increase significantly comparing the end-of-diuresis samples to the specimens that were diagnostic of ascitic fluid infection. Patients who survive spontaneous bacterial peritonitis are able to increase their ascitic fluid total protein and opsonic activity in response to diuresis. This increase in endogenous antimicrobial activity may help prevent recurrence of ascitic fluid infection.

Amiloride↗