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PubMed1988

Cardiac ascites: a characterization.

In a prospective study, there were 13 patients with cardiac ascites among a group of 262 ascites patients (5% of the total). I compared the characteristics of 20 ascitic fluid samples from these patients with heart failure to those of 20 patients with cirrhotic ascites. The serum-ascites albumin concentration gradient was greater than or equal to 1.1 g/dl in all patients in both groups. The ascitic fluid total protein concentration was greater than or equal to 2.5 g/dl in all patients with cardiac ascites whereas only 10% of patients with cirrhotic ascites had such high values. The ascitic fluid lactate dehydrogenase and red cell counts were significantly higher in cardiac ascites than in cirrhotic ascites--although cardiac ascites was not visibly bloody. The peripheral hematocrit of patients with cardiac ascites was also significantly higher than that of patients with cirrhotic ascites. The ascitic fluid analysis in patients with cardiac ascites is characteristic and may assist in the differential diagnosis of ascites.

Ascites↗
PubMed1996

Ascites in Nephrotic syndrome. Incidence, patients' characteristics, and complications.

The pathophysiology of ascites in patients with cirrhosis is complex and includes increases in hepatic sinusoidal pressure, the formation of hepatic and splanchnic lymph, renal sodium retention, and hypoalbuminemia. However, the role of hypoalbuminemia in ascites formation is controversial. Evaluating ascites in hypoalbuminemic patients with nephrotic syndrome could add to our understanding of the role of hypoalbuminemia in ascites development. We conducted a retrospective analysis of 52 adults and 21 children with nephrotic syndrome who were hospitalized in the Hadassah University Hospital on Mount Scopus during 1981-1994. There was a significant difference in the prevalence of ascites between pediatric (52%) and adult patients (23%) (p = 0.024). Pediatric patients had lower serum albumin levels than adults (1.70 +/- 0.08 g/dl vs. 2.10 +/- 0.07 g/dl, p = 0.001). Adult patients with ascites had lower serum albumin levels than adult patients without ascites (1.80 +/- 0.13 g/dl vs. 2.20 +/- 0.07 g/dl, p = 0.01). This difference was not found in pediatric patients. Temporary fluctuations in liver enzymes (up to four times the upper limit of normal for transaminases) were evident in five patients from the pediatric group with ascites, whereas all pediatric patients without ascites had completely normal liver enzymes (p = 0.035). Among the 12 adult patients with ascites, seven had liver disease (three with cirrhosis and four with amyloidosis), and two had right-sided congestive heart failure. Among the 40 adult patients without ascites, only four had liver disease (amyloidosis). The plasma albumin levels of the patients with amyloidosis without ascites were higher than patients with amyloidosis with ascites (1.90 +/- 0.10 g/dl vs. 1.50 +/- 0.07 g/dl, p = 0.03). Two patients with nephrotic syndrome and ascites (one without liver disease) had episodes of spontaneous bacterial peritonitis. Ascites in nephrotic syndrome is more common in children than in adults. Although in most pediatric patients ascites formation is probably a common manifestation of the general fluid retention, in most adult patients with nephrotic syndrome ascites can be attributed to both hypoalbuminemia and the presence of liver disease or congestive heart failure, with increased hepatic sinusoidal pressure.

Adolescent↗
PubMed1988

Bile constituents in ascitic fluid.

Bile acids and other bile constituents were determined in serum and ascites from eight patients with liver cirrhosis and in ascites secondary to malignancy in six patients. In cirrhotic ascites, total bile acid levels averaged 53% of the serum levels. A positive correlation was evident between ascites and serum levels for both cholic and chenodeoxycholic acid. For cholic acid, the ascites to serum ratio was higher in all patients compared with the corresponding ratio for chenodeoxycholic acid. The ascites to serum ratios for glycine, taurine and sulphate conjugates were similar, no tendency being shown by any of the conjugates to leak more easily into ascites. The high levels of bile acids in cirrhotic ascites suggests that the abdominal cavity harbours a fraction of the bile acid pool, which should be taken into account when studying bile acid turnover in liver cirrhosis. Bilirubin levels in cirrhotic ascites averaged 24% of the serum values. A positive correlation between ascites and serum levels for unconjugated bilirubin was recorded, whereas the occurrence of bilirubin conjugates in ascites was variable. Albumin levels in cirrhotic ascites were 25% of the serum levels. The ascites to serum ratios for other proteins such as IgG, IgA and IgM and also cholesterol and phospholipids were lower than that for albumin. In malignant ascites, a pattern different from that in liver cirrhosis was seen, low bile acid levels being found. No difference between bilirubin levels was observed, while albumin and cholesterol levels were higher in malignant ascites, with no overlap between the patient groups. These results indicate that the complex mechanisms of ascites formation result in variable levels of bile constituents in ascitic fluid, which are further dependent on the underlying disease.

Aged↗
PubMedDate not supplied

Vascular endothelial growth factor activating matrix metalloproteinase in ascitic fluid during peritoneal dissemination of ovarian cancer.

The role of vascular endothelial growth factor (VEGF) during peritoneal dissemination of ovarian carcinoma and the association with tumor microvessel density (MVD) and matrix metalloproteinase (MMP) activity was investigated. To this end, MVD, tumor tissue and ascitic fluid levels of VEGF, and MMP activity of ascitic fluid were examined in patients with ovarian cancer and benign ovarian tumor. The effect of ascites on cell growth, cell invasion activity and angiogenesis was investigated in vitro. Ascitic fluid and tumor tissue samples were obtained from 15 patients with benign ovarian tumor and 24 patients with ovarian carcinoma. Tissue extract and ascitic fluid levels of VEGF were measured using enzyme immunoassay. Tumor microvessels were detected immunohistochemically. MMP activity was measured by gelatin zymography. For the in vitro experiment, the SKOV-3 human ovarian carcinoma cell line was utilized. Cell growth was examined using MTT-assay, cell invasion activity was measured by Matrigel in vitro invasion assay, and neovascularization was assessed using an angiogenesis kit. VEGF levels in tissue extract and ascitic fluid, MVD, expression of active form MMP-2 in ascitic fluid and ascites volume were higher in ovarian cancer patients than in benign ovarian tumor patients. In addition, these were elevated in stage III and IV diseases compared to stage I and II diseases in ovarian cancer patients. MVD and expression of active form MMP-2 in ascitic fluid were closely correlated with VEGF level in tissue extracts, and MVD and ascites volume were closely correlated with VEGF level in ascitic fluid. Cell invasive activity and angiogenesis activity increased when cells were exposed to ascites. These increases were apparent when exposed to ascites obtained from ovarian cancer patients and were related to VEGF concentrations of ascitic fluid and expression of active form MMP-2 in ascitic fluid. The increased VEGF secreted from tumor cells is suggested to enhance tumor growth through angiogenesis, to produce ascites and to elevate ascitic VEGF concentrations and expression of active form MMP-2. The progression of peritoneal involvement may be induced by elevated VEGF and expression of active form MMP-2, followed by increased VEGF in the primary tumor. Control of VEGF in the primary tumor may become an effective strategy against peritoneal dissemination of ovarian carcinoma.

Adenoma↗
PubMed2005

Infected and noninfected ascites in pediatric patients.

OBJECTIVES: To determine the prevalence of spontaneous bacterial peritonitis, ascites with bacterial infection and noninfected ascites in pediatric patients with portal hypertensive ascites and to compare the clinical and laboratory features of infected and noninfected ascites. METHODS: Forty-one episodes of portal hypertensive ascites (serum-ascites albumin gradient >1.1 g/dL) in 31 patients were studied. Median age was 2.9 years. Twenty-four (77.4%) patients were cirrhotic and 20 (83.3%) were classified as Child-Pugh C. Median pediatric end-stage liver disease score was 18.5. The following ascites features were assessed: polymorphonuclear neutrophil cell count, cytology, pH, concentration of glucose, lactic dehydrogenase, total protein and albumin, Gram stain and bacteriological culture. Blood was sampled for complete blood count, coagulation studies, liver and renal function tests. Groups were compared by Mann-Whitney and chi tests (P < 0.05). RESULTS: Noninfected ascites were observed in 29 of 41 samples, spontaneous bacterial peritonitis in eight of 41 and ascites with bacterial infection in four of 41. The most prevalent clinical features were fever, voluminous ascites and encephalopathy, but there were no significant differences in the clinical features of the groups. All patients with infected ascites were cirrhotic. There was no statistical difference in Child-Pugh or pediatric end-stage liver disease status between patients with infected and noninfected ascites. Culture of ascetic fluid was positive in four of eight cases of spontaneous bacterial peritonitis. Gram-negative rods were the most prevalent bacteria cultured. Except for serum albumin, no statistical differences in biochemical markers were observed between patients with infected and noninfected ascites. CONCLUSIONS: The prevalence of infected ascites was 29.2%. With the exception of serum albumin, there were no differences in the clinical and biochemical features of patients with infected ascites and noninfected ascites.

Ascites↗
PubMed2003

Elevation of serum and ascites cancer antigen 125 levels in patients with liver cirrhosis.

BACKGROUND AND AIM: Serum cancer antigen (CA) 125 elevation has been reported in patients with liver disease, but it is poorly characterized. The present study aimed to evaluate the range of serum and ascitic CA 125 levels in patients with liver cirrhosis and to explore possible factors associated with CA 125 elevation. METHODS: A total of 70 patients were studied. Group I consisted of 30 patients with liver cirrhosis with or without ascites. Group II consisted of 30 patients with digestive malignant tumors with or without ascites. Group III consisted of 10 patients with benign ascites. The CA 125 levels were measured in the serum of all patients and also simultaneously in the ascitic fluid of 15 patients. RESULTS: Serum CA125 levels in 80% of (24/30) patients from group I were elevated, particularly in those with ascites, irrespective of the etiology of cirrhosis. Serum CA 125 levels were correlated with Child-Pugh scores (r = 0.38), but not significantly (P = 0.06). All patients from group II with ascites and from group III had elevated serum CA 125 levels, but there was no difference in the serum CA 125 levels between patients with ascites from group I (275 +/- 175 U/mL), group II (368 +/- 190 U/mL) or group III (396 +/- 287 U/mL), nor was there a significant difference in ascitic CA 125 levels (P > 0.05). The levels of serum CA 125 (198 +/- 108 U/mL) were lower than, but correlated with that of ascites (460 +/- 234 U/mL, r = 0.58, P = 0.026). The elevation of serum CA 125 accompanied by abnormalities of other tumor markers was more common in malignant ascites than in benign ascites (90% compared with 6%, P < 0.05). CONCLUSION: The elevation of serum CA 125 is common in patients with liver cirrhosis. It is related to the presence of ascites, and possibly to the insufficiency of liver function, but not the etiology of cirrhosis and ascites. Serum CA 125 probably comes from ascites. It usually predicts benign disease if the elevation of serum or ascites CA 125 is not accompanied by the abnormalities of other tumor markers.

Adult↗
PubMed2005

Ascites after orthotopic liver transplantation in children.

Ascites is a poorly understood postoperative complication of orthotopic liver transplantation (OLT). It is associated with additional morbidity and can prolong hospitalization considerably. The incidence, the factors predictive of occurrence and the etiology of this complication are not known. The charts of 118 patients with 138 OLT were analyzed according to the following criteria: ascites lasting longer than the first 10 postoperative days, assessed by loss of ascitic fluid through drainage tubes, surgical wounds or paracentesis, with a peak volume of > or =10 mL/kg/day. Patients were divided into three groups: Group 1, no ascites; Group 2, ascites associated with postoperative complications, including chylus ascites; and Group 3, ascites not associated with postoperative complications. Postoperative ascites occurred in 43 of 138 OLT (31.2%). Patients with biliary atresia, preoperative portal hypertension, postoperative pleural effusion or at retransplantation had ascites significantly more often. In 32 of 138 (23.2%) OLT, ascites was associated with postoperative complications, including thrombosis, abdominal infections, intestinal perforation, biliary leak, pancreatitis, and chylus ascites. In 11 of 138 (7.9%) OLT, ascites was the only postoperative complication (group 3). Group three patients were significantly older, and had lower preoperative platelet counts and preoperative ascites more often than group 1 patients. The primary liver diseases were mainly cystic fibrosis of the pancreas, congenital hepatic fibrosis, and North American Indian childhood cirrhosis. The serum-ascites albumin gradient suggested a hepatic origin of ascites. Postoperative ascites is associated with the duration and degree of preoperative portal hypertension. We speculate that the mechanism involved includes a disproportion between venous blood volume and liver uptake capacity of the donor organ.

Ascites↗
PubMedDate not supplied

Symptomatic ascites after discontinuation of continuous peritoneal dialysis.

OBJECTIVE: To analyze pathogenetic associations, clinical features, management, and outcome of ascites following discontinuation of continuous peritoneal dialysis (CPD). DESIGN: Retrospective analysis of symptomatic ascites, defined as ascites requiring at least one therapeutic paracentesis, developing in patients who discontinued CPD. SETTING: Dialysis unit of one tertiary care center. PARTICIPANTS: Twelve patients with 13 episodes of symptomatic ascites diagnosed soon after (a few days to 2 months) discontinuation of CPD. INTERVENTIONS: Diagnostic tests to characterize the pathogenesis of ascites; management of ascites by hemodialysis or CPD. MAIN OUTCOME MEASURES: Evolution of clinical features and nutritional parameters, survival. RESULTS: Ascites was infectious in 3 episodes (non-tuberculous mycobacterial peritonitis) and noninfectious in the remaining 10 episodes. Serum-to-ascites albumin concentration gradient (AG) was 6.3 +/- 1.5 g/L in infectious ascites and 17.3 +/- 2.7 g/L ( >11 g/L in every episode) in noninfectious ascites. Infectious ascites was managed with hemodialysis, prolonged courses of antimicrobial agents, and repeated paracentesis. Paracentesis ceased after 3-9 months. The patients were alive after 52 +/- 19 months. Seven episodes of noninfectious ascites were managed by hemodialysis and repeated paracentesis. Five patients died within 6 months from cardiac causes or sepsis. The remaining 2 patients died after 14 and 16 months from cardiac causes. Three episodes of noninfectious ascites in 2 patients were treated by restarting CPD within 2-5 months. Patients were alive at 16.9 +/- 13.2 months. They were asymptomatic and achieved fluid control. On the same CPD schedule, peritoneal clearances of urea and creatinine and normalized protein nitrogen appearance were unchanged between the initial and restarted CPD. Serum albumin was 33.3 +/- 2.5 g/L at the end of the first CPD period, 23.6 +/- 2.5 g/L soon after restarting CPD, and 31.3 +/- 5.5 g/L 4 months after restarting CPD. CONCLUSIONS: Noninfectious ascites after discontinuation of CPD is often characterized by an AG > 11 g/L, suggesting portal hypertension. Restarting CPD in noninfectious ascites may be associated with improvement in ascites symptomatology and nutritional parameters and with satisfactory survival.

Adult↗
PubMed2005

The utility of lactate dehydrogenase isoenzyme pattern in the diagnostic evaluation of malignant and nonmalignant ascites.

OBJECTIVE: Lactate dehydrogenase (LDH), a tetrameric protein composed of four monomers, is expressed as five isoenzymes. Serum LDH isoenzymes may be useful in differential diagnosis of ascites etiology since tissue damage releases isoenzymes contained therein, leading to a change in their pattern. MATERIALS AND METHODS: We determined ascitic fluid LDH level and LDH isoenzyme activities in patients with malignant and nonmalignant ascites in a total of 76 patients (43 males and 33 females). RESULTS: LDH level, LDH-4 activity and LDH-5 activity were found to be significantly higher, and LDH-1 activity was found to be lower in malignant ascites when compared with nonmalignant ascites. LDH-1 activity was detected to be significantly higher in the sterile cirrhotic ascites when compared with spontaneous bacterial peritonitis, malignant ascites, tuberculous ascites and congestive heart failure-related ascites. LDH-2 activity was found to be higher in spontaneous bacterial peritonitis when compared with the other groups. LDH-3 activity was detected to be higher in spontaneous bacterial peritonitis, malignant ascites and tuberculous ascites when compared with the sterile cirrhotic ascites. In the diagnosis of malignant ascites, the sensitivity and specificity were 96% and 76% for LDH level, 90% and 70% for LDH-1 activity, 94% and 62% for LDH-4 activity, and 100% and 56% for LDH-5 activity, respectively. CONCLUSION: Ascitic LDH and its isoenzyme pattern may be helpful for the differential diagnosis of the most common causes of ascites: cirrhosis, spontaneous bacterial peritonitis, congestive heart failure, tuberculosis and malignancy.

Ascites↗
PubMed1999

Markedly elevated levels of vascular endothelial growth factor in malignant ascites.

BACKGROUND: Vascular endothelial growth factor (VEGF) is a potent angiogenic factor that also has the ability to increase vascular permeability. Malignant ascites has significant morbidity, but the mechanism of its development is unknown. Because of the permeability-inducing properties of VEGF, we hypothesized that malignant ascites formation is associated with high levels of VEGF. The purpose of our study was to determine the role of VEGF in malignant ascites formation. METHODS: Ascites from 25 patients with gastric (n = 6), colon (n = 7), or ovarian (n = 12) cancers was collected by paracentesis or surgery. VEGF protein levels were determined by enzyme-linked immunosorbent assay. The effect of ascites on endothelial cell permeability was assessed by evaluating propidium iodide uptake by human umbilical vein endothelial cells (HUVECs) exposed to ascites. Neutralizing antibodies to VEGF added to ascites were used to determine the causal effect of VEGF in permeability induction. RESULTS: VEGF protein levels were markedly increased in malignant ascites compared with levels in nonmalignant cirrhotic ascites (controls). VEGF protein levels in ovarian, gastric, and colon cancer ascites were found to be increased 45, 23, and 12 times, respectively, compared with levels in cirrhotic ascites. Malignant ascites from patients with colon and gastric cancer caused an increase in permeability in HUVECs in all cases. Neutralizing VEGF activity in colon cancer ascites decreased in-vitro HUVEC permeability in three of four cases. CONCLUSIONS: VEGF protein levels are markedly elevated in malignant ascites. VEGF may play a role in malignant ascites formation by increasing endothelial cell permeability.

Angiogenesis Inducing Agents↗
PubMed2002

Hyper- or hypothyroidism: its association with the development of ascites syndrome in fast-growing chickens.

The ascites syndrome in broiler chickens is attributed to the progress in genetic selection for rapid growth, coupled with the metabolic burden imposed by exposure to a relatively low-ambient temperature (T(a)). The syndrome is mainly characterized by hematocrit elevation, decline in blood oxygen saturation, accumulation of fluid in the abdominal cavity, and finally, death. Ascitic chickens have demonstrated hypothyroidism coupled with a marked stress response (high corticosterone concentration) and reduction in the hemoglobin content. The objective of the present study was to examine the role of thyroid and corticosterone hormones in the development of the syndrome. Ascites was induced by exposure to a gradually declining T(a) and supplementation of a pellet-form diet. Exogenous thyroxin (T(4)) and propylthiouracil (PTU) (in Experiments 1 and 2, respectively) were supplemented in drinking water to induce hyper- or hypothyroidism, respectively. Ascites syndrome was developed in 21.5% and 23% of the birds exposed to ascites-induced conditions (Exps. 1 and 2, respectively). Excess T(4) (Exp. 1) significantly reduced the percentage of ascites (down to 7%), whereas PTU (Exp. 2) significantly increased the appearance of the syndrome (35%). In the T(4)-treated chickens, although the T(4) concentration reached pharmacological levels, the triiodothyronine (T(3)) concentration remained within physiological levels, whereas T(3) in the ascitic birds exhibited a reduction pattern similar to that observed in the ascitic non-supplemented ones. In the PTU-treated chickens, however, both ascitic and non-ascitic birds demonstrated significant reductions in both T(4) and T(3) concentrations. In both experiments, ascitic chickens exhibited a considerable stress response, characterized by a significant and persisted elevation in plasma corticosterone concentration, which was in accordance with a similar elevation of hematocrit, and the PTU-treated non-ascitic birds exhibited a similar stress response. At 5 weeks of age, ascitic birds and the PTU-treated non-ascitic ones exhibited significant reductions in the hemoglobin content of their red blood cells. It may be concluded that deficiency in the thyroid hormones and elevated corticosterone may play a key deleterious role in the development of the ascites syndrome.

Aging↗
PubMed2003

Detection of type IV collagenase activity in malignant ascites.

AIM: Type IV collagenase participates in invasion and metastasis of cancer cells. Malignant ascites is a manifestation of advanced malignant disease that is associated with invasion and metastasis of the peritoneal cavity. Thus, it is reasonable to hypothesize that type IV collagenase is linked to malignant ascites. The purpose of our study was to detect type IV collagenase activity in malignant ascites so as to provide the scientific basis for clinic diagnosis and treatment of malignant ascites. METHODS: Cirrhotic ascites (n=36), tuberculous ascites (n=8) and malignant ascites (n=23) from patients with gastric cancer (n=6), colon cancer (n=5), ovarian cancer (n=8) and other cancers (n=4), including 2 hepatocellular cancers, 1 pancreatic cancer, 1 primary peritoneal carcinoma were collected by paracentesis. The ascites were made cell-free by centrifugation and stored frozen at -70 degrees C before determination. Type IV collagenase activity was determined by gelatin zymography. RESULTS: The activity of matrix metalloproteinases-2 and -9 could not be detected in ascites of hepatic cirrhosis and tuberculous peritonitis but could be detected in 20 and 18 out of 23 malignant ascites respectively. The positive rate of type IV collagenase (MMP-2, 87.0% and MMP-9, 78.3%) was higher than that by routine ascites tests (P<0.01) in malignant ascites. Furthermore, the activity of MMP-2 was higher than that of MMP-9 (P=0.022<0.05). CONCLUSION: Type IV collagenase is positive in malignant ascites. Detection of type IV collagenase activity is useful in qualitative diagnosis of ascites. Type IV collagenase may play an important role in malignant ascites formation.

Ascites↗
PubMed2003

Role of VEGF and CD44v6 in differentiating benign from malignant ascites.

AIM: To detect the vascular endothelial growth factor (VEGF) and soluble splice variant 6 of CD44 (sCD44v6) levels in ascites and to explore their role in differentiating benign from malignant ascites. METHODS: Cirrhotic ascites (n=36), tuberculosis ascites (n=8) and malignant ascites (n=23) were collected and studied. Concentrations of soluble VEGF and sCD44v6 in various kinds of ascites (n=67) were measured using a sandwich enzyme-linked immunoadsorbent assay. RESULTS: VEGF and sCD44v6 levels in malignant ascites were 640.74+/-264.81 pg/ml and 89.22+/-38.20 ng/ml, respectively, both of which were significantly higher than those in cirrhotic ascites and tuberculous ascites (q=18.98, 11.89 and q=8.92, 5.09; P<0.01). However, the levels of VEGF and sCD44v6 in cirrhotic and tuberculous ascites had no significant difference (q=0.48, 0.75; P>0.05). Furthermore, VEGF levels in malignant ascites in patients with ovarian cancer were higher than those with gastric and colon cancer (q=5.03, 6.79; P<0.01, respectively). But differences of VEGF levels between gastric and colon cancer were not significant (q=1.90, P>0.05). Whereas, sCD44v6 levels in malignant ascites from patients with ovarian, gastric and colon cancer had no significant difference (q=0.06, 0.91, 0.35; P>0.05, respectively). In comparison with cirrhotic and tuberculous ascites, when the upper limit of its VEGF mean levels 119.44 pg/ml (70.90+/-48.54) and sCD44v6 mean levels 63.59 ng/ml (44.42+/-19.17) was taken as the minimum cutoff limit, the sensitivity and specificity of VEGF and sCD44v6 of this assay to the diagnosis of malignant ascites were 91.3%, 90.9% and 73.9%, 88.7% respectively. CONCLUSION: Elevated levels of VEGF and sCD44v6 may be useful in differential diagnosis of benign and malignant ascites.

Adult↗
PubMed2001

Bradykinin in the ascitic fluid of patients with liver cirrhosis.

Bradykinin, a nonapeptide with vasodilatory and permeabilizing activity, is generated through the cleavage of high-M(r) ('high-molecular-weight') kininogen by kallikrein, and its generation is facilitated by plasmin. In the ascitic fluid of patients with cirrhosis, there is massive cleavage of high-M(r) kininogen and activation of fibrinolysis, but bradykinin has never been measured directly. In the ascitic fluid of 24 patients with cirrhosis, we measured bradykinin-(1-9)-nonapeptide levels by RIA after liquid-phase and subsequent HPLC extraction, and those of its catabolic product bradykininin-(1-5)-pentapeptide by ELISA after liquid-phase extraction. Cleaved high-M(r) kininogen, activated factor XII and plasmin-antiplasmin complexes were measured in ascitic fluid and plasma. Plasma renin activity (PRA) was also determined. As a control, we also analysed plasma from 24 healthy subjects matched for sex and age with the patients. In the ascitic fluid from patients with cirrhosis, the median bradykinin-(1-9) concentration was 3.3 fmol/ml (range 0.2-29.0 fmol/ml), and the median bradykinin-(1-5) concentration was 210 fmol/ml (range 58-7825 fmol/ml). The levels of bradykinin-(1-5) in ascitic fluid were higher in patients with refractory ascites [median 1091 fmol/ml (range 58-7825 fmol/ml)] than in patients with responsive ascites [134 fmol/ml (72-1084 fmol/ml)] (P=0.010). Ascitic fluid levels of bradykinin-(1-9) were not related to the severity of ascites. PRA was higher in patients with refractory ascites [23.0 ng x h(-1) x ml(-1) (7.9-80.0 ng.h(-1).ml(-1))] than in patients with responsive ascites [6.9 ng x h(-1) x ml(-1) (0.9-29.4 ng x h(-1) x ml(-1))] (P=0.002). In ascitic fluid, 48% (19-68%) of high-M(r) kininogen was cleaved, and plasmin-antiplasmin complexes were more concentrated than in plasma (P=0.0001). In conclusion, in the ascitic fluid of patients with cirrhosis, both bradykinin-(1-9) and bradykinin-(1-5) are present, with cleavage of high-M(r) kininogen and activation of fibrinolysis. The highest levels of the long-lived metabolite bradykinin-(1-5) were found in the ascitic fluid of patients with refractory ascites and high PRA. Activation of the kinin system may therefore be involved in decompensating cirrhosis, but a cause-effect relationship remains to be established.

Adult↗
PubMed2004

[Clinical significance of detecting VEGF, CD44v6, MMP-2, and MMP-9 in malignant ascites].

BACKGROUND & OBJECTIVE: Cytological examination, despite of its high specificity, has been found to have a low sensitivity in the diagnosis of malignant ascites due to the high percentage of false negative results. So it is indispensable to seek appropriate cancerous markers in ascites. The aim of this study was to determine vascular endothelial growth factor (VEGF), CD44v6 levels and matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) activities in ascites so as to provide scientific basis for clinical diagnosis and treatment of malignant ascites. METHODS: A total of 67 samples were collected, including cirrhotic ascites (36), tuberculosis ascites (8), and malignant ascites (23). VEGF and CD44v6 levels were determined using enzyme-linked immunosorbent assay (ELASA). MMP-2 and MMP-9 activities were determined by gelatin zymography. RESULTS: VEGF and CD44v6 levels in malignant ascites were 640.74+/-264.81 ng/L and 89.22+/-38.20 microg/L, respectively, which were significantly higher than those in cirrhotic ascites (67.05+/-51.91 ng/L, 44.79+/-18.02 microg/L) and tuberculosis ascites (88.25+/-24.12 ng/L, 50.25+/-12.57 microg/L) (P< 0.01, respectively). The activities of MMP-2 and MMP-9 could not be detected in cirrhotic ascites and tuberculosis ascites but could be detected in 20 and 18 out of 23 malignant ascites respectively. CONCLUSION: VEGF, CD44v6 levels increase significantly and MMP-2, MMP-9 activities are obvious in cancerous ascites. The detection of VEGF, CD44v6 levels and MMP-2, MMP-9 activities are useful in differential diagnosis of benign and malignant ascites.

Adult↗
PubMed2004

[Changes of ascites nitric oxide according to the treatment course in cirrhotic patients with spontaneous bacterial peritonitis].

BACKGROUND/AIMS: Nitric oxide (NO) is a molecule involved in vascular dilatation and pathogen suppression. It also has immunologic and regulatory functions. Liver cirrhosis is characterized by an increased risk for bacterial infections, including spontaneous bacterial peritonitis (SBP). The role of NO in SBP which develops in cirrhosis has not been clearly established. The aim of this study was to investigate the role of NO in the pathogenesis of SBP and its clinical usefulness for prediction of disease prognosis. METHODS: This study was designed to investigate the changes of ascites NO in the course of treatment. Nitric oxide metabolite (nitrites+nitrates [NOx]) was measured by chemiluminescence in 84 ascites samples obtained from 84 cirrhotic patients. Among them, the 38 patients with SBP were treated with cefotaxime 2.0 g, q 12hr for 7 days. In 24 of SBP patients, ascites was obtained consecutively before treatment (day 0), during treatment (day 2), and after treatment (day 7). RESULTS: Ascites NO levels in the patients with SBP (n=38; 82.3 +/- 14.4 microM) were not different from those in patients with sterile ascites (n=46; 54.6 +/- 13.0 microM). There was no significant change of NO levels in sequential ascites samples during antibiotic treatment. Ascites NO level before treatment was significantly higher in SBP patients who responded to antibiotics (n=26; 101.86 microM/L) than that in SBP patients who did not respond to antibiotics (n=12; 40.03 microM/L, P=0.044). A significant direct correlation was found between ascites and serum NO levels before treatment (Pearson correlation, r2=0.86, P=0.001). Among the SBP patients, treatment response rate to antibiotics were significantly higher in those patients with pretreatment NO level > or = 80 microM/L in multivariate analysis. CONCLUSIONS: Ascites NO level was not different between ascites from SBP patients and ascites from cirrhotic patients with sterile ascites. There were no changes of ascites NO in SBP patients during treatment. Therefore ascites NO was not useful to predict the progress of SBP. Ascites NO levels reflect serum NO levels, and the patients with higher NO level may have better response to antibiotics.

Adult↗
PubMed1994

Diagnostic parameters for spontaneous bacterial peritonitis in hepatitis B-related cirrhosis: comparison of ascitic fluid polymorphonuclear cell count, lactate and pH values.

BACKGROUND: The clinical value of ascitic fluid pH or lactate in the diagnosis of spontaneous bacterial peritonitis was debated in alcoholic cirrhosis. It was rarely discussed in hepatitis B-related cirrhosis. We investigated the best rapid diagnostic method in spontaneous bacterial peritonitis of patients with hepatitis B-related cirrhosis. METHODS: Ascitic fluid polymorphonuclear cell count, ascitic fluid pH, arterial-ascitic fluid pH gradient, ascitic fluid lactate, and arterial-ascitic fluid lactate gradient were analyzed in 79 patients with sterile portal hypertension-related ascites, 31 patients with spontaneous bacterial peritonitis, 16 patients with hepatocellular carcinoma, 15 patients with malignancy-related ascites and 9 patients with other miscellaneous diseases. RESULTS: The sensitivity, specificity and accuracy of the diagnosis of spontaneous bacterial peritonitis were 100, 94 and 95% with the cut-off value of an ascitic fluid polymorphonuclear cell count > or = 250 cells/mm3, and were 86, 98 and 96% with that value > or = 500 cells/mm3, respectively. The sensitivity, specificity and accuracy were 29, 92, 80% using ascitic fluid pH < or = 7.35 as a cut-off value; 38, 91, 82% using arterial-ascitic fluid pH gradient > or = 0.1 as a cut-off value; 52, 92, 85% using ascitic fluid lactate > or = 32 mg/dL as a cut-off value, and 38, 96, 85% using arterial-ascitic fluid lactate gradient > or = 20 mg/dL as a cut-off value. CONCLUSIONS: The sensitivity of ascitic fluid pH or lactate was too low to aid in a diagnosis of spontaneous bacterial peritonitis in hepatitis B-related cirrhosis in spite of the acceptable specificity. An ascitic fluid polymorphonuclear cell count > or = 250 cells/mm3 or > or = 500 cells/mm3 was the major and appropriate aids in the rapid diagnosis of spontaneous bacterial peritonitis.

Adult↗
PubMed1996

[Study of nitric oxide synthases, nitric oxide and tumor necrosis factor in different types of ascites].

The purpose of this study was to elucidate the clinical significance of nitric oxide synthases (NOS), nitric oxide (NO) and tumor necrosis factor (TNF) in different types of ascites. NOS, NO and TNF in ascitic transudates of 21 patients with liver cirrhosis, ascitic exudate of 32 patients with liver cirrhosis and carcinogenesic ascites of 19 patients were measured by Griess, ELISA and colorimetric methods. Compares to the value in ascitic transudate of 21 patients with liver cirrhosis, NOS (7.32 +/- 3.13 nmol.min-1.g-1), NO (15.4 +/- 7.6 mumol/L) and TNF (331.7 +/- 121.2 mumol/L) in ascitic exudate of 32 patients with liver cirrhosis were significantly higher (P < 0.01). The NO (10.7 +/- 3.2 mumol/L) and TNF (185.6 +/- 84.1 mumol/L) in carcinogenesic ascites of 19 patients were between those in ascitic exudates and those in ascitic transudates of patients with liver cirrhosis (P < 0.05 or 0.01). The NOS activity was highest in carcinogenesic ascites. The decrease of 24h urine volume in patients with cirrhosis was relative to the increase of NO level in ascites. Those suggested that measurements of NOS, NO and TNF in ascites are helpful in differential diagnosis of ascites. The separation between NO level and NOS activity in ascites indicates that the ascites is carcinogenesis.

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