Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASCITES”

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

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

At least 433 records · Page 24Linked to original sources

Enhancement of ascites on MRI following intravenous administration of Gd-DTPA.

OBJECTIVE: The enhancement of ascites following intravenous administration of Gd-DTPA on MRI was investigated. MATERIALS AND METHODS: Magnetic resonance imaging was performed in 20 patients with ascites (8 peritoneal carcinomatosis, 2 tuberculous peritonitis, 8 liver cirrhosis, 1 nephrotic syndrome, 1 peritoneal adhesion), and T1-weighted SE images were obtained before and 15-20 min following intravenous administration of Gd-DTPA (0.1 mmol/kg). RESULTS: There were 10 exudative ascites and 10 transudative ascites. Eight of 10 exudative ascites showed enhancement, in contrast to none of 10 transudative ascites. The precontrast signal intensity ratios (SIRs) of exudative ascites were significantly higher (p < 0.05) than those of transudative ascites, and the postcontrast SIRs of exudative ascites were significantly higher (p < 0.01) than those of transudative ascites. This difference was thought to be caused by increased peritoneal permeability and higher protein concentration in the cases with exudative ascites in this study. CONCLUSION: It is concluded that enhancement of ascites on MRI obtained 15-20 min after intravenous administration of Gd-DTPA is not an uncommon finding in exudative ascites (especially associated with peritoneal carcinomatosis).

Ascites↗

Ascites fluid as a possible origin for hyperfibrinolysis in advanced liver disease.

OBJECTIVES: Advanced liver disease is associated with both exaggerated fibrinolysis and with ascites. This study was undertaken to determine whether fibrinolytic activity exists in the ascites fluid of patients with liver disease and to see whether such activity is associated with evidence of plasma fibrinolysis. METHODS: Both the ascites fluid and plasma from 15 patients with cirrhotic ascites (group A) were evaluated for markers of fibrinolysis: fragment D-dimer, plasminogen, fibrinogen, and fibrin split products. In addition, the euglobulin lysis time, a test highly specific for fibrinolysis, was evaluated in the ascites fluid samples. As a control group, the plasma from 15 cirrhotic patients without ascites (group B) was evaluated for markers of fibrinolysis. RESULTS: In group A, elevated fragment D-dimer and fibrin split products were uniformly found in ascites fluid in concentrations that would be considered pathologically elevated if in plasma. Ascites fluid was also depleted, compared with plasma, of both plasminogen and fibrinogen. These results, along with the short euglobulin lysis time in 83% of the patients, suggest that increased fibrinolytic activity is present in ascites fluid. In 93% of these patients, plasma D-dimer was elevated. The mean plasma plasminogen was also low in these patients. In group B, only 33% of patients had elevated plasma D-dimer. CONCLUSIONS: Ascites fluid has fibrinolytic activity. Because ascites fluid reenters the systemic circulation via the thoracic duct, via a natural peritoneovenous shunt, ascites fluid warrants serious consideration as a pathological fluid that contributes to the systemic fibrinolytic state found in the majority of our patients with ascites.

Ascitic Fluid↗

Pharmacotherapy of ascites associated with cirrhosis.

Cirrhotic patients frequently develop ascites during the course of their disease. The appearance of ascites is the final consequence of profound disturbances in systemic and splanchnic haemodynamics, and in renal and hormonal function. The alterations in renal function consist of a decreased ability to excrete sodium and water, and in more severe cases, a reduction in renal blood flow and glomerular filtration rate. No effective drug therapy is yet available for water retention and renal failure in these patients. Sodium retention, however, may be treated by the administration of diuretics. The diuretics most commonly used in the treatment of cirrhotic patients with ascites are loop diuretics, particularly furosemide (frusemide), and distal, or 'potassium-sparing' diuretics such as spironolactone. Although furosemide has a much greater natriuretic potency than spironolactone in healthy individuals, studies in cirrhotic patients with ascites have shown that spironolactone is more effective than furosemide in the elimination of ascites. Nowadays, however, therapeutic paracentesis associated with plasma expanders has replaced diuretic therapy as the initial treatment for cirrhotic patients hospitalised with tense ascites since it is more effective and is associated with a lower rate of complications than diuretic therapy. Diuretics should be given after the elimination of ascites by paracentesis to avoid the reaccumulation of the abdominal fluid. Only cirrhotic patients with mild ascites should be treated initially with diuretics. Cirrhotic patients with ascites frequently develop a spontaneous infection of the ascitic fluid which is usually caused by Gram-negative bacilli from enteric origin and has a great tendency to recur after therapy. The antibiotics of choice for this infection are third-generation cephalosporins. Long term administration of norfloxacin, which causes a selective elimination of Gram-negative bacilli from the intestinal flora, is effective in preventing the recurrence of ascites infection in these patients. Finally, cirrhotic patients with ascites are prone to develop renal failure when treated with a variety of pharmacological agents, particularly aminoglycosides and nonsteroidal anti-inflammatory drugs. The administration of the latter drugs may also cause dilutional hyponatraemia and refractory ascites since they induce water retention and impair the renal response to diuretics.

Acute Kidney Injury↗

Tuberculous peritonitis: diagnostic value of ascitic fluid pH and lactate.

BACKGROUND: The analytical pattern of ascitic fluid in peritoneal tuberculosis is frequently similar to that found in other causes of ascites. The diagnostic value of the ascitic fluid pH and lactate in cases of tuberculous peritonitis has not yet been established. METHODS: Ascitic fluid pH, lactate, total proteins, cell count, lactate dehydrogenase, glucose, and their blood-ascitic gradients were determined in 10 patients with tuberculous peritonitis (group I). These results were compared with those obtained from 40 patients with cirrhotic sterile ascites (group II), 16 patients with spontaneous bacterial peritonitis (group III), and 18 patients with malignant ascites (group IV). RESULTS: A decreased pH and an elevated lactate level in ascitic fluid were found in patients in group I in comparison with those in group II (p < 0.001). No significant differences were found between group I and groups III and IV. The arterial blood-ascitic fluid pH gradient was more than 0.10 (p < 0.001), and the ascitic fluid-serum lactate gradient was greater than 15 mg/dl (p < 0.001) in group I when compared with group II. No significant differences were found between group I and groups III and IV. CONCLUSIONS: Ascitic fluid pH and lactate are useful markers in differentiating tuberculous peritonitis from cirrhotic sterile ascites. However, these variables lack specificity, as they are also decreased and increased, respectively, in cases of malignant ascites and spontaneous bacterial peritonitis.

Adult↗

Immunoreactive human chorionic gonadotropin and its free beta subunit in serum and ascites of patients with malignant tumors.

Human chorionic gonadotropin (hCG) is a clinically relevant marker of trophoblastic and nontrophoblastic malignancies. In the present studies, in addition to determining serum hCG, we investigated the presence and properties of hCG immunoreactivity in ascites of patients with nontrophoblastic malignant tumors and, for comparison, in ascites caused by cirrhotic liver disease. Total hCG immunoreactivity [hCG (+hCG-beta)] was found to be elevated above the reference value (greater than 5 IU/liter) in the serum of 2 of 20 patients with cirrhosis and 11 of 20 patients with malignant tumors. For comparison, in ascites, hCG (+hCG-beta) concentrations were frequently higher than in the corresponding serum samples and exceeded 10 IU/liter in 0 of 20 cirrhotic samples and in 16 of 20 malignant samples. In order to elucidate the nature of the hCG immunoreactive material, all samples were then assessed by immunoradiometric assays specific for the intact hCG molecule (holo-hCG) and the free hCG-beta subunit, respectively. In the holo-hCG assay, elevated values were detected in 0 of 20 (0 of 20) cirrhotic ascites (serum) samples and 0 of 20 (1 of 20) malignant ascites (serum) samples. In the free hCG-beta assay, on the other hand, no positive results were obtained in the ascites or serum of 20 patients with liver cirrhosis; however, 8 of 20 serum samples and 16 of 20 ascites samples derived from tumor patients were positive. In accord with the immunological data, gel chromatographical studies of malignant ascites revealed the abundance of free hCG-beta subunit rather than that of holo-hCG. In contrast to malignancy-related ascites, in ascites of patients receiving hCG injections for treatment of infertility, holo-hCG was more abundant than free hCG-beta immunoreactivity. Incubation experiments of purified holo-hCG in ascites for 24 h at -20, 20, or 37 degrees C showed no substantial dissociation of the hCG molecule and release of free hCG-beta immunoreactivity, thus arguing against production of free hCG-beta by degradation of holo-hCG and in favor of its tumor-related secretion. In conclusion, hCG-beta immunoreactivity is frequently elevated in malignancy-related ascites and appears to be related to the presence of free beta subunit of hCG rather than that of the intact hCG molecule. Interestingly, hCG-beta determination in ascites proved to be clearly superior to serum measurement in discriminating between tumor and cirrhosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Essential requirement of toll-like receptor 4 expression on CD11c+ cells for locoregional immunotherapy of malignant ascites using a streptococcal preparation OK-432.

Toll-like receptors (TLRs) are important molecules that stimulate the innate immunity in order to eradicate microbial pathogens, after which the adaptive immunity emerges. The involvement of TLRs in the action mechanism of OK-432, a bacterial preparation, was investigated in the locoregional treatment of malignant ascites from gastric cancer. The expression of TLRs in ascites cells was analyzed using reverse-transcription polymerase chain reaction specific for TLRs and by flow cytometry using anti-TLR2, -TLR4, -CD4, -CD8, and -CD11c antibodies. These measurements were compared with the locoregional response of OK-432 immunotherapy for malignant ascites, as well as TNF-alpha producing potential, which was measured by ELISA, of ascites cells stimulated in vitro with OK-432. It was observed that OK-432 immunotherapy for malignant ascites showed 8 positive (67%) and 4 negative responses with the tolerable adverse effects of fever elevation and abdominal pain. The TNF-alpha production of ascites cells by in vitro OK-432 stimulation was significantly higher in responder patients than in non-responders. The clinical responses were correlated with the expression of the TLR4 gene of ascites cells. The TNF-alpha-producing potential of ascites cells by in vitro OK-432 stimulation was dependent on the existence of a CD11c + TLR-4+ cell population in ascites cells. OK-432 was highly stimulatory for TNF-alpha production of ascites cells compared with other biological response modifiers of PSK and LEM. These results suggest that TLR-4 expression on ascites cells of a macrophage lineage is essential for ascites cells to produce TNF-alpha in relation to OK-432 stimulation and for subsequent positive clinical responses in locoregional immunotherapy using OK-432 for malignant ascites from gastric cancer.

Ascites↗

Clinical significance of complements in ascitic diseases: elevated complement levels disapproving the liver disease origin.

In a two-year period, ascitic fluid concentrations of complement 3c and complement 4 were measured in 110 patients with sterile cirrhotic ascites, 31 patients with spontaneous bacterial peritonitis, 65 patients with hepatocellular carcinoma, 36 patients with peritoneal carcinomatosis and 12 patients with miscellaneous diseases (nephrotic syndrome 4, systemic lupus erythematosus 3, secondary peritonitis 2, cardiac ascites 1, eosinophilic peritonitis 1 and tuberculosis peritonitis 1) to assess the clinical utility of ascitic fluid complements. The ascitic fluid level of complements 3c or C4 was significantly higher in patients with peritoneal carcinomatosis (32.8 +/- 10.2, 13.4 +/- 7.4 mg/dL) than in patients with sterile cirrhotic ascites (9.2 +/- 5.2, 4.5 +/- 3.9 mg/dL, p < 0.001), spontaneous bacterial peritonitis (8.2 +/- 4.1, 3.8 +/- 2.4 mg/dL, p < 0.001) or hepatocellular carcinoma (12.8 +/- 8.3, 5.6 +/- 4.4 mg/dL, p < 0.001). However, it was not significantly different from the miscellaneous disease group. To verify that ascites formation is not related to liver disease origin, diagnostic sensitivity, specificity and accuracy were 83.3%, 92.7% and 90.9%, respectively, by the ascitic fluid level of complement 3c higher than the cut-off value (20 mg/dl); or 60.4%, 89.8% and 84.3%, respectively, by the ascitic fluid level of complement 4 higher than the cut-off value (10 mg/dL). A direct correlation was found between the ascitic fluid protein level and the ascitic fluid complement 3c (r = 0.70) or complement 4 (r = 0.57) level. Based on results in this study, we can conclude that measuring ascitic fluid complements is clinically useful in disapproving the liver disease origin of ascites formation. However, it is of little value in diagnosing spontaneous bacterial peritonitis or hepatocellular carcinoma.

Ascites↗

Experimental, clinical, and metabolic results of side-to-side portacaval shunt for intractable cirrhotic ascites.

BACKGROUND: Intractable ascites, refractory to medical therapy, occurs in approximately 10 percent of patients with ascites from cirrhosis and is almost always fatal. Sinusoidal hypertension resulting from hepatic venous outflow obstruction plays a primary role in the pathogenesis of cirrhotic ascites and provides the rationale for decompression of the liver by side-to-side portacaval shunt in treatment of intractable ascites. This report presents the experimental basis for the use of side-to-side shunt and long-term results of a prospective study in 34 selected patients with intractable cirrhotic ascites. STUDY DESIGN: In the experimental studies, hepatic venous outflow obstruction and massive ascites were produced in dogs by ligation of the hepatic veins, and the effect of portacaval shunts on ascites, thoracic duct lymph flow, and aldosterone secretion were measured. In the clinical study, 34 carefully selected patients with cirrhosis (91 percent alcoholic) and truly intractable ascites (failure of medical therapy for 5 to 24 months) underwent side-to-side portacaval shunt. The effects on ascites, survival, metabolic abnormalities, and quality of life were studied prospectively during follow-up that was longer than 5 years in all but two patients. Quantitative Child's risk classes in percent of patients were A in 0, B in 68, and C in 32. RESULTS: In the experimental studies, side-to-side portacaval shunt permanently relieved severe ascites, reduced the 13-fold increase in thoracic duct lymph flow rate to almost normal, and abolished the aldosterone hypersecretory response to minimal hepatic venous outflow obstruction. End-to-side portacaval shunt was much less effective. In the clinical study, side-to-side portacaval shunt reduced mean portal vein-inferior vena cava pressure gradient from 282 mm saline to 4 mm and permanently relieved all patients of ascites without subsequent requirement of diuretic therapy. Two patients who died of hepatoma, and one who died of heart failure developed terminal ascites. Thirty-day mortality rate was 6 percent, and long-term survival rates at 5, 10, and 15 years were 75 percent, 74 percent, and 73 percent. In metabolic studies, side-to-side shunt produced marked diuresis and natriuresis and abolished hypersecretion of aldosterone. Quality of life was generally improved as a result of a low incidence of recurrent portal-systemic encephalopathy (6 percent), abstinence from alcohol in 91 percent, improvement in liver function in 81 percent, and improvement in Child's risk class. The portacaval anastomosis remained permanently patent in every patient. CONCLUSIONS: Side-to-side portacaval shunt is very effective treatment of intractable ascites from cirrhosis. Our results are attributable to careful selection of patients, an organized system of care, and a program of rigorous, lifelong follow-up that emphasizes abstinence from alcohol and dietary protein restriction.

Adult↗

Analysis of ascitic fluid in cirrhosis.

In order to determine the composition of "normal" ascitic fluid, the results of analysis of the first paracentesis on 347 consecutive cirrhotic patients with ascites at the West Haven Veterans Administration Hospital between 1955 and 1976 were examined. The ascites was considered "normal" in 259 patients. Bacterial peritonitis was present in 51, malignant ascites in 18, pancreatitic ascites in 15, and ascites of other types in 4 patients. Normal ascites is sterile, usually clear, and contains 281 +/- 25 leukocytes/mm3 (mean +/- SEM), 27 +/- 2% of which are polymorphonuclear. In spontaneous bacterial peritonitis the fluid is usually cloudy, contains 6084 +/- 858 white blood cells/mm3, 77 +/- 4% of which were PMN and culture is positive for a single bacterial species, usually enteric in origin. Malignant and pancreatitis ascites are sterile, often cloudy, and contain an average of 696 +/- 273 and 1821 +/- 833 leukocytes/mm3, respectively, about half of which are polymorphonuclear. Amylase activity is increased in pancreatitic ascites, but not in other types of ascites. Stained smears of sediment for bacteria are often positive in bacterial peritonitis, but not in the other categories. Neither the specific gravity, protein concentration, nor glucose level is useful in the differential diagnosis of ascites. Based on the critical number of leukocytes alone, (500/mm3), one can accurately differentiate infected from uninfected fluid in over 90% of ascitic patients.

Amylases↗

Albumin to ascites: demonstration of a direct pathway bypassing the systemic circulation.

The transport of plasma albumin and newly made albumin into ascitic fluid was studied in eight patients with cirrhosis and ascites. The thoracic duct was cannulated in two patients and lymph collected over a period of 2 hr. Simultaneously albumin-(131)I and carbonate-(14)C were injected intravenously. The albumin-(131)I measured the transfer of plasma albumin into ascites and into thoracic duct lymph. The carbonate-(14)C, by labeling newly formed albumin, permitted the estimation of the transfer of newly formed albumin into plasma, ascites, and lymph. If the newly synthesized albumin entering ascites and thoracic duct lymph is delivered initially into the plasma, then the ratios of the albumin-(14)C and -(131)I in ascites and lymph compared with the content of albumin-(14)C and -(131)I in plasma would be identical. However, if some newly formed albumin is delivered directly into ascites or lymph, the ratio for albumin-(14)C would be higher than that for albumin-(131)I in lymph or ascites. The ratios of both labeled albumins found in ascites or lymph are expressed as per cent of the total plasma pool. In the eight patients studied 4.2-11.7% of the albumin-(14)C in plasma was found in ascites in 2 hr whereas only 0.4-2.2% of plasma albumin-(131)I entered in this same period. In the two patients studied during thoracic duct lymph drainage 6.1 and 13.5% of newly made albumin-(14)C appeared in lymph in 2 hr whereas only 2.8 and 3.8% of plasma albumin-(131)I was found in the lymph. In cirrhosis with ascites some newly formed albumin entered ascites and thoracic duct lymph by a direct pathway from the liver bypassing the systemic circulation.

Albumins↗

Pancreatic ascites.

Pancreatic ascites is rarely considered in the differential diagnosis of exudative ascites, and is in fact missed in a majority of patients. Eleven cases of pancreatic ascites are described. 63.6% were chronic alcoholics. The clinical diagnosis was cirrhosis of liver (5/11), tuberculous peritonitis (5/11) or malignant peritonitis (1/11). In all patients ascites was exudative and the ascitic fluid amylase was markedly elevated (mean +/- SD: 7815 +/- 6507 SU/dl). Endoscopic retrograde pancreatography (ERP) performed in 4 patients demonstrated the site of leak in 3. Laparoscopy performed in 8 patients helped in the diagnosis of pancreatic ascites in all, which was confirmed on histology. Laparoscopy ruled out other causes of exudative ascites in all. We conclude that pancreatic ascites should be suspected in any patient with exudative ascites, especially chronic alcoholics and that ascitic fluid amylase should be routinely performed in all such cases. High ascitic fluid content is virtually diagnostic of pancreatic ascites. ERP is essential in preoperative assessment or planning endoscopic treatment. Laparoscopy is an invaluable investigation to rule out other conditions such as tuberculous or malignant peritonitis and cirrhosis of liver.

Adolescent↗

[Chylous ascites in cirrhotic and non-cirrhotic patients].

Chylous ascites is an accumulation of lymph in the abdominal cavity. The diagnosis is established when the concentration of triglycerides in plasma is greater than in ascitic fluid over a level of 200 mg/dl. The clinical and biochemical characteristics of 22 patients with chylous ascites (11 cirrhotics and 11 non cirrhotics) were studied in order to assess differences between patients with and without hepatic cirrhosis. The cirrhotic patients with chylous ascites showed lower protein (1.3 +/- 0.74 mg/dl, p = 0.002) and cholesterol concentration (46.0 +/- 45.2 mg/dl, p = 0.02) in ascitic fluid than non cirrhotic patients (3.1 +/- 1.09 mg/dl, and 100.85 +/- 41.7 mg/dl, respectively). In addition, the cellularity in the ascitic fluid was also lower in cirrhotic patients (209.09 +/- 113.96 cel/mm3) versus (831.8 +/- 945.08 cel/mm3; p < 0.05). Four patients (18.18%) presented high adenosine deaminase levels (ADA) in the ascitic fluid in the absence of tuberculous peritonitis. The authors conclude that the biochemical differences observed in the ascitic fluid of the cirrhotic patients with chylous ascites may be explained by a dilutional mechanism due to the combination of "clear" ascites secondary to portal hypertension and chylous ascites. Furthermore, chylous ascites could be the cause of an elevation in ADA in the absence of tuberculous peritonitis.

Adenosine Deaminase↗

Pancreatic ascites as a powerful inducer of inflammatory cytokines. The role of known vs unknown factors.

OBJECTIVES: To determine if pancreatic ascites will induce interleukin 1 beta (IL-1 beta) or tumor necrosis factor alpha (TNF-alpha) production outside the pancreas and examine the possible components responsible. DESIGN: Severe pancreatitis was induced in rats (n = 30) by pancreatic duct infusion with 4% glycodeoxycholic acid; pancreatic ascites was collected 18 hours later. In vitro studies used quiescent murine splenic or pulmonary macrophages (10(5)/mL) which were exposed to media alone (control), trypsin, chymotrypsin, cathepsin-B, 20% ascites (vol/vol), 50% ascites, or endotoxin (lipopolysaccharide, 10 micrograms/mL, positive control) for 4 hours. Subsequently, pancreatic ascites was cultured for bacteria and assayed for endotoxin and cytokines (interleukin 1, interleukin 6, interleukin 8, TNF-alpha, or interferon gamma). The experiments were then repeated using 20% and 50% ascites that was sterile and cytokine-free (SCF ascites). In vivo studies used 100% (n = 8) or 50% (n = 12) SCF ascites or normal rat serum (control, n = 12) for a 10-second pulmonary lavage (100 microL) in adult mice, with lungs collected at 6 hours for cytokine gene analysis. SETTING: Surgical basic science research laboratory. MAIN OUTCOME MEASURES: Interleukin 1 beta and TNF-alpha gene induction was assessed by quantitative competitive reverse-transcription polymerase chain reaction and cytokine protein production was determined by enzyme-linked immunosorbent assay. RESULTS: Macrophages responded to untested and SCF ascites in a dose-dependent fashion, with a multifold increase in both IL-1 beta and TNF-alpha messenger RNA (mRNA) and protein, which was often more potent than lipopolysaccharide. Expression of IL-1 beta and TNF-alpha mRNA could not be induced by trypsin, chymotrypsin, or cathepsin-B. All animals undergoing lavage with 100% SCF ascites died within 2 hours, while those undergoing lavage with 50% SCF ascites showed a multifold increase in pulmonary IL-1 beta and TNF-alpha mRNA. CONCLUSIONS: Pancreatic ascites contains factors that are capable of inducing IL-1 beta and TNF-alpha production in vitro and in vivo. This effect cannot be reproduced by activated digestive enzymes and is propagated despite the absence of known inducers of cytokines such as bacteria, endotoxin, or other inflammatory cytokines.

Animals↗

Interleukin-6 level in serum and ascites as a prognostic factor in patients with epithelial ovarian cancer.

BACKGROUND: Interleukin-6 (IL-6) is a multifunctional cytokine that can be produced by human ovarian cancer cells. Elevated IL-6 levels have been found in the serum and ascites of patients with ovarian cancer, but its role in this disease has not been clearly established. METHODS: The authors studied the relationship between IL-6 levels in serum and ascites, various tumor parameters, and survival in 70 patients with newly diagnosed, untreated epithelial ovarian cancer. Ascites and serum specimens were obtained at the time of initial surgery, and IL-6 levels were determined using the B9 bioassay. RESULTS: All patients underwent platinum-based chemotherapy after initial surgery. The median age of the group was 62 years (range, 28-87 years), and the median follow-up time was 13 months (range, 12-59 months). Significantly higher IL-6 levels were detected in patients' ascites (median, 49,612 pg/ml [range, < 1 to 680,330 pg/ml]) compared with serum (median, 10 pg/ml [range, < 1 to 1221 pg/ml]) (P < 0.0001). IL-6 levels in ascites correlated significantly with the volume of ascites (P < 0.0001) and nearly so with the size of tumor found at initial surgery (P = 0.05). Serum and ascites IL-6 levels did not correlate statistically with overall survival time, tumor stage, grade, histologic findings, residual tumor volume after debulking, and serum CA 125 levels. Although not statistically significant, patients who responded to chemotherapy tended to have lower ascites IL-6 levels (median, 21,102 pg/ml) compared with patients who did not respond to chemotherapy (median, 40,200 pg/ml). CONCLUSIONS: IL-6 is present in very high amounts in the ascites of patients with epithelial ovarian cancer. IL-6 levels in ascites correlated significantly with ascites volume and initial tumor size. IL-6 levels in ascites and serum did not correlate statistically with other tumor parameters or with survival time.

Adult↗

The pH of ascitic fluid in the diagnosis of spontaneous bacterial peritonitis in alcoholic cirrhosis.

Fifty-six patients with alcoholic cirrhosis and ascites were studied. The ascitic fluid was analyzed for pH, PO2, PCO2 glucose, protein, specific gravity, amylase, lactic dehydrogenase, white blood cell count, polymorphonuclear count, and cytology. It was also cultured aerobically and anaerobically. Simultaneously, arterial blood was analyzed for pH, PO2, and PCO2. Venous blood was analyzed for complete blood count, protein, aspartate transaminase, and it was also cultured under aerobic and anaerobic conditions. Six patients had spontaneous bacterial peritonitis (SBP), i.e., culture was positive for Escherichia coli in five and Streptococcus faecalis in one. The mean (+/- S.E.) ascitic fluid pH in the SBP group wa 7.25 +/- 0.06 with a range of 7.12 to 7.31, while the ascitic fluid pH in the group with sterile ascites was 7.47 +/- 0.07 with a range of 7.39 to 7.58. The pH of the blood in both groups was 7.47 +/- 0.03. The pH of the ascites in the SBP group was significantly different from the pH in the group with sterile ascites, p less than 0.001. It was also significantly different from the blood pH, p less than 0.001. Highly significant inverse correlations existed between the ascitic pH in the SBP group and the ascitic white blood cell count (r = 0.84, p less than 0.01) and between the ascite pH in the SBP group and the ascitic polymorphonuclear count (r = -0.87 ,p less than 0.01). The ascitic fluid pH is recommended as an easy, quick, sensitive, and specific means of diagnosing SBP and it overcomes the problem of the present SBP diagnostic methods of utilizing an absolute white blood cell count greater than 500 per mm3 or a polymorphonuclear count greater than 250 per mm3 in which false positive interpretations occur.

Adult↗

Bioelectrical impedance analysis is a useful bedside technique to assess malnutrition in cirrhotic patients with and without ascites.

Protein-calorie malnutrition is associated with poor prognosis in chronic liver disease, but reliable assessment is hampered by changes in body water. We prospectively evaluated the effect of fluid retention on bioelectrical impedance analysis (BIA) as a simple method for the estimation of body cell mass (BCM(BIA)) in 41 patients with cirrhosis (n = 20 with ascites; n = 21 without ascites) using total body potassium counting (BCM(TBP)) as a reference method. Arm muscle area and creatinine-derived lean body mass were compared with total body potassium data. In patients total body potassium was 24.4% lower than in controls and this loss was more severe in patients with ascites (-34.1%; P<.01). BCM(BIA) and BCM(TBP) were closely correlated in controls (r(2) =.87, P<.0001), patients without ascites (r(2) =.94, P <.0001) and patients with ascites (r(2) =.56, P<.0001). Removal of 6.2 +/- 3 L of ascites had only minor effects on BCM(BIA) (deviation of -0.18 kg/L ascites). Limits of agreement between both methods were wider in patients with ascites than in patients without (6.2 vs. 4.2 kg). In patients without ascites arm muscle area (r(2) =.64; P<.001) and lean body mass (r(2) =.55; P<.001) correlated significantly with total body potassium, but not in patients with ascites. For assessment of protein malnutrition in patients with cirrhosis, body cell mass determination by use of BIA offers a considerable advantage over other widely available but less accurate methods like anthropometry or the creatinine approach. Despite some limitations in patients with ascites, BIA is a reliable bedside tool for the determination of body cell mass in cirrhotic patients with and without ascites.

Adult↗

Pathogenesis of ascites in broilers raised at low altitude: aetiological considerations based on echocardiographic findings.

This study reports novel insight into the aetiology of pulmonary hypertension and ascites in broiler chickens. The scope of measurements was focused on anatomical and functional parameters, and blood flow patterns in leghorns (resistant to ascites), fast-growing broilers (susceptible to ascites), broilers developing ascites, and ascitic broilers evaluated in vivo using echocardiography, and further examined in the context of postmortem findings. Both, in vivo observed features and postmortem findings, showed clear differences between broilers and leghorns, and between normal and ascitic broilers. Abnormalities in the heart chamber geometry and blood flow patterns were detected upon echocardiographic examination in all ascitic broilers. Right and left atrio-ventricular (AV) valve regurgitation were common findings in ascitic broilers and some apparently normal broilers, with left AV valve insufficiency being a predominant feature with respect to degree and frequency of occurrence. Blood flow disturbances were not detected in leghorns. Left ventricular fractional shortening (functional parameter) was considerably reduced (P < 0.01) in ascitic birds (mean: 21.7 +/- 2.0 SE) in comparison with normal broilers (mean: 39.1 +/- 3.6 SE), or leghorns (mean: 43.3 +/- 2.4 SE). The presented findings indicate that pathological and functional changes in the left ventricle and atrium play a significant role in the pathogenesis of ascites in broilers. Severe dilation of the left atrium and pulmonary veins seen on postmortem examination, as well as regurgitant blood flow in the left atrium, demonstrated by Doppler study in ascitic birds, provide evidence that chronically elevated pressure in the left atrium is involved in the aetiology of pulmonary hypertension and ascites in fast-growing broilers.

Altitude↗

Cancer antigen 125: a sensitive marker of ascites in patients with liver cirrhosis.

OBJECTIVE: Cancer antigen 125 (CA 125) is a high molecular mass glycoprotein, usually used for monitoring the course of epithelial ovarian cancer. Recently it has been shown that liver cirrhosis is associated with increased levels of CA 125, particularly in the presence of ascites. The aim of this study was to evaluate CA 125 as a marker for the detection of ascites in patients with chronic liver disease. METHODS: A total of 170 patients were studied. All had ultrasound scanning for detection of ascites. Group I consisted of 123 patients with chronic liver disease without ascites; whereas group II consisted of 47 patients with chronic liver disease with ascites. CA 125 levels were measured in all patients and also simultaneously in the ascitic fluid of 31 patients from group II. RESULTS: Of 47 patients, 46 (97.8%) of group II had elevated serum levels of CA 125 (mean 321 +/- 283 U/ml) as compared with only nine of 123 (7.3%) patients of group I [mean 13 +/- 15 U/ml]), p < 0.001. The mean CA 125 concentration in the ascitic fluid of 31 cirrhotic patients (group II) was 624 +/- 397 U/ml and was always higher than corresponding serum levels (p < 0.01). Serum CA 125 levels correlated with the amount of ascitic fluid (r = 0.78). A profound decrease in serum CA 125 concentration was noted 2-3 and 10 days after large volume paracentesis. CA 125 was more sensitive and preceded ultrasonography in detection of ascites in few cirrhotic patients. CONCLUSIONS: CA 125 is a highly sensitive marker to detect ascites in patients with liver cirrhosis. This marker may be useful to detect small to moderate amounts of ascitic fluid in cirrhotic patients when physical examination is difficult or equivocal for ascites.

Adult↗